Social anxiety disorder (SAD) is a very common psychiatric disorder. The lifetime prevalence, or in other words, the proportion of a population that at some point in their life has experienced symptoms of social anxiety disorder is 6,7% in Europe and 12,1% in the USA. Symptoms of social anxiety disorder can have a big impact on someone’s life and are related to outcomes such as poor social functioning, poor adjustment at work, lower levels of academic and professional achievement, lower quality of life and high levels of comorbidity with other mental disorders. Comorbidity means that someone with social anxiety disorder also often has another disorder, for example depression.
Even “subthreshold” or “subclinical” social anxiety, which means that someone experiences symptoms of social anxiety disorder, but not enough to be diagnosed with the disorder, can have a big impact on someone’s life. In the general population, 20% of the people report subclinical symptoms of social anxiety.
Social anxiety has different effects. For instance, the subjective experience of a person during social interactions is often characterized by high negative affect and low self-efficacy or feelings of inferiority. It is also often seen that social anxiety leads to increased self-focused attention and negative interpretation biases during social situations. It may also be the case that both social anxiety disorder and subclinical social anxiety symptoms go together with altered biological reactivity to stress. Some studies have suggested that the hypothalamic-pituitary-adrenal (HPA) axis, a biological stress response system, may be dysregulated in people with anxiety disorders. A dysregulated HPA axis may also cause medical health problems and could be the cause of the high comorbidity of social anxiety disorder with other medical conditions.
There is limited information about the relationship between cortisol levels and the severity of social anxiety symptoms. This study looked at multidimensional responses to social stress. Social stress was induced by means of the Trier Social Stress Test (TSST). This is a widely used procedure that triggers cortisol responses by combining elements of uncontrollability and social-evaluative threat. There was also controlled for the menstrual cycle phase and oral contraceptives, because these are known to influence the cortisol reactivity in the Trier Social Stress Test. Previous studies showed that social anxiety is linked to altered responses under stress. Therefore, in this study, there was looked at new associations between HPA axis reactivity to stress and ratings of behavioral anxiety and cognitive biases that are central to social anxiety disorder.
Participants
There were 262 participants who filled in the Liebowitz Social Anxiety Scale (LSAS-SR). Only the participants who scored over 30, had no anxiety and mood disorders, were free of HPA-related medical conditions and, in the case of women, had a regular menstrual cycle, were included. Therefore, only 52 out of 262 participants were included in de final sample. These were people with increased social anxiety symptoms.
Social anxiety symptoms
The Liebowitz Social Anxiety Scale consists of 24 items or questions. It measures fear and avoidance of social situations. However, this was a self-report version of an otherwise clinical test.
State Anxiety
State anxiety can be defined as a transitory emotional state consisting of feelings of apprehension, nervousness and physiological sequelae such as an increased heart rate or respiration.
Speech Anxiety Behaviors
The participants’ speech performance during the Trier Social Stress Test was assessed by three evaluators. These evaluators made use of the Behavioral Assessment of Speech Anxiety (BASA). With the help of BASA, the speech of the participants is evaluated on six behavioral categories: voice, verbal fluency, mouth and throat, facial expression, arms and hands, and gross bodily movements. Each category contains a specific behavior. For example, for the category ‘voice’, a specific behavior could be: quivering or tense voice, talking too fast, talking too soft, and monotonous or lack of emphasis. Each evaluator watched a video of the participant and scored the BASA items on a 10-point scale which indicates the severity of anxiety. This rating is based on both the frequency and the intensity of a particular behavior. So, three independent ratings for each of the six behaviors was reached.
Cognitive biases
To assess cognitive biases, the probability and cost of negative evaluation scale was used. This means that participants were asked about how high the likelihood is that their Trier Social Stress Test performance will be evaluated negatively. So, a statement could be: “The raters will think you are incompetent”. These items would then be rated by the participant on a 5-point scale.
Out of this study, it became clear that the intensity of social anxiety symptoms was positively associated with self-reported state anxiety and cognitive biases to negative social evaluations. Several observable anxiety behaviors as seen in the Trier Social Stress Test were also positively correlated with social anxiety symptoms, but only the correlation with facial expression was significant after adjusting for multiple comparisons. Cortisol reactivity was negatively associated with the severity of social anxiety symptoms. So, reduced cortisol may be a risk factor for socially anxious individuals. Reduced cortisol may be the result of chronic stress. In people with social anxiety, their inability to adapt to social situations could lead to allostatic load and reduced cortisol reactivity. Allostatic load is defined as the cost of chronic exposure to elevated or fluctuating endocrine or neural responses resulting from chronic or repeated challenges that the individual experiences as stressful. So, in the case of social anxiety symptoms, it could be that lower cortisol reactivity leads to an inappropriate energy supply during social situations, which lead to that socially anxious individuals are unable to adapt and are susceptible to poor performance. This can in turn lead to cognitive biases. The reduced cortisol reactivity may also lead to increases comorbidity with medical problems.
An alternative explanation for the lower cortisol reactivity is that it is a way of coping in the form of disengagement from social settings which involve possible negative evaluations or social rejection. This idea fits the recently developed model of protective inhibition: the protective inhibition of self-regulation and motivation (PRISM). The PRISM states that during social situations that lead to hyperarousal (a lot of stress) or which allow for disengagement coping, social anxiety is linked to decreased cortisol. This is then seen as a protective disengagement mechanism against extremely high emotional arousal. In this study, the participants who were hypo responders for cortisol (so, they showed a lower reactivity to cortisol), scored higher on measures of arousal.
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