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Abstract

The aim of the present study was to identify and synthesize recent research findings in the aetiology and psychological treatment of social anxiety disorder and consider how these might improve outcome through more effective intervention. The electronic databases Medline, EMBASE and PsychInfo were searched for January 2000–December 2008. Publications of interest referred to in relevant articles were also reviewed. Case reports and publications not in English were excluded. The greatest variance in social anxiety disorder is accounted for by temperamental and personality factors and these may be associated with significant heritability. The environmental contribution is smaller and mainly due to non-shared factors, with a small contribution from shared environmental factors. Epidemiological research confirms that social anxiety disorder is chronic, and among the anxiety disorders has the lowest rates of treatment seeking, receipt of evidence-based treatments and recovery. Effective psychological treatments have been available for some time, and the research emphasis is on increasing the efficacy of treatments through innovations in programme content and delivery. Cognitive science research has contributed a better understanding of cognitive factors that maintain social anxiety disorder and informed enhancement of the cognitive elements of therapy. Internet-based programmes show promise as a novel way to deliver and improve access to effective therapy. Genetic, personality and temperamental factors contribute to the risk for social anxiety disorder. Given the associated comorbidity and disability, energy needs to be directed towards early recognition and treatment, and to increasing engagement and retention in effective therapy. Ongoing professional education is required to ensure that the disorder is recognized and evidence-based treatments received by patients who do seek help. Current cognitive behavioural treatments are being enhanced as the results of cognitive science research are being applied, and novel forms of treatment delivery show promise in increasing access.

Keywords

anxiety disorders cognitive therapy phobic disorders social phobia

Social anxiety disorder (SAD) is one of the commonest psychological illnesses.1 Community-based studies put the 12 month prevalence rate for DSM-IV social phobia (SAD) in western countries at between 3% and 7% depending to some extent on the threshold for diagnosis of the instrument used [1–5]; it may be somewhat lower in Asian countries [6]. SAD is the focus of intense research effort, and yet it has one of the lowest rates of treatment. Despite the availability of effective treatments, many individuals with the illness do not come forward, and many who do, do not receive an evidence-based treatment [7]. There continues to be a long delay after the onset of illness before treatment is sought [8]. Cognitive behavioural interventions are well established, with a robust treatment literature, but still have significant dropout rates and fail to achieve recovery for all participants. A substantial research effort is focused on the elucidation of cognitive factors that underlie SAD, and the application of this knowledge to improving the outcome of therapy. At the same time, a number of different psychological approaches is being trialled, including a number of mindfulness based strategies.

Aetiology of social anxiety disorder

Anxiety runs in families [9–13]. A heritable component for anxiety disorders has been established over the past 30 years, following observations about frequent clustering of comorbid disorders in epidemiological and clinical populations. This led to predictions of a ‘common vulnerability factor’ to ‘affective spectrum’ or ‘internalizing’ disorders [14–17]. Although it was established some time ago that concordance rates for anxiety were approximately twice as high in monozygotic as in dizygotic twins, it was famously noted that no two monozygotic twins in that early sample had the same anxiety disorder [15]. Most studies suggest two main clusters of anxiety disorders with shared heritable factors: a cluster of generalized anxiety/depression and another based on phobias [18, 19], although one recent study suggested a cluster with panic-generalized-phobic anxiety (with overlap with depression) and a cluster of specific phobias, with social phobia intermediate between these [20]. Results are likely to vary depending on methodology and what markers are chosen to measure heritability.

Heritability appears stronger for generalized than for non-generalized (i.e. <2–4 social situations involved) SAD [21, 22]. Most studies suggest a significant role for genetic factors, with estimates that they may account for approximately 30–60% of the variance in SAD [8, 23], although it may be that the bulk of this represents one or more common genetic risk factors for anxiety and depression, with a relatively small component specific to social fears or social anxiety [10, 24]. One recent negative twin study has reported only a minor role for genetic factors in SAD but, because the study group was only aged 6 years it may be that there was a floor effect; that study did support a general vulnerability for genetic factors [12]. Genetic factors appear to account for more variance in adult than in child samples [25].

