Social Anxiety Help is a founding regional clinic of the National Social Anxiety Center (NSAC):
by Lata K. McGinn
Ferkauf Graduate School of Psychology, Yeshiva University;
Michelle G. Newman
The Pennsylvania State University
[Note: this article is excerpted for public educational purposes from the International Journal of Cognitive Therapy, volume 6, number 2, June 2013. All references and footnotes, some 200 in total, have been removed. This is a publication of the International Association for Cognitive Psychotherapy (IACP). To learn more about and to join this organization, visit www.the-iacp.com. To order the complete version of this article and to subscribe to this journal, see www.guilford.com/ijct.]
Although descriptions of social anxiety date back to ancient times, the modern description of the syndrome was first provided in the 1970s. Social phobia became part of the diagnostic nomenclature with the third edition of the Diagnostic and Statistical Manual (DSM-III; American Psychiatric Association, 1980). However, revisions of the DSM indicate that the more common clinical presentation consists of a pattern of fear and avoidance across a wide range of situations.
Approximately 20-40% of nonclinical samples report feeling shy, which suggests that social anxiety is on a continuum of severity within the general population, with Social Anxiety Disorder (SAD) toward one extreme of this continuum. The characteristic symptoms of SAD include an intense and unremitting fear of social or performance situations in which individuals are in the presence of people unacquainted to them and/or are being examined by others. The overriding concern is that they will be negatively evaluated by other people and will show visible symptoms of anxiety and/or behave in a way that will cause them to be embarrassed or humiliated.
Individuals with SAD often have negative beliefs about themselves (e.g., thoughts of inadequacy, inferiority) and tend to be excessively self-focused during social interactions. Common physical symptoms include anxiety; blushing, heart palpitations, trembling, sweating, muscle tension, stomach pain, dry throat, hot or cold flashes, and headaches. Anxiety may reach the level of a full-blown panic attack in some cases. Common situations feared by individuals with SAD include public speaking, formal or informal social gatherings, meeting new people, making small talk, eating or writing in public, using public restrooms, disagreeing with others or asserting themselves, and speaking to authority figures. The underlying concern is typically that of being negatively evaluated or doing something embarrassing or humiliating. Individuals either avoid or escape the feared situation or tolerate it with extreme discomfort. Trigger situations may be hierarchically arranged, as some individuals fear specific situations like public speaking on one end of the severity continuum, whereas others have broad-based fears, such as the possibility of being evaluated negatively by others.
To meet diagnostic criteria, individuals must recognize that their fears are excessive or unreasonable and they must invariably feel anxious in social or performance situations. Also, the social avoidance or distress must interfere significantly with individuals' daily routine or functioning or they must experience extreme distress about their symptoms. The majority of individuals fear two or more social situations. Nonetheless, the DSM has specified two subtypes since its third edition: a fear of a discrete social situation such as public speaking (specific subtype) and broad based fears of social contact (generalized subtype).
Although inclusion in the DSM has raised awareness of severe social anxiety; several problems still exist, such as a lack of clear boundaries between normal and pathological social anxiety; lack of criteria defining the generalized subtype and the high degree of overlap between the generalized subtype and avoidant personality disorder. As discussed below, some of these issues have been addressed in the proposed revisions for the DSM-5.
A number of proposed changes for DSM-5 have been made based on empirical evidence in an attempt to correct prior problems. For example, given the continued difficulty in determining the boundaries between normal and pathological social anxiety, the term marked has been operationalized as intense. Other changes include more prominence for the fear of showing anxiety symptoms, a focus on three types of fears (observation, performance, and interaction), placing humiliation or embarrassment under the umbrella of negative evaluation, and operationalizing the term excessive or unreasonable as meaning "out of proportion to the danger posed." The DSM notes that the clinician is in a better position than the client to determine if fear is excessive or unreasonable, as most clients do not feel their fears are excessive or unreasonable.
