by Amaya Patel
art by Kai Do
Dear (Gentle) Reader, I'd like to start by painting a picture for you. For some, this may be fresher in your memory than for others. I would like you to dig through these memories and reflect on your first day of college, the herds of people walking in, the possibility of so many new friends but also the anxiousness of not knowing them at all. A crowd that was supposedly your home but completely unfamiliar, how did you feel?
For every one in five college students who struggle with social anxiety, these weeks can be especially challenging. The prevalence of social anxiety can hinder college students’ education by isolating them from study groups or more generally, from connections with their peers. Social anxiety disorder (SAD) is defined as an intense fear of being judged, negatively evaluated, or rejected in a social or performance situation [1]. It is crucial to keep in mind that both biological processes and sociocultural factors influence the prevalence of SAD. This disorder was first recognized by the Diagnostic and Statistical Manual of Mental Disorders (DSM) in 1980 [1, 2]. Since then, the idea that social anxiety primarily arises from developmental experience—such as those encountered during childhood and adolescence—has been researched and discussed in connection with biological factors. To put it simply, with respect to SAD the relationship between nature and nurture, it is not either or, but instead a codependent relationship.
The Nature Perspective
Immanuel Kant says, “Science is a beautiful gift to humanity; we should not distort it.”
The complexity of the nurture-nature relationship is entangled by the fact that most psychological and social factors above are also represented by biological processes within our neural circuits. These biological processes associated with SAD are mainly observed in the amygdala. The amygdala is a part of the limbic system, which is involved in processing emotionally striking external stimuli and initiating the appropriate behavioral response—usually fight, flight, or fear [19].
In 2020, Suor and her lab conducted a study measuring the differences in amygdala volume between participants with SAD, healthy controls, and comorbid conditions (groups diagnosed with more than one condition [3]. Participants were assessed for SAD using the Liebowitz Social Anxiety Scale, a tool that measures the severity of SAD symptoms by assessing fear of social behavior and avoidance of those behaviors, alongside other scales [4, 5]. MRI scans, a non-invasive imaging technique used to show detailed internal structures of the human body, were then conducted on all the participants [3, 9]. The results showed that the SAD and comorbid groups exhibited larger right and left amygdala volumes than the healthy participants. However, the same difference was not shown in participants with generalized anxiety disorder in comparison to healthy participants.
Now, why is it relevant that the amygdala in SAD participants is larger?
This data is relevant because it shows that SAD is not purely driven by emotions but also built up through physical aspects. The larger amygdalas in SAD patients are also indicative that the amygdala is being overactivated in these participants. Neurologically, this occurs when a certain brain region is overactivated by the constant firing of action potentials and frequent use of neural pathways [3, 6]. This overactivation can trigger neurogenesis (an increase in neurons) and dendritic branching (extension of dendrites to form larger networks), which can lead to the area growing in size [7].
The physical size of the amygdala, however, is not the only aspect influenced by SAD. The activity of this brain region is also influenced, which is researched using functional magnetic resonance imaging (fMRI) scans. It is a research method of tracking blood flow to certain brain regions as a subject executes a cognitive function. fMRI scans in the
experiments I will be discussing are used to show differences in activity between certain brain regions and the amygdala [8, 9]. Many researchers use the stimulus of “fearful faces,” or images of faces that represent sadness or anger, to elicit activity in the amygdala and other brain regions associated with SAD, such as the prefrontal cortex (PFC) [10, 11]. The PFC is the region signaled by the amygdala when a fear circuitry is sparked. It is the higher-order association center of the brain, which is mainly responsible for higher levels of processing and thinking, primarily centered around goal-directed behavior. The PFC, specifically the ventromedial prefrontal cortex, plays a crucial part in associating fearful faces with the emotions of fear and anxiety. Research has shown that the ventromedial prefrontal cortex is largely activated when participants with social anxiety disorder see ‘fearful faces’ [12]. However, repeated exposure to these faces may cause habituation, reducing activation. Habituation refers to the reduced responsiveness to a stimulus upon repeated exposure to the stimulus over time. When researchers use habituation, they are desensitizing the participant to the stimulus, which may reduce the firing of action potentials and a diminished excitatory response [13]. This leads to an overall less dramatic/shocked reaction to the stimulus. This is related to the PFC and the amygdala, as during habituation, the PFC suppresses the amygdala to diminish the sparking of the fear circuitry. This is used as a common research method in experiments [14]. For example, imagine that you go to the same haunted house every year. The pop-out ghosts/axe murderers that scare you the first time trigger a less intense fear response when you go the next year and the year after that, as you have become habituated to the stimuli of the haunted house pop-outs. In SAD experiments, habituation can be a risk. If the participants have been overexposed to the stimuli, their responses may be invalid for what the researchers are testing [15].