Neuroticism, considered to be a personality factor and characterized as the tendency to emotional distress or negative affectivity, has a significant genetic component [11, 26] and appears a likely candidate for much of the shared risk, while introversion may underlie some of the more specific risk [11]. One twin study estimated that introversion and neuroticism together, proposed to be endophenotypes, accounted for all the genetic vulnerability observed [11]. A recent meta-analysis of serotonin transporter promoter polymorphism (5-HTTLPR) studies supports a relationship between the 5-HTTLPR short allele and neuroticism [27]. Further, positron emission tomography (PET) studies have demonstrated an association of 5-HTTLPR and increased amygdala activity in response to social threat [28]. Interestingly, recent PET studies have suggested that the increased left amygdala activation seen in response to viewing pictures of angry faces is more closely related to possession of a 5-HTTLPR short allele than it is to diagnosis of SAD [29, 30].

It has also been proposed that personality factors such as introversion and neuroticism may contribute to the development of the cognitive biases that have been identified as maintaining factors in SAD [31]. Findings from a large twin study suggest that, although genetic factors appear to be strong in both genders, environmental influences may play a slightly greater role in accounting for personality factors in women [26].

Temperamental factors, such as trait anxiety, harm avoidance and behavioural inhibition (BI) that appear to be associated with increased rates of anxiety disorders, including SAD, have also been described and may represent phenotypic manifestations of the underlying genetic factors [11]. Of interest for some time now is the temperamental factor referred to as ‘behavioural inhibition to the unfamiliar’ [32]. BI is identifiable in infancy, but manifests differently, and is triggered by different situations at different ages. For example, the earliest triggers include noise, to which the infant will react with a startle response. A few years later, BI is manifest by withdrawal from the situation, often with clinging or maintaining proximity to the mother when the trigger is a stranger. Physiological markers of sympathetic arousal in children high in BI have been demonstrated [33]. Although many children may grow out of these reactions, there is some evidence that extremes of BI or behavioural disinhibition may be more stable, and that stable levels of these factors may have some association with later psychological problems – externalizing or conduct disorders in the disinhibited, and anxiety disorders in the inhibited. Although BI can be assessed in quite young children, it appears that the trait may be more stable in children from 2 to 8 years. Recent research also suggests that BI may have two components: physical fear and social fear. The social fear components may be more stable and more closely associated with later SAD, while the presence of physical fear components may explain the broader associations of BI with other anxiety disorders [24, 33]. The neurobiological correlate of BI may be an increased reactivity (compared to non-BI individuals) in the limbic circuits and amygdala [21, 33, 34]. This might represent a lower threshold for arousal, especially by threat-related cues.

BI may also represent a risk factor for future depression for individuals with SAD, according to data from a prospective, longitudinal community study that followed adolescents with SAD for 10 years [35]. Comorbid depression complicates the prognosis of SAD and is associated with more suicidal ideation and attempts. The identification of BI in adolescents with SAD might thus present secondary prevention opportunities with respect to future depression.

Neuroimaging research offers some support for these hypotheses. Neuroimaging studies consistently support a finding of increased reactivity in the amygdala in subjects with high social anxiety [34]. Studies of adults characterized as high BI at the age of 2 years have demonstrated persisting differences in activity in the amygdala in response to viewing novel faces but not familiar faces, irrespective of a diagnosis of SAD [36]. The neural circuitry involved in the cognitive processing that reduces the anxiety provoked both by painful and emotionally distressing stimuli has been identified in both PET and functional magnetic resonance imaging (fMRI) studies, implicating increased activity in the dorsolateral prefrontal cortex (dlPFC) and reduced activity in the amygdala [37, 38]. A simulated social rejection paradigm during fMRI resulted in increased activity in the dorsal anterior cingulate cortex (dACC), left amygdala and left peri-aqueductal grey areas (the latter two regions known to be associated with processing of affective and pain stimuli) [39]. In that study increased activity in the dACC was associated with higher levels of everyday social distress, measured prospectively. Personality measures including social anxiety, neuroticism and rejection sensitivity also predicted day-to-day social distress, but were no longer significant when the neural activity was controlled for [39]. This would seem to provide a possible neural link between personality factors and social anxiety, as well as demonstrating the applicability of neuroimaging findings to the lived experience of social anxiety. Studies have also looked for changes in these circuits following treatment. Changes in regional cerebral blood flow (rCBF) were demonstrated when responders had greater decreases in dlPFC, ACC, hippocampus and peri-amygdaloid regions than non-responders, whether treated with cognitive behaviour therapy (CBT) or citalopram [40]. There were some differences in rCBF changes between CBT and citalopram that may reflect differences in the mode of action. In a 1 year follow up, the level of post-treatment reduction in rCBF in the peri-aqueductal grey (shown in the CBT but not citalopram group), left thalamus (seen in the citalopram but not CBT group), right and left amygdala predicted the level of sustained improvement [40].