A new criterion has also been added, which is that the symptoms SAD should last at least six months, although there is a caveat to not apply this criterion too rigidly. Also, it has been proposed that the DSM-IV (American Psychiatric Association, 2000) exclusion of social fears or avoidance associated with medical conditions be removed based on research showing that such fears can be treated in the same way as other social anxieties. Also, data regarding the prior specifier of generalized versus specific SAD suggests that these subgroups simply represent a continuum of severity and therefore these subtypes have been replaced with performance only in circumstances where this is the individual’s only fear. For the latter subtype, there appears to be some evidence suggesting that those whose fears are solely around performance are qualitatively different than those who fear other types of interpersonal situations. The DSM workgroup concluded that there is sufficient evidence that avoidant personality disorder is a separate diagnostic category, and that more research is needed before merging the two. Finally, the official designation of social phobia has been made a secondary label to SAD (with social phobia in parentheses) as social phobia seems more like a specific phobia and SAD connotes broader and more diverse fears.
The national comorbidity replication study showed that SAD was the most common anxiety disorder and the fourth most common psychiatric disorder in the United States. The prevalence of SAD varies considerably, ranging from 3-14% in Western populations. Twelve-month prevalence rates also vary from 1.2-7.1%. Although methodological and procedural differences may account for some of the dissimilarities observed, it is noteworthy that the prevalence in the U.S. consistently seems to be higher than the prevalence observed in European countries. This discrepancy has been attributed to differences in assessment tools used, number of social situations probed, and language. However, it could also be due to a lower tolerance for social inhibition in the U.S. than elsewhere. Writers have documented the rise of the extrovert ideal in the U.S. beginning in the twentieth century and research shows a corresponding increase in the rates of SAD in younger cohorts in the U.S.
Other countries, especially those in Southeast Asia, also show markedly lower rates of SAD in comparison to the U.S.. Again, these results may be due to a greater acceptance for social inhibition in these countries as proposed here, but may also be the result of language and methodological differences or of the fact that symptoms in the East are captured by other culturally syntonic expressions such as taijin kyofusho (a fear of causing offense to others).
SAD is more common in women than men, as the 12-month prevalence rates in the U.S. range from 1.5-3.4% among women and 0.9-2.1% among males. The National Epidemiologic Sample on Alcohol and Related Conditions reports lifetime prevalence of 5.67% among women and 4.2% among males. Although female adolescents and adults are far more likely than their male counterparts to suffer from SAD, boys and girls below age 5 appear to present with similar rates. The growing gender discrepancy as individuals get older may indicate that cultural factors influence the expression of SAD. Shyness and withdrawn behaviors are less permissive in men across most cultures. In males, such behavior is typically perceived more negatively by parents, and is associated with more problems and functional impairment.
AGE OF ONSET
SAD typically begins in childhood or adolescence, and rarely after 25 years of age. The mean age of onset is 15.1 years with individuals often reporting a history of shyness or behavioral inhibition in early childhood. However, closer examination of the Epidemiological Catchment Area study data shows a bimodal distribution of age of onset with the first peak occurring before 5 years of age and a second peak occurring around 13 years old.
COURSE AND IMPAIRMENT OF UNTREATED SYMPTOMS
SAD may become chronic and unremitting if left untreated, and is associated with significant functional impairment. Those who have 3 or more social fears are more impaired, more likely to have comorbid disorders including alcohol abuse and depression, and may have a poorer treatment outcome. Individuals with comorbid disorders, and in particular comorbid mood disorders, are more likely to take medications to control their symptoms, and are more likely to attempt suicide. Although individuals with SAD may recover without treatment, they may also suffer for years. The costs of SAD to both the individual and society are tremendous. Individuals with SAD are unable to effectively fulfill social roles and work obligations, are more likely to be under-educated, Native American, have a low SES [socio-economic status], and are more likely be single, separated, or divorced.
Over 46% percent of people with SAD also meet criteria for another disorder. Some studies show even higher rates of comorbidity, with rates ranging from 70-80%. However, SAD onset tends to precede the onset of other disorders. Between 45 to 56% meet criteria for a comorbid anxiety or mood disorder with specific phobia (37.3%), generalized anxiety disorder (17.3%), and panic disorder (15.3%), being the most common. Thirty eight percent meet criteria for a mood disorder alone (lifetime rates 56%) with 20%, 13.2%, and 6.6% presenting with major depression, bipolar I, and dysthymia, respectively. Thirteen percent have comorbid alcohol abuse or dependence. Individuals with SAD also have an increased prevalence of comorbid personality disorders (61%), with obsessive-compulsive (33.1%), avoidant (30.3%), paranoid (28.7%), schizoid (21.2%), antisocial (10.8%), and dependent personality disorders (5.6%) among the most common. However, Avoidant Personality Disorder (APD) is the most common personality disorder (61%) and APD reduces the likelihood of remission from SAD.
