“To avoid criticism, do nothing, say nothing, be nothing.” – Elbert Hubbard

Social anxiety disorder (SAD), also known as social phobia, is a disorder in which an individual experiences excessive and unreasonable fear of social situations, most often arising from fear of being closely watched, judged, or criticized by others [1]. It is one of the most common types of anxiety disorders, affecting roughly 8% of the population at some point in their life [2].

Treatment plans for chronic and severe SAD typically include anti-anxiety medication, most of which are selective serotonin reuptake inhibitors (SSRIs) [3]. These are one of the most prescribed medications and are known to treat both anxiety and depression [4].

According to the well-known “chemical imbalance” theory, depression and anxiety are due to low serotonin levels in the brain [5]. Serotonin is usually described as being the “happiness molecule” within the brain. Thus, it would make sense that low levels are attributed to low mood, whereas higher levels can correspond with an elevated mood. SSRIs are designed to improve mood by preventing serotonin reuptake in the brain, thus increasing the amount of serotonin available for brain cells to communicate with [6].

More recent findings, however, suggest that this widely accepted chemical imbalance theory may be wrong, and that we might actually have it backwards. A recent study by Andreas Frick and colleagues, published in the journal JAMA Psychiatry, found that SAD is actually linked with higher than usual levels of serotonin in the brain [7].

Frick and colleagues used positron emission tomography (PET), which is a brain imaging method that injects a radioactive tracer molecule into the bloodstream and tracks how this molecule is processed within the brain. In this study, they radioactively labelled the serotonin molecule “5-HT”, making it traceable, and monitored its levels in the brain’s fear centre. An elevated level of 5-HT was found in this brain region in individuals with SAD, as compared to control subjects who did not have SAD. The researchers concluded that there is an overactive serotonin synthesis system present in those with SAD. More serotonin in the brain’s fear region intensifies anxiety [8].

These findings have caused quite a bit of confusion amongst researchers and pharmacologists, as it seems counterintuitive to treat something by exacerbating the very thing that could be responsible for it.

However, a meta-analysis conducted by G.J. Linden and colleagues in 2000 on the efficacy of SSRIs for SAD, which was published in the Journal International Clinical Psychopharmacology, concluded “with a high degree of confidence that SSRI treatment for SAD is effective, both in reducing levels of social anxiety and in improving patient’s overall clinical condition” [9]. An even more recent meta-analysis and systematic review conducted in 2014 by Evan Mayo-Wilson and colleagues, published in The Lancet Psychiatry, stated that SSRIs show the most consistent evidence of benefit for those with social anxiety, second only to treatment through cognitive behavioral therapy [10].

So how can SSRIs be effective in treating SAD, if high serotonin levels are possible risk factors for SAD onset?

Tomas Furmark, who worked alongside Frick on the study, reports that “SSRIs are effective for anxiety disorders, including social anxiety disorder. However, the exact mechanism whereby SSRIs exert their anxiety reducing effects is still not known” [8].

The take home message here is that the brain is complex beyond belief.

When talking about how brain activity is influenced by psychopharmacological agents, there is a process known as a “cascade”, in which one event that takes place leads to a divergent domino effect of other brain events. Maybe SSRIs could be effective in such a way that serotonin interacts with other brain molecules in other regions of the brain previously not thought to be involved in influencing anxiety. Either way, it should be noted that these findings that suggest SAD corresponds with an overactive serotonin system, come from one single study. There have been countless other studies supporting the clinical efficacy of SSRIs when used to treat social anxiety disorder, and so these more recent findings should be taken with a grain of salt.

Further investigation delving into the role of serotonin on the brain’s functioning, and thus, the manifestation of abnormal behaviours and feelings, needs to be conducted. Is serotonin really just a “happiness molecule”? The chemicals in the human brain may be more complex than we thought, which is important to consider when treating mental illnesses that affect a person’s day-to-day functioning.


By: Christina Gizzo

Edited by: Veerpal Bambrah

Image by: Alexa Battler




[1] WebMD. (2015). Anxiety and Panic Disorders Guide. Retrieved from:


[2] Canadian Mental Health Association. (2013). Social Anxiety Disorder. Retrieved from:


[3] WebMD. (2015). Anxiety and Panic Disorders Related Topics. Retrieved from:


[4] WebMD. (2015). Depression Health Center. Retrieved from:


[5] Mercola.com. (2015). Social Anxiety Disorder Linked to High Serotonin Levels, Throwing Treatment with SSRIs into Serious Question. Retrieved from:


[6] Mayoclinic. (2015). SSRIs. Retrieved from:


[7] Frick, A., Åhs, F., Engman, J., Jonasson, M., Alaie, I., Björkstrand, J., … Furmark, T. (2015) Serotonin Synthesis and Reuptake in Social Anxiety Disorder: A Positron Emission Tomography Study. JAMA Psychiatry, 72(8), 794-802.   

[8] Forbes. (2015). Pharma & Healthcare. Retrieved from:


[9] van der Linden, G. J., Stein, D. J., van Balkom, A. J. (2000) The efficacy of the selective serotonin reuptake inhibitors for social anxiety disorder (social phobia): a meta-analysis of randomized controlled trials. Int Clin Psychopharmacol., 15(2), 15-23.

[10] Mayo-Wilson, E., Dias, S., Mavranezouli, I., Kew, K., Clark, D. M., Ades, A. E., Pilling, S. (2014) Psychological and pharmacological interventions for social anxiety disorder in adults: a systematic review and network meta-analysis. The Lancet Psychiatry, 1(5), 368-376.

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