Environmental factors are also of some aetiological significance. Shared environmental factors of attachment and parenting have been studied. The anxious–resistant style of attachment, evident in early childhood, does seem to be associated with the later development of anxiety disorders [21]. Studies of parenting styles show some consistency in reporting an association with an over-controlling parental style, in which parents appear to grant less autonomy to their children [41, 42]. Much of this literature suffers from the drawback of relying on retrospective reports by anxious, sensitive individuals, many of whom have anxious parents. A recent meta-analysis of mainly cross-sectional studies of anxious children and their parents confirmed a role for parenting but estimated it to be very limited: parenting style accounted only for approximately 4% of the variance in childhood anxiety [42]. Similarly, prospective studies have not consistently supported a role for over-controlling parenting style. Other confounders include the fact that parents may be coping with their own high levels of anxiety by being over-protective/over-controlling, or that over-protectiveness may be a response to an anxious child that would not occur with a non-anxious sib.

Non-shared environmental factors of interest include the experience of sustained bullying or victimization at school. Research suggests that neither the bullied nor the bully may be well adjusted. The victim of the bully may be more likely to have an internalizing style of coping with emotional distress, while the bully is likely to externalize [43] although some of these differences may be related to gender [44]. Hence the victim may be less likely than others to retaliate, thus perpetuating themselves as a target. Although the short-term effects of bullying are reasonably well established (negative affect, anxiety, low self-esteem, loneliness) there is as yet only a small literature looking at the long-term associations with anxiety. In a non-clinical sample, an association was found between self-reports of being verbally teased in childhood and current levels of social anxiety and anxiety sensitivity [45]; a history of bullying was significant only for male subjects with SAD in a sample recruited through the media [46]. In a sample of adults attending a depression clinic, retrospective reports of distressing levels of bullying were associated with higher rates of SAD and agoraphobia, and generally higher state anxiety [43]. But this certainly does not prove a causal association and reports could be amplified by the greater emotional sensitivity in this group, resulting in recall bias. In fact, the strongest predictor for SAD in this and other studies [47] was BI, which, together with parental over-control, was itself found to be a risk factor for bullying.

It is difficult to reconcile the findings in studies of adults with SAD that shared environmental factors account for little of the variance in risk, with studies in childhood that consistently show a role for environmental factors. Recently, aetiological models of SAD have been proposed in which temperamental and genetic factors (mainly shared with other emotional disorders but some specific to SAD) account for the greatest risk but may be acted upon by environmental experiences [31], possibly via cognitive factors [24]. For example, if the presence of temperamental attributes such as BI resulted in a lower threshold of activation of neuroendocrine responses to threat, given the aversiveness of such experiences an individual might develop strategies aimed at avoiding threat, which in turn might lead to the development of attentional and interpretive cognitive biases – being on the lookout for threat, and interpreting ambiguous cues as potentially threatening. Some recent fMRI research also implicates cognitive factors. Findings in that study suggested to the authors that individuals with SAD may show less coordinated, possibly less effective, cognitive control strategies when faced with social threat [38].

In the Rapee and Spence model it was proposed that shared environmental factors may be relatively more important in early childhood and non-shared environmental factors of more impact in adolescence and adulthood [24]. Complementing this, Fox et al. discussed a neurobiological model for the gene × environment interaction [48]. There is a pressing need for longitudinal studies to investigate these factors further.