Several models have been proposed to account for the development and maintenance of SAD. These models differ in the degree to which they emphasize hardwired (ethology, genetics, temperament, neurobiology) versus psychosocial factors (life events, parenting styles and interactions, peer relations, cognitive and behavioral models). However, recent formulations emphasize a multifaceted approach to understand who eventually goes on to develop clinical symptoms and how their symptoms are maintained.
Evolutionary theories suggest that we may be biologically prepared to acquire social fears and that social fears may have evolved as a by-product of dominance hierarchies wherein defeated primates typically displayed fear and submissive behaviors to avoid conflict against dominant primates. In support of the notion that social anxiety may have been evolutionarily adaptive, social anxiety is normative across species and characteristic SAD behaviors (e.g., blushing, averting gaze) are similar to primate appeasement displays in dominance hierarchy situations. Hence, social fears and coping responses in humans are seen as adaptive for inhibiting behaviors that are likely to lead to social exclusion or conflict. A keen sensitivity to social disapproval, which may be adaptive in certain situations, may just be exaggerated and/ or distorted in those that develop social phobia.
Hence, from an evolutionary perspective, SAD along with other anxiety disorders may represent an instance of evolution gone askew. Anxiety disorders may arise from a cultural misalliance between our biological nature and the current environment. Situations that were inherently dangerous for our primitive ancestors are no longer usually dangerous, and consequently pathological anxiety may be an “over-responsive, culturally maladaptive mechanism rather than a qualitatively different disease entity” as presently classified in the DSM [according to Stefan Hofmann, PhD].
Although some coping responses may still be adaptive in situations in which there is a true dominance hierarchy (e.g., averting a gaze when being threatened), these responses may not be as adaptive in other situations (e.g., averting a gaze in a romantic situation). Still other coping responses (e.g., physical escape or aggression) that were adaptive for the largely physical dangers faced by our primitive ancestors may now be obsolete given that individuals are usually required to be present, and stay calm and focused in the face of social dangers.
Research suggests a moderate genetic component to SAD, with approximately 30 percent of the variance being heritable. In a large twin study conducted by Kendler and colleagues there was a concordance rate of 24.4% for identical compared to 15% for fraternal twin pairs. Another study found that as much as l3% of the variance in social anxiety was accounted for by genetic factors. However, in two other studies, the concordance rates did not differ between monozygotic and dizygotic twins. Other findings suggest that social fears may be linked to specific genetic and environmental factors, that social fears may only share a small genetic overlap with other anxiety disorders, and that such fears may have a sizable genetic commonality with neuroticism.
Children of adults with social anxiety disorder appear to be more likely to meet criteria for SAD as compared to children of normal controls. First degree relatives of persons with SAD exhibit a higher risk for SAD compared to relatives of normal controls. Patients with three or more fears appear to have a higher percentage of first-degree relatives with social anxiety as compared to others with social phobia. Although the greater incidence of SAD among family members who are more closely linked genetically supports the fact that heritability contributes to the development of SAD, these findings do not rule out the contribution of the environment to the etiology of SAD. Additionally, findings of genetic etiology are mixed to date and suggest that environmental influences are important in the development of social phobia.
TEMPERAMENT AND PERSONALITY STYLES
Several temperamental and personality styles have been implicated in the development of social anxiety disorder. Behavioral inhibition (BI), defined as a tendency to approach novel situations with restraint, avoidance, and distress appears to increase the risk of developing anxiety disorders, especially SAD. Given that characteristics of BI have been observed across cultures and across species, it is likely that the tendency toward being behaviorally inhibited is an "evolutionarily conserved temperamental phenotype" [according to Jordan Smoller, MD]. About 61% percent of individuals with BI versus 27% of those without BI go on to develop SAD in adolescence or adulthood. It appears that behavioral inhibition toward social stimuli as opposed to physical stimuli may confer the greatest and most specific risk.
