Anxiety Disorders

Anxiety disorders are the most common class of mental disorders with an estimated 12-month prevalence of 18.1% in the population.[1] . Among them, social anxiety disorder (SAD), also defined as social phobia, is characterized by fear and avoidance of oneself under the supervision of others.[2] It is a condition involving significant anxiety about performance and social situations. The lifetime rate is 12% and the annual prevalence is 7% of the population[3] . Individuals may experience anxiety when they have social anxiety disorder, and their behavior may result in embarrassment and humiliation. As a result of overt anxiety, individuals avoid or endure interpersonal encounters with severe discomfort.[2] . Individuals with social anxiety disorder have a basic notion that other people have a negative evaluation of them. Because of this core maladaptive belief, they have some difficulty interacting with a range of social activations, such as eating or typing in a crowded place, starting or maintaining a conversation, attending parties, dating, meeting strangers, or communicating with authority figures.[4] . As a result, their functionality in daily life is negatively affected and their behavior in the social environment is restricted. of DSM-V[5] Several changes have been made to the definition of SAB with its publication. Individuals with SAD typically have multiple social fears and social disorders, but some individuals may simply be afraid of public speaking or performing. In addition to humiliation and embarrassment, other consequences such as rejection by others in the social environment occur in SAD.

Epidemiological studies have shown that SAD is commonly associated with other psychiatric disorders such as depression, substance abuse, and other anxiety disorders [6,7]. Moreover, SAD starts earlier than many other mental disorders.[1]and its association with anxiety risk factors such as behavioral inhibition[8] indicates a significant psychological disorder. This condition requires treatment.

Risk Factors in the Development and Course of Social Anxiety Disorder

Various risk factors including familial factors, conditioning events, temperament factor and cognitive factors have been associated with the development and course of SAD.

Familial Factors

Familial studies have shown that first-degree relatives of patients with SAD are three times more affected than relatives of control subjects [9,10]. First-degree relatives of 129 SAD patients were evaluated by applying interview and family history methodologies. Their findings showed that relatives of general SAD patients had a three-fold higher rate than patients with the non-generalized subtype. In parallel with these results, it was found that the relatives of SAD patients were significantly higher than the families of other anxiety disorders. On the other hand, Stein et al. (1998) evaluated 106 first-degree relatives of 23 patients with generalized SAD using direct interview methodology. In this study, the risk ratio for general SAD was 9.7 in patient relatives compared to control subjects, but there was no significant difference in non-generalized SAD.[11] . Although all these studies confirm the familial background in SAD occurrences, they show that differences in risk ratios may occur due to methodological differences such as different assessment methods. Larger studies using more standard methodologies are needed.

When parenting practices are taken into account, higher parental rejection and higher parental overprotection have been shown to increase rates of SAD in children. If the parents have psychopathology, the relationship between parental rejection and SAD formation in adolescents was found to be higher.[12] . Additionally, Bruch (1989) showed that children who experience criticism and rejection are more likely to have SAD later in life through fear of negative evaluation and avoidance of social scrutiny.[13].

The family environment can also affect adolescents’ perceptions and promote social anxiety. Caster, Inderbitzen, and Hope (1999) found that adolescents reporting higher levels of social anxiety had different perceptions of their family environment than adolescents with lower levels of social anxiety. However, parents of adolescents with higher social anxiety did not perceive their families as different from parents of adolescents with lower social anxiety. In addition, the high social anxiety group perceived their parents as more socially isolated and less socially active compared to the low social anxiety group.[14].

Conditioning Events

Traumatic social conditioning experiences and shyness have been shown to be risk factors in the development of SAD.[15] . Repetitive and cumulative experiences, such as rejection by peers, can lead to the development of fear in social interactions or scrutiny.[15] . In addition, studies show that shy adolescents and shy adults have unpleasant experiences with their peers.[16]and children neglected by their peers show higher SAD and fear of negative evaluation.[17] has shown. Consequently, both neglect and unpleasant experiences with peers may have an interactive relationship in the emergence of SAD.

Temperament Factors

Behavioral inhibition of the unknown (DI) is a hypothesis that suggests that behavioral responses to strangeness, threat, or challenge occur due to tonic differences in threshold reactivity in the amygdala and hypothalamus, parts of the limbic lobe. Children of different ages have different physiological responses to strangers. For example, increased urinary 3-methoxy-4-hydroxy phenylglycol between the ages of 4 and 5.5 in children and an increase in morning salivary cortisol at baseline between the ages of 5.5 and 7.5 years were observed in children, and these events are regulated by limbic-hypothalamic stimulation.[18] . In addition, Calkins, Fox, and Marshall (1996) examined the physiological and behavioral antecedents of uninhibited and inhibited behavior in 9-10 month old infants.[19] . Their findings showed a frontal activation pattern and asymmetry in brain activation in highly reactive and inhibited infants. It has been previously shown that differences in preactivation in infants are distressing after brief maternal separation. In line with these data, hypoactivation in the left frontal region increased the development of SAD and depression in adults, and similar differences were found in the brains of these individuals.[20] . On the other hand, several studies have linked DI occurring in children with the development of SAD. For example, early maternally reported DI has been shown to increase the lifetime probability of SAD occurrence in adolescence by approximately four times.[21] . In a meta-analytical study, it was shown that BI was associated with more than seven-fold higher occurrences of SAD and the largest single risk factors for the development of SAD.[22] . These results show that BI is associated with the development of SAD in children, adolescents, and adults.

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