Treatment seeking

Several studies have examined patterns of help seeking in SAD. The National Comorbidity Survey in the USA found that only 19% of those who met criteria for social phobia had ever sought help [49]. In the first Australian National Survey of Mental Health and Wellbeing (NSMHWB), 61.6% of persons who met criteria for DSM-III-R social phobia in the preceding 12 months had had at least one consultation with a health professional for a mental problem within the same time period [7], and only 20.8% were receiving care for social phobia at the time of the survey [50]. Recent research confirms early observations of a long delay from onset of the disorder to treatment seeking. Epidemiological research has consistently identified one of the commonest reasons for not seeking treatment as being a preference to manage independently [7, 51], although fear of negative evaluation and, in the USA, concerns about affordability are also commonly reported [51]. Qualitative research in the UK involving members of a phobia support group sought to identify barriers to effective treatment [52]. Respondents reported that they feared that their doctor would not take them seriously, that their condition was not serious enough to take up the doctor's time, and that they felt embarrassed or ashamed of their anxiety. They reported a relative absence of any informational literature in the doctor's surgery, and felt that had this been available along with the myriad of informational pamphlets on physical health problems, it would have helped to reduce stigma and helped them access effective help sooner. Respondents identified that accurate diagnosis by their general practitioner (GP), and information about the illness and its optimal treatment – not only what might be available through the local health service (usually little) – would be most helpful. Unfortunately, research suggests that the diagnosis of SAD is often missed in primary care [53, 54]. Respondents in the UK survey also highlighted that their GPs were generally pessimistic about the treatments available within the health service because it was clear to all that ‘serious and enduring mental illness’ was interpreted in practical terms as psychosis and severe mood disorder.

Effectiveness of psychological treatments

Cognitive behaviour therapy

CBT has a well-established efficacy literature for SAD both in adults and in children. Effect sizes (ES) are robust and long-term maintenance of gains has been shown in both groups [41, 55–57]. Although exposure therapy alone is more effective than wait-list control, the weight of evidence suggests that the addition of cognitive strategies enhances outcome [58–60]. There is continued interest in the question of whether group or individual treatment is more effective. Early studies suggested some superiority for group treatment [61], and arguments were raised that the group setting would provide a richness of exposure experiences not easily replicated in individual treatment; by the late 1990s the weight of evidence suggested that there was no clear superiority between group and individual treatment [62]. More recently, this issue has been revisited, using CBT incorporating a number of developments, including factors related to attention focus, safety behaviours and post-event processing (PEP). This more recent research shows a trend towards superiority for the individual setting [59, 63–65]. Pragmatic factors may dictate whether individual or group CBT is offered to patients of a service, and the literature reassures that both formats are superior to wait-list and psychological placebo.

Good-quality CBT for SAD includes a number of elements [8, 65]. Development of an individualized cognitive model, or case conceptualization, of the disorder is seen as an essential beginning to good quality CBT [66, 67]. Psychoeducation about the disorder is important, with information about typical underlying beliefs and fears, followed by assistance to develop an understanding of the individual's own habits of thinking about their interactions with others, and their own habitual patterns of responding to the anxiety occasioned by social situations. Psychoeducation also assists individuals to understand how their own responses to anxiety, for example, avoidance or safety-seeking behaviours, may reinforce their fears [68]. The cognitive model represents a hypothesis linking all these factors to explain the development and maintenance of SAD in this individual, and becomes the template for treatment planning. Behavioural and cognitive interventions are planned to target elements of the model related to the maintenance of problematic social anxiety.

Because anxiety disorders are seen at rates in excess of population norms in the families of anxious children, studies of CBT for children have often included a condition wherein the parents receive some training in anxiety management. Although this may enhance the outcome for affected children in the short term, both in terms of greater numbers achieving remission and better scores on outcome measures, Cobham et al. failed to find an advantage for children who did not have a parent with an anxiety disorder [69], and Barrett et al. found that the initial advantage was no longer evident at long-term follow up, 5–7 years after treatment [41].