Shyness is a distinct risk factor for developing SAD. Not all shy people develop SAD and as many as 90 percent of adults report that they were shy at one time in their life. Researchers suggest that higher levels of shyness may bestow a greater risk for those with a more chronic course of SAD as compared to individuals whose symptoms remit more quickly. Although temperamental and personality factors such as shyness and behavioral inhibition both clearly play a role in the development of SAD, they do not fully explain its development. Multiple temperamental and personality styles likely interact to confer a vulnerability to develop SAD. For example, greater levels of emotion combined with inadequate coping resources appear to increase the risk for developing anxiety. The trait of neuroticism appears to be common to both anxiety and depressive disorders. Individuals with SAD may also have difficulties with effortful control, particularly voluntary attentional regulation of excessive emotions. Low voluntary attentional control may also lead to the development of anxiety above and beyond the trait of neuroticism. In fact, neuroticism and low attentional control together appear to both increase the risk for anxiety, and in combination with socially inhibited temperament, these may be the best predictors of the development of SAD.
Although the HPA [hypothalamic-pituitary-adrenal axis] axis has been implicated in SAD, there is correspondingly less attention on the neurobiology of SAD in comparison to other anxiety disorders. The literature has implicated an increased release of cortisol, an increased activation of norepinephrine, an exaggerated sensitivity of serotonin receptors, decreased levels of dopamine, and oxytocin dysfunction. However, findings are mixed in most cases with some studies finding increased HPA responsivity to socially specific fears in SAD and other studies finding no evidence for a sensitized HPA [adrenal glands] response. Similarly, whereas some findings showed that individuals with SAD did not have abnormal circadian rhythms, cortisol levels, or a DST [dexamethasone suppression test] response, others demonstrated elevated cortisol levels in patients with SAD. Imaging studies have found both a hypofunction of the prefrontal cortex associated with a decreased ability to modulate fear responses as well as a hyperarousal of the amygdala, which is associated with increased anxiety.
Negative Life Experiences. Studies have linked a variety of negative life experiences to social anxiety: separation from or death of parents, marital discord, family violence, sexual or physical abuse, childhood illness, and bullying by peers. Temperamental factors may either lead directly to anxiety, or they may increase the likelihood of anxiety dependent on the experience of negative life events (e.g., bullying by peers). It is also possible that negative life events may represent an independent risk factor for social anxiety (e.g., death of parents).
Parenting Styles and Interactions. Over-controlling and overprotective parenting styles have been linked to the development of anxiety disorders in general and may be more strongly associated with SAD than other anxiety disorders and to shyness in general. However, findings regarding this causal relationship are mixed and the link may represent a temperament-environment relationship, as parents may be more inclined to be overprotective of shy, inhibited children, and thereby inadvertently reinforce shyness and more inhibited behaviors in such children. A recent prospective study showed that greater behavioral inhibition was only associated with SAD in the context of high maternal over-control but not in the context of low maternal over-control. Higher maternal over-control at 7 years also predicted higher SAD symptoms and lifetime rates during adolescence.
Children may also acquire social fears through information learned from parents or through observation of parents' behaviors and attitudes. Parents may model fear responses in social situations by enacting and reinforcing avoidant responses, highlighting information about risk, and expressing doubts about their own competence in social situations. Although many studies use retrospective recall, which is subject to memory bias, adults with SAD rate their parents as less warm and more controlling, and remember their parents as being socially isolated, encouraging family isolation, limiting contact with others, using shaming to discipline them, and being overly mindful of the opinions of others.
An insecure attachment style, independent of behavioral inhibition or maternal anxiety, has also been linked to anxiety disorders in general although findings are still mixed with some studies demonstrating that insecure attachment to parents is associated with anxiety, whereas others show no relationship between the two.
Peer Relationships. Peer relationships have also been associated with and etiologically linked to anxiety in general and may be particularly influential in the development of SAD. Individuals with social anxiety often have fewer friendships, experience less intimacy and support in relationships, and are less likely to be married. Peer rejection, teasing, or bullying in childhood may also be causally related to the development of social anxiety. Possible reasons for peer victimization or neglect include the presence of poor social skills in individuals with SAD. Shyness and social anxiety also tend to be negatively evaluated by both children and adults, which may lead directly to negative outcomes with peers. In either case, peer neglect, victimization, or rejection may lead to a cycle of increased social anxiety; poorer social skills, and a greater avoidance of social relationships over time.