Looking beyond our current scope, exploring the possibility of a larger amygdala as a biomarker for SAD could be key to the field of diagnosis. By examining patterns of increased amygdala volume, researchers could determine if they are a biomarker for SAD, a correlation, or a consequence that follows the disorder [3].
Shifting to functional measures of SAD, spikes of neuronal activity in the brain can be measured during socially anxious behaviors [9]. Recent studies of fMRI have highlighted strong correlations between highly active brain regions, regions receiving the most electrical synaptic flows and blood, and the presentation of social anxiety symptoms [6, 16]. The study sampled 22 participants: 11 diagnosed with SAD by the Liebowitz scale (for social anxiety score and 11 healthy controls.) The researchers concluded that fMRI results using angry
faces compared to neutral faces showed hyperactivity in the amygdala within the SAD group compared with the healthy controls [2,16].
While sufficient evidence supports hyperactivity in the amygdala as the primary brain pattern shown during a response involving social anxiety, other regions exhibiting less brain activity may also play a role [12]. Ultimately, these results indicate that other regions of the limbic area may also be associated with social anxiety disorder and that it may not be solely associated with the amygdala but within the wider limbic area.
The amygdala assigns positive and negative associations to situations, therefore the nurture aspect is intertwined with nature. In simpler terms, this means that when we process a situation, our brains draw on past experiences to categorize the situation as either leading to beneficial or unpleasant outcomes, resulting in comfort or discomfort. For example, if you were to see a student being bullied, your amygdala would categorise that as a negative situation. This categorisation of negative and positive association is known as valence and is necessary for our survival in this world as it helps us perceive danger and form relationships [17]. You must be wondering, how is this relevant to social anxiety disorder (SAD), and furthermore to the nurture perspective? This biological relationship between the amygdala and attribution of valence establishes the interconnectedness of biological and socio-cultural factors with regards to SAD. This is because participants with SAD tend to be more sensitive to negative valence and tend to predict less positive valence i.e., these individuals may tend to downplay how positive a situation is and overplay how negative a situation is [17]. Therefore, the biological aspect of the amygdala being responsible for this and SAD is tied in with the socio-cultural aspect of the self-fulfilling policy––the propagation of an already false negative state of mind based on individual emotions and societal expectations––and sensitivity to negative valence in SAD associated with fear of social exclusion [18, 19].
The Nurture Perspective
How are sociocultural factors associated with social anxiety disorder?
At one point or another, we have all felt lonely, even when surrounded by people. How can we feel so isolated even around lively crowds? It could be that we lack shared values and morals, or the crucial elements of a deep friendship. But how do we know if we are uncomfortable because of ourselves or the people we are surrounded by? A study conducted on the occurrence of anxiety and depression in individuals who were bullied revealed that these individuals reported higher levels of depression and anxiety compared to their counterparts, as well as lower self-esteem [20, 21].