Cognitive factors had been increasingly recognized as highly significant in SAD when Clark and Wells described a model of social phobia emphasizing the role of cognitive factors [70]. The publication of this model stimulated clinical and laboratory research directed towards achieving a better understanding of the cognitive experience of SAD. CBT programmes have subsequently been enhanced by incorporating clinical applications of these findings. Important findings that have shaped CBT in recent years include recognition of the relationship between state anxiety and the perceived likelihood and cost of a feared outcome [8, 58, 71, 72], the greater self-focus of individuals with SAD compared to those without the disorder [70, 73–75], the role of safety-seeking behaviours or subtle avoidance [76–78], the impact of cognitive biases on the experience of social events [79, 80], and the problems caused by post-event rumination [81]. Strategies to address these psychopathological elements have been incorporated into current CBT programmes.

Recent research suggests that focusing on achieving more realistic estimates of the cost of a feared outcome (e.g. how distressing negative evaluation would be) may be more effective in achieving a good outcome than reducing estimates of the probability of feared social outcomes [82].

It appears that social interaction is a stimulus to greater self-awareness (or self-consciousness) for both high and low socially anxious individuals. Two types of self-awareness have been described: public self-awareness (seeing oneself from an ‘observer’ perspective) and private self-awareness (being more aware of one's internal experiences). When social anxiety is high, the level of self-focused attention may become intense and include both public and private self-consciousness [83, 84]. Self-focused attention can actually improve performance when there is no particular concern about evaluation, but for those with increased social anxiety it appears to have detrimental effects [78, 85]. Psychological interventions that include directions to participants to focus their attention externally showed superiority over packages without this instruction in a number of studies [75, 85, 86]. It may even be effective in the absence of more abstract cognitive interventions such as cognitive challenging [87] and, as such, may be useful for participants who find the cognitive elements of CBT programmes difficult.

In SAD, self-focused attention is usually accompanied by unhelpful analytical evaluation of performance [88], resulting in negative self-attributions, and studies have shown that the main difference from persons without SAD has to do with making more negative attributions [83, 89, 90]; some studies have demonstrated an approximately equivalent number of positive attributions, but these seem not to be attended to. Perspective taking has also been considered from another dimension, that is, ‘field’ versus ‘observer’ perspective. The former may be likened to the view from behind a camera and the latter to feeling as if one is the focus of the camera. It appears that individuals with SAD engage more in the observer perspective when highly socially anxious. This is then compounded by PEP.

The role of post-event negative rumination around performance has been highlighted by a number of investigators. PEP is a common occurrence and not limited to anxious individuals. It may arise more commonly, however, and be more intense, after anxiety-provoking social situations than in response to phobic situations [91, 92]. Non-clinical studies and two out of three studies using clinical populations have found that PEP is most closely linked to baseline levels of social anxiety and fear of negative evaluation [81, 89, 93, 94]. PEP can have a negative or positive valence. Negatively valenced PEP appears most likely to be triggered in highly socially anxious individuals when the outcome of the social situation was perceived negatively [92, 95, 96]. Not surprisingly, there appears to be a link with post-event (state) anxiety but this, too, is related to baseline social anxiety, as well as being mediated by a number of cognitive variables including maladaptive focus of attention, negative perception of performance, and probability and cost estimates of a poor performance [92, 97]. Treatment can reduce the occurrence of negative PEP [89].

PEP research contributes to our understanding of why socially anxious individuals often do not seem to benefit from self-directed exposure, in contrast to those with other types of phobias. It is hoped that incorporating education and interventions around the role of PEP in maintaining SAD will enhance treatment outcome, but this is yet to be demonstrated. A corollary of so much unhelpful focusing of attention, negative interpretation of outcome and PEP, not surprisingly, is predicted to be negative autobiographical memories of the event, which in turn contribute to anticipatory anxiety about future events, a model that has received some support [98]. Alcohol is a popular choice of anxiolytic for many, and interesting recent research suggests that it may be that alcohol does not so much reduce state anxiety as interfere with the negative processing of the event and the laying down of unpleasant memories [99].