Early behavioral models, including stimulus-response models, used a respondent conditioning paradigm to explain the development and maintenance of anxiety disorders. For example, [O. H.] Mowrer's two-stage model suggests that a neutral stimulus leads to social anxiety through its pairing with an unconditioned stimulus. The now conditioned stimulus gets maintained by the negative reinforcement individuals derive from their efforts to avoid or escape it. In support of this model, many but not all individuals with SAD recall a history of one or more traumatic social events although a history of traumatic conditioning is more common among those with a specific subtype. There is more support for the second stage of the model, which suggests that avoidant or escape behaviors used as methods to cope with symptoms serve to maintain social fears in the long run. [R. E.] Zinbarg and [S.] Mineka also suggest that normal, adaptive fear becomes pathological when the conditioned response is out of proportion to the degree of actual threat, becomes generalized to other stimuli that are not threatening, and is rigidly maintained despite the fact that the contingencies that led to its development are no longer present.
Newer models also incorporate other methods of conditioning such as modeling, observational or vicarious learning, verbal or instructional learning, direct social reinforcement and verbal instruction as well as learning conveyed through culturally relevant rules and norms. Finally, other behavioral models emphasize social skills deficits as risk factors for SAD. Individuals with social anxiety may have primary social skills deficits or secondary deficits related to their anxiety about social situations, despite being socially fluent. In either case, social fluency may eventually be affected, and thereby lead to negative social consequences.
Given that a fear of negative evaluation is the hallmark of social anxiety disorder, cognitive models suggest that SAD is the result of cognitive processes. Proximal models suggest that people with SAD have a series of negative biases before, during, and following social situations that increase their anxiety and potentially impair their performance.
Individuals with SAD have unrealistic standards of performance, overestimate the likelihood of being scrutinized and the probability of being negatively evaluated, predict catastrophic outcomes, and underestimate their ability to cope with negative outcomes. Additionally, these individuals form a mental representation of themselves during social situations along with a self-evaluation of their performance, as well as a mental representation of others who they perceive are observing and evaluating their performance. Their cognitive biases are maintained post-performance, even if negative events do not occur, and typically include a harsh self-appraisal of their performance as well as a perceived harsh evaluation by others.
Individuals with SAD also appear to be less likely to form benign or positive interpretations in social situations and appear to have cognitive biases even when they are in nonevaluative situations. They are also far more likely than those without SAD to rank dominant others as being high in status and to rank themselves as having a low status. Individuals with social anxiety also appear to have entrenched beliefs about their lack of desirability or adequacy in social situations as well as beliefs that others are critical, harsh, and evaluative.
According to these models, social avoidance, escape, and safety behaviors employed by socially anxious individuals prevent them from having their negative biases disconfirmed and thereby perpetuate the cycle of social anxiety and impaired functioning. The use of safety behaviors may also inadvertently worsen their performance, increase the likelihood that they will be negatively evaluated, and hence maintain their social fears in the long run.
Studies have confirmed the presence of cognitive biases in individuals with social anxiety, even in those as young as 8 years old. However, a distal-causal relationship between these biased cognitions and the development of SAD has not yet been fully established. Further, although studies have observed a relationship between negative environments and social anxiety as well as between negative cognitions and social anxiety, the role of negative beliefs in mediating this relationship has yet to be determined.
Other models have also proposed cognitive processes in the etiology of social anxiety disorder. These models implicate both distal factors such as over-controlling parenting styles, uncontrollable stressors, or repeated social defeat and proximal factors such as low perceived control or perceptions of uncontrollability in the etiology of social fears. Support for these processes comes from animal studies which show that uncontrollable shock leads to increased submissiveness and repeated social defeat leads to learned helplessness. Further support also comes from studies with humans that have demonstrated a link between perceptions of low control or uncontrollability to anxiety.
The average age when individuals present for treatment is in their thirties suggesting that most individuals suffer for years before they present to a provider. Individuals with SAD are generally less likely to seek treatment than people with other illnesses ( < 23%) and tend to come to the attention of a provider only if they develop a comorbid disorder. Primary care physicians are also less likely to correctly assess for the presence of SAD compared to other anxiety disorders. Given that SAD may cause more impairment in roles traditionally expected of men, treatment samples show equivalence among the genders or men are overrepresented.
Cognitive Behavior Therapy (CBT) and serotonergic medications both have a strong empirical basis in the treatment of social anxiety. Various CBT techniques such as cognitive therapy, exposure-based treatments, rational emotive behavior therapy, self-instructional training, social skills training, and relaxation training have been studied separately or in combined CBT. Meta-analyses suggest that CBT is effective. When delivered individually, CBT has also demonstrated evidence of generalizability to the real world. [T. M.] Lincoln and colleagues have also found that the application of typical exclusion criteria used in randomized controlled trials does not increase individual treatment effectiveness.