Various environmental conditions and experiences can alter how our neural circuits develop and function over time [6, 7, 22]. Another study conducted by Carolein J.W.H. Brujien examined the effects of childhood trauma on the release of cortisol, a hormone released through the bloodstream [23]. Cortisol, which provides people with the energy required to counter a stress response, is released when they are put in stress-inducing situations [23, 24]. The amount of cortisol released depends on the individual. Some individuals can have an exaggerated response, while others have a more blunted response. For those who experience exaggerated responses, more cortisol is secreted, making it more challenging for normal levels to be re-established. Linking the biological explanation behind cortisol activity to Carolein’s research, individuals with childhood trauma demonstrate desensitised cortical reactivity associated with trauma behaviour. This has been further supported by work showing that stressful experiences affect key stress mediating systems [25].
Desensitization is commonly associated with “avoidance behaviors,” due to the stress-response involved, which are in turn highly indicative of SAD [8, 23]. Avoidance behaviors are maladaptive behavioral responses to excessive fear and anxiety; these contribute largely to SAD [8]. These avoidance behaviors can be emotional or social, and both have the commonality of individual dissociation from the people around us. This is highly linked with SAD, as social avoidance behavior involves the avoidance of others and isolation from the social world altogether [20]. Carolien and researchers assessed participants for childhood trauma through three metrics: neuro psychiatric interviews, therapist referrals, and guidelines from The Diagnostic and Statistical Manual of Mental Illnesses (DSM-5), which is used as the main way of diagnosing mental health disorders and conditions [26, 2]. These participants were then assessed for SAD. Results showed that “the severity of SAD symptoms was significantly correlated with the level of reported childhood trauma” [26]. Therefore, childhood trauma, resulting in desensitization of cortisol activity, is linked with SAD. This evidence supporting the neurological connection of cortisol activity with childhood trauma highlights the complexity of the neuro-sociological nature of SAD.
Interestingly, simply thinking you are under medication or treatment for SAD can relieve your symptoms of this disorder. This is known as the placebo effect––a phenomenon where a person’s physical or mental health appears to improve after a change in mindset under false pretenses—and is associated with the treatment of social anxiety disorder [27, 28]. The placebo effect is prevalent in our daily lives. Imagine you have just bought a new pair of running shoes, and you feel like you’re running on air or that you are now able to run quicker. Research has shown that the placebo effect has had statistically significant effects in alleviating symptoms of SAD [28, 29]. The study compared active drug treatment with placebo treatment to test if an inactive substance is an alternative option for the treatment of SAD [28]. This research shows us that non-medical treatments indeed exist for SAD, however, it doesn’t mean that taking a placebo pill before public speaking is the only non-
medical way to alleviate SAD symptoms. Other psychotherapies also exist, such as exposure-based cognitive behavioral therapy, where you gradually face the situations that you fear [8]. For example, this could be approaching a group of three people you have never met before, in a group of people you know, and then the next week approaching more new people. The effectiveness of these nature-based therapies in alleviating symptoms of SAD highlights the nurture perspective, specifically that socio-cultural factors heavily influence the occurrence of SAD. However, this support from the nurture perspective is not indicative of an either/or relationship. These phenomena have been largely viewed as psychological, socio-cultural paradigms that remain largely connected to neurochemical processes.
So, what threads connect this research and article to our own experiences? It proposes that SAD is a biopsychosocial phenomenon and not simply rooted in nurture: our life events
and experiences are not its sole influences. The biopsychosocial approach provides a more holistic view of SAD and the multiple factors that contribute to its occurrence. The ratio between nature and nurture is specific to each individual, but acknowledging both sides of this spectrum is integral in diagnosing and treating this disorder. This proposes the idea of a cyclical relationship between the socio-cultural and biological factors of SAD. Both the amygdala and SAD affect each other: changes in social behavior may cause hyperactivity in the amygdala, or the amygdala may be prone to hyperactivity due to the presence of SAD. In other words, nature and nurture are codependent in forming the roots of SAD.
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