Traditional exposure-based strategies remain a mainstay of therapy, and understanding of the neurobiological basis of extinction is growing. The exposure-based extinction of fear is now thought to involve new learning that actively inhibits the fear reaction to a given cue [100]. Repeated exposure can provide the opportunity to learn that a particular cue is not necessarily linked to a disastrous outcome.

The repertoire of behavioural strategies in CBT for SAD has expanded. Identifying and seeking to eliminate the use of safety-seeking behaviours (often referred to simply as ‘safety behaviours’) has become a standard part of treatment over the past 10 years or so. Safety behaviours may also be conceptualized as a subtle form of avoidance. Their purpose is to prevent a feared outcome from occurring or, in the case of SAD, to make signs of anxiety or social incompetence less obvious to others should these outcomes occur. Individuals believe these behaviours to be helpful in managing their anxiety [78], but a number of detrimental effects of using these strategies have been identified by various authors. When a socially anxious individual uses safety behaviours in a situation in which they are anxious, they are likely to attribute a successful outcome to the use of these strategies, rather than a more realistic appraisal of their performance and the expectations and impressions of others. Safety behaviours also prohibit the acquisition of experience disconfirmatory to unrealistic negative beliefs about how others will react to an imperfect performance or signs of anxiety. Safety behaviours may also of themselves contribute to a relatively less skilled social performance (e.g. avoiding personal disclosure, holding something so tightly in an effort to control shaking that behaviour appears stilted, or shaking of tense muscles occurs in any case), which may then reinforce negative self-beliefs. Attempts have been made to determine the impact of safety behaviours on performance in both high and low socially anxious individuals, but methodological challenges have proven difficult to overcome, such as instructions that confound safety behaviours and self-focused attention, the use of generic rather than personally relevant social situations, and the difficulty of identifying when safety behaviours are being used. It has been demonstrated that individuals with high social anxiety do use more safety behaviours in a broader range of social situations than non-socially anxious individuals [78], and there is some evidence to support claims that identifying and reducing the reliance on safety behaviours may enhance outcome from CBT [101].

Behavioural experiments represent another addition to the repertoire of behavioural strategies. They promote cognitive insight as a result of behavioural change, and reflect a greater emphasis on finding the answer for oneself. For example, an individual can learn for themselves the detrimental effects of focusing on a negative internal self-representation by trying the same type of social or performance activity once while deliberately focusing on a negative view of themselves, and on another occasion with a positive or even neutral self-image in mind. In a controlled trial utilizing this methodology, it was indeed the case that holding a negative self-image in mind made participants more anxious as well as having detrimental effects on task performance [102]. Behavioural experiments are generated from the individualized cognitive model, ideally by the individual themselves, often following discussion, or Socratic dialogue, with the therapist.

The situations utilized as the basis of many behavioural experiments may not be very different to those that untreated individuals with SAD are pushing themselves to engage in repeatedly without any improvement in their symptoms. It may be that it is the ‘cognitive preparation’ [82, 103, 104] that occurs in the therapeutic setting prior to such exposure that makes the difference. That is, participants are approaching the task in a particular way and are primed to study the outcome more objectively, judging it against pre-generated hypotheses. In one study utilizing videotaped speeches by participants in a SAD programme, later reviewed by the speakers, those who were primed to judge their performance against a predicted outcome gained more from the experience and were less anxious and apprehensive about doing another speech [103]. This particular type of behavioural experiment appears so helpful clinically that it is now a standard part of many CBT packages.

Novel psychological approaches

A number of other psychological approaches have been developed in recent years including dialectical behaviour therapy, cognitive behavioural analysis system of psychotherapy, mindfulness-based stress reduction (MBSR), mindfulness-based cognitive therapy (MBCT) and acceptance and commitment therapy (ACT), and their effectiveness has recently been reviewed [105]. To this author's knowledge, however, only MBSR, MBCT and ACT have been evaluated in individuals with SAD.