COGNITIVE BEHAVIORAL GROUP THERAPY
Cognitive behavioral group therapy (CBGT) is one of the most well studied treatments for SAD. It is typically delivered to groups of 6-8 individuals by two co-therapists over 12 weekly sessions. The most common comparison group for CBGT, a waitlist control consistently has been found to be inferior. Most studies also found that CBGT was superior to an educational supportive group therapy, as well as to medication placebo. CBGT also led to improved quality of life, reduced tendency to interpret ambiguous stimuli as negative, as well as good long-term efficacy, with maintenance or improvement of gains up to a 5-year follow-up. Moreover, CBGT has been studied in naturalistic settings, showing favorable comparisons to randomized controlled trials with respect to effect sizes. Also, [P. M.] McEvoy found that restricting samples on the basis of comorbidity, older age, or alcohol abuse did not moderate effect sizes. Nonetheless, a group format is not always logistically possible as it typically means that some clients need to wait until a cohort of individuals seeking group treatment is available. In addition, tailoring treatment is less possible within a group compared to individual treatment.
Although meta-analyses have found no difference between the efficacy of group and individual therapy, two direct comparison studies found that individual therapy for SAD was more effective than group or medication focused treatments. Thus, there may be reason to favor individual therapy over group therapy in terms of efficacy.
COMPARISONS BETWEEN CBT AND ITS COMPONENTS
Meta-analyses generally report few differences between standard CBT and its various components, and that cognitive or behavioral changes are unrelated to the treatment modality. A recent study reported a trend for greater gains with the combined treatment over exposure and cognitive restructuring alone, while another study found that the combined treatment was more effective only over cognitive therapy alone.
Research has shown that social skills training was equivalent to cognitive therapy, exposure, and combined cognitive behavioral therapy. However, one recent study suggested that social skills training augmented the impact of standard CBT and another suggested that cognitive therapy was superior to exposure or applied relaxation.
CBT VERSUS OTHER THERAPEUTIC INTERVENTIONS
A small number of more recent studies have compared standard CBT to other forms of therapy. For example, Koszycki and colleagues found that CBT was more effective than mindfulness-based stress reduction. However, another study found that mindfulness-based stress reduction led to greater reduction in negative emotion than aerobic exercise during emotion regulation, but there was otherwise no difference between these two treatments. In comparisons between CBT and interpersonal therapies, one study found that CBT conducted in a residential facility was not significantly different from interpersonal therapy on main outcome measures, but CBT was better on a measure of social role security. On the other hand, another study found that cognitive therapy was superior to interpersonal therapy in an outpatient setting. Also, sudden gains in both CT and IPT were predictive of long term outcome but sudden gains were greater in CT compared to IPT. Finally, one study found that psychodynamic therapy augmented the effects of information, self-exposure and anxiolytic medications and that this intervention was equally effective to information, self exposure, anxiolytic medications and therapist-directed exposure. However, these findings are in need of further replication.
Many individuals self-medicate with alcohol or drugs to cope with their anxiety in social situations. Prescribed agents include beta-blockers, selective serotonin reuptake inhibiters (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs), benzodiazepines, tricyclic antidepressants, and reversible and irreversible monoamine oxidase inhibitors (MAOIs). When comparing classes of drugs, the most effective one appears to be the irreversible nonselective MAOI, phenelzine. However, this drug has problematic side-effects including risky food and drug interactions. Therefore, it is not considered to be the first-choice option. Among the other choices of drugs, many have demonstrated similar rates of efficacy, but the first-line pharmaceutical recommendations are typically SSRIs and SNRIs due to their efficacy combined with less aversive side-effects. On the other hand, tricyclic antidepressants have shown unsatisfactory results and although benzodiazepines are superior to placebo, these drugs have negative side-effects as well as the risk for dependency.