MBSR was developed by Jon Kabat-Zinn and colleagues at the Stress Reduction Clinic (now the Centre for Mindfulness in Medicine, Health Care and Society) at the University of Massachusetts in the 1980s. Based on techniques of Vipassana Buddhist meditation, the programme also included psychoeducation about somatic and cognitive correlates of stress [106]. MBSR has been well evaluated as a treatment for stress and various somatic conditions, and mindfulness-based techniques have recently been reviewed in conjunction with the literature on possible neurobiological correlates of their effects on the brain [107], but only two studies were identified in which MBSR was used to treat SAD. In a non-clinical sample, high and low socially anxious students experienced less anxiety and more positive thoughts when asked to focus on the experience of anxiety without evaluating its meaning using word lists of anxious sensations [88]. An uncontrolled pilot study of mindfulness strategies together with training in task-focused attention (to replace self-focused attention) resulted in improvement on symptom measures of SAD [87]. In a well-designed controlled trial, MBSR was compared to group CBT (CBGT) for generalized SAD. Although both conditions resulted in better quality of life, reductions in scores for depression and interpersonal sensitivity, and reduced disability ratings, CBGT was more effective than MBSR in reducing core symptoms of SAD, such as self-rated fear and avoidance of social and interactional situations, and on overall ratings of illness severity [108]. CBGT also resulted in significantly greater rates of response and remission compared to MBSR.

ACT was described by Hayes et al. in 1999 as ‘an experiential approach to behaviour change’ [109]. It includes elements of a mindfulness approach, and adds an emphasis on acceptance rather than avoidance of unpleasant emotional experience. ACT is reported to focus on values clarification and linking behaviour to personally identified goals and values [110]. Unlike CBT it does not explicitly identify symptom reduction as a goal. There is overlap, however, with the incorporation of exposure techniques. Additionally, the goal of ACT for participants of ‘living with’ anxiety symptoms [111] shows considerable overlap with current CBT approaches, which emphasize reduction of cost perceptions rather than attempts to eliminate anxiety. To date there are no controlled studies of ACT in SAD. A recent uncontrolled pilot study was actually a combination of ACT, exposure therapy and social skills training [110]. No attempt to change cognitions was made and the emphasis was on identifying and pursuing life goals in spite of thoughts or feelings that might arise. Improvements were noted on symptom measures, quality of life and Clinical Global Impressions (CGI) scales comparable to uncontrolled studies of CBT, although this was to be expected given the inclusion of exposure and social skills components.

The number of trials of newer psychological approaches remains very small, and it is not yet possible to draw robust conclusions about the effectiveness of these treatments in SAD.

The Internet is being increasingly explored as a means of providing treatment for mental disorders. Research so far has suggested that computerized treatment is most effective, and otherwise high attrition rates (>50%) are lowest when it is combined with some therapist interaction [112, 113]. A recent study compared Internet-based treatment of SAD with a wait-list control [114]. Participants in the active condition completed nine web-based modules of CBT, and associated homework, for which an online therapist gave feedback. Participants were required to pass a quiz before being able to proceed to the next module. Two 3 h group sessions were offered in conjunction with modules 4 and 8, although only approximately half the Internet-treated group attended the second session: this was linked with both severity (the more severe were less likely to attend) and outcome (those who attended both sessions did better on primary outcome measures). Outcomes indicated that the Internet-based treatment was effective at reducing symptoms of SAD (ES[Q1] averaged 0.8), with gains reasonably well maintained at 1 year follow up. In a subsequent study the same investigators were able to increase the rate of full completion of the programme to 93% of participants by adding a short weekly telephone call from a therapist [115]. The average ES was also slightly higher at 0.93. These effect sizes are comparable to those found after face-to-face treatment [64], and the attrition rates were actually better than those for many face-to-face programmes.

Two Australian studies of Internet-based CBT with therapist contact via email (approximately 2 h of contact over 10 weeks of treatment) demonstrated within-group ES of 1.0–1.2 on measures of social anxiety, with attrition rates of only approximately 20% [116, 117]. Importantly, the mean pre-treatment scores were comparable to those seen in face-to-face treatment programmes, at least on social anxiety-specific measures, suggesting that these were not simply less symptomatic individuals. Long-term maintenance of gains remains to be demonstrated, as does the suitability and effectiveness of Internet-based treatment for individuals with the higher levels of depression commonly encountered in outpatient clinics, but Internet-based CBT with therapist support shows promise in providing a cost-effective treatment option with the benefit of being accessible even to those in rural and remote areas.