STUDIES COMPARING CBT AND PHARMACOTHERAPY
Comparisons between CBT variants and pharmacological treatments, have found no significant difference between SSRIs and exposure alone or between SSRIs and cognitive behavioral therapy alone. However, one study found that cognitive therapy was superior to an SSRI and 2 other studies showed superiority of exposure therapy to an SSRI. Studies that compared monoamine oxidase inhibitors (MAOIs) to CBT generally have reported no significant differences between treatments, although one study found CBT to be superior. On the other hand, clonazepam was superior to cognitive behavioral group therapy after 12 weeks of treatment. Additional studies found that CBT was superior to buspirone and that flooding was superior to atenolol. However, when studies compare CBT to medications on long-term maintenance of gains, CBT is consistently superior. Although pharmacological agents appear to be more cost effective in the short run and have a relatively rapid onset of treatment effects, the primary drawback is a high risk of relapse following medication discontinuation. By comparison CBT is more durable than medication, even up to 5 years.
Whereas one study suggested a slight advantage for combined CBT plus SSRI medication to CBT alone, two others have found no significant advantage. One study found a significant advantage of combining CBT with MAOIs over CBT alone whereas another study found that CBT was superior to combined treatment. Nonetheless, as noted earlier, MAOIs have strong interactions with certain foods and are therefore not optimal choices.
Several studies have examined whether exposure therapy could be enhanced by the use of medications that are thought to act as cognitive enhancers. Findings suggested that d-cycloserine augmented the impact of exposure for public speaking anxiety compared to a placebo plus exposure in individuals with SAD. Another randomized trial found that oxytocin did not enhance the impact of exposure on symptoms of SAD.
Over the last several years, several technology-guided CBT protocols have been developed for the treatment of SAD. Advantages in using different technologies to deliver CBT are that they can provide greater access to CBT and that they may be more cost-effective than therapist delivered formats.
Studies have shown that virtual reality CBT is effective in individuals suffering from SAD. Computerized programs designed to modify cognitive biases have also demonstrated efficacy in the treatment of SAD with up to 72% no longer meeting diagnostic criteria after a 4 week training program.
Internet Guided CBT (I-CBT) has also shown promising results in various settings and preliminary results suggest that it may be as effective as in-person CBGT. I-CBT produces greater decreases in social anxiety and increases in self-efficacy compared to waitlist conditions and the gains made in I CBT appear to be durable. Three recent studies showed that gains in I-CBT were maintained at 1 year, 2.5 years, and 5 years. Although technology guided CBT formats appear to show promise, more studies are needed to compare them to traditional CBT.
SAD is a chronic and debilitating condition that affects a large percentage of individuals and appears to be growing in the United States. A number of proposed changes are slated for the DSM-5 diagnosis of SAD and have been made based on empirical evidence and in an attempt to correct prior problems with the diagnosis. Several models account for the development and maintenance of social anxiety disorder. These models differ in the degree to which they emphasize hard-wired (ethology, genetics, temperament, neurobiology) versus psychosocial factors (life events, parenting styles and interactions, peer relationships, cognitive and behavioral models), and recent formulations emphasize a multi-faceted approach to understanding who eventually goes on to develop clinical symptoms and how their symptoms are maintained. More research is necessary to understand the variance contributed by each of the distal and proximal factors implicated in the onset and maintenance of social anxiety disorder as well the interplay between them. A better integration among cognitive and learning theory formulations is especially needed. Additional studies are also required to investigate both the developmental origins and the proposed mediators. Studies using prospective designs, especially with experimental manipulations are essential.
Cognitive Behavior Therapy (CBT) and serotonergic medications both have a strong empirical basis in the treatment of social anxiety and appear to have similar rates of efficacy, although CBT appears to be more durable and better tolerated, but has a slower onset of treatment effects. Various forms of CBT have been studied in the treatment of social anxiety. Such techniques include cognitive therapy, exposure based treatments, rational emotive behavior therapy, self-instructional training, social skills training, and relaxation training studied separately or in combination. Findings from component analyses suggest that treatments that emphasize cognitive or behavioral strategies have similar rates of efficacy and that combining cognitive and behavioral therapies may be more effective than either one alone. Preliminary results show that technology-guided CBT protocols are effective in treating SAD, provide greater access to treatment, and may be more cost-effective. However, more studies are needed to compare I-CBT and other technology-guided protocols to traditional CBT treatments. Finally, although some characteristics have been linked to treatment outcome (e.g., earlier age of onset, broad-based fears), future studies need to examine additional factors that may impact or mediate therapeutic outcomes in order to maximize effects of treatment.
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