Future directions

Aside from the longstanding focus on improving treatment effectiveness, three problems remain to be solved to improve outcomes in SAD: the low rate of engagement with treatment, provision of effective treatment, and reduction of the treatment attrition rate.

The Harvard Brown Anxiety Research Program (HARP) has now reported on 12 years of follow up of patients with anxiety disorders [118, 119]. The long-term recovery rates for SAD are poor, even when defined as generously as in the HARP study (at least one period of at least 8 consecutive weeks with no or only mild symptoms). SAD had the lowest remission rates of all the anxiety disorders in the HARP study, with the cumulative probability for recovery over 12 years of only 0.37 (compared to major depression at 0.73) [119]. The problem of low rates of treatment seeking is compounded by the fact that many who do seek help do not receive effective treatment [7, 50, 118]. In the NSMHWB only 32.2% of those in contact with health services (approx. 7% of all those meeting criteria for 12 month social phobia) reported receiving a treatment known to be effective, the lowest rate of any anxiety disorder in the survey [50]. There is a role for continuing education of general and mental health professionals about evidence-based treatments for SAD.

Although results for individuals who complete treatment with either (or both) pharmacotherapy or CBT are good, there is a significant number of patients who drop out of treatment at various stages, and who do not then benefit. Attrition rates of 25% are probably average. A recent German study examining the stages and reasons for discontinuing CBT found that 16% of patients refused treatment after the first assessment, and a further 12% dropped out after being provided with an individualized model of SAD and an explanation of the nature and rationale for the CBT on offer [120]. These authors found that dropouts (but not refusers) were significantly more likely than treatment completers to be married, more avoidant, and to have comorbid diagnoses. There was a trend towards higher measures of impairment, severity and depression. Other studies, however, have failed to support a significant difference between dropouts and completers on measures of severity [64, 121]. Nevertheless, the German data are clearly worrying in that they suggest that many of the most severely affected individuals may not be getting the treatment that could benefit them; it will be important to study this further and in any case it is a call to find better ways to attract individuals to and keep them in effective treatment. In this regard the Internet and computer-based treatments may offer the promise of reaching more individuals, although the problem of attrition remains to be solved.

Conclusion

A genetic vulnerability shared with depression, anxiety and other emotional disorders, and a smaller genetic vulnerability specific to SAD, are likely to account for a large proportion of the variance in the risk for SAD. The phenotypic expressions of this vulnerability may include BI and shyness. Environmental factors may act on underlying vulnerability in variable ways at different developmental stages, to shift an individual from preclinical to clinical levels of symptoms and distress. Typically, this happens relatively early in life. Once SAD is established, a number of cognitive processing biases can be identified that play a major role in the maintenance of disorder. Cognitive behaviour therapy is effective at relieving symptoms and improving disability. Effectiveness may be improved by targeting beliefs about the realistic cost of negative social outcomes, addressing subtle forms of avoidance such as safety behaviours, redirecting the focus of attention away from the self and reducing negative PEP. Development of individualized cognitive models and an approach incorporating behavioural experiments is recommended. Computerized cognitive behaviour therapy programmes with minimal therapist support are increasingly being shown to be effective. Novel approaches requiring further assessment include mindfulness-based strategies and ACT. Problems warranting future research and intervention include relatively low rates of treatment seeking, even lower rates of receipt of evidence-based treatments, and significant attrition rates. Professional and public education may assist in addressing some of these problems and improving the access of individuals to effective treatments.

Footnotes

Based on a keynote address presented at the Australasian Anxiety Disorders Conference, 2008.

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Social Anxiety Disorder: Recent Developments in Psychological Approaches to Conceptualization and Treatment

Abstract

Keywords

Aetiology of social anxiety disorder

Treatment seeking

Effectiveness of psychological treatments

Cognitive behaviour therapy

Novel psychological approaches

Future directions

Conclusion

Footnotes

References