New perspectives in the treatment of body dysmorphic disorder

Clinical presentation

Body dysmorphic disorder (BDD), once called dysmorphophobia¹, manifests as an excessive concern with minor or wholly nonexistent defects in physical appearance; patients believe themselves to be unacceptably deformed and unattractive when actually they remain normal in appearance^2,3. Patients respond to these beliefs with compulsive behaviors, such as repeatedly combing hair or covering up perceived blemishes, that are unpleasant and difficult to control⁴. BDD is often associated with low quality of life and frequently is comorbid with major depressive disorder, substance use disorders, obsessive–compulsive disorder (OCD), and social phobias^5–8. Patients often are unaware that effective treatments are available and will hide symptoms because of feelings of shame or guilt^9,10. BDD is usually associated with increased suicidal ideation¹¹, delusional ideas, and poor or absent insight¹². The delusional variant of BDD is considered more severe^12,13. Both delusional and non-delusional variants present challenges in treatment compliance; many patients seek unnecessary dermatologic, dental, and other cosmetic interventions in hopes of removing their perceived flaws^14–16. These procedures typically have poor outcomes and lead to patient distress, often worsening symptoms and leading to patient dissatisfaction and loss of self-esteem¹⁶. Some patients undergo repeated surgeries without achieving the expected outcome and thus have increased risk for depression and suicide.

Epidemiology

The prevalence of BDD in the general population is approximately 2%¹⁷ and is strongly associated with a history of cosmetic surgery and higher rates of suicidal ideation and suicide attempts^17,18. Patients who present for cosmetic surgery treatment are also affected by BDD at rates markedly higher than in the general population, ranging from 3 to 53%^16,19. Its prevalence is markedly increased in the inpatient psychiatric setting, at approximately 16%⁹. Prevalence in outpatients with OCD, social phobia, and other disorders ranged from 10 to 40%^9,19. It is often initially undetected¹⁰, suggesting the importance of BDD-specific screening practices and their role in achieving better outcomes^9,10.

Pathophysiology

The pathogenesis of BDD has yet to be fully elucidated but likely involves a combination of social, psychological, and biological factors^20,21. Individuals with BDD were found to be more likely to self-report a history of physical or sexual abuse (or both) in childhood or adolescence in comparison with healthy controls²². A total of 78.7% of patients with BDD surveyed reported a history of childhood maltreatment, which included emotional neglect (68.0%) and emotional abuse (56.0%), physical abuse (34.7%), physical neglect (33.3%), and sexual abuse (28.0%)²³. These abusive experiences were also associated with a history of the following: attempted suicide, a substance use disorder, and a mood disorder. The average age of onset is about 17 years associated with gradual rather than sudden onset^2,24.

An emerging body of neuroimaging research has led to the development of a working neurobiological model of BDD pathophysiology, one that involves the large-scale disorganization of neural networks involved in cognitive control and interpretation of visual and emotional information²⁵. Functional magnetic resonance imaging (fMRI) studies have shown that patients with BDD demonstrate left-sided hyperactivity in several regions within the lateral-temporal-parietal cortices upon exposure to low spatial frequency (LSF) images (which test the processing capacity of holistic information); in contrast, control subjects showed similar activity within the right hemisphere upon exposure to LSF images and showed left-sided activity only in processing of high spatial frequency (HSF) images (which test the processing of detailed featural information)^26,27. This result suggests that patients with BDD will interpret even solely holistic visual information via pathways that interpret detailed, focused information. Functional network pathway analysis studies have also found that patients with BDD demonstrated hypoactive structural connectivity and poor transfer of information between primary and secondary occipital regions^25,28. This may be the cause of the relative hypoactivation of the lingual gyrus, parahippocampal gyrus, and the precuneus in the aforementioned fMRI studies²⁹.

A separate fMRI study comparing visual processing in anorexia nervosa (AN) and BDD used psychophysiological interaction analyses, which estimate functional connectivity between target brain regions and the rest of the brain, to find that patients with BDD demonstrated uniquely heightened functional connectivity in occipitotemporal networks for LSF (testing the processing of holistic information) facial information³⁰. Patients with AN and those with BDD showed similar patterns of higher-order connectivity between the right fusiform face area, the precuneus, and the posterior cingulate cortex; they also showed decreased connectivity of the insula and the central opercular cortex^25,30. The authors support the hypothesis that this may show impaired introspection and also cause patients with BDD and patients with AN to overattribute importance to aberrantly processed visual information^25,30,31. Another study of neural networks has also found that patients with BDD demonstrate disturbances in whole-brain structural topological organization³². This study also found evidence of abnormal connectivity between regions responsible for lower-order visual processing and higher-order visual and emotional processing³².

There is also evidence for a genetic component in the pathogenesis of BDD. A total of 8% of patients with BDD have a family member with similar disease, and this represents four times the prevalence in the general population²⁴. A total of 7% of patients with BDD have a first-degree relative with OCD³³. Although there is no clear explanation to date, this co-occurrence may be explained by genetic or environmental factors or both. A recent study in 2,148 female twins (1,074 pairs) found a covariance of genetic influences common to OCD and BDD phenotypes (64%, 95% confidence interval 0.50–0.80)³⁴. In the same study, environmental factors of influence remained unique for each phenotype. Of notice, the GABA (A)-gamma-2 1(A) allele was associated with BDD, although this did not survive correction for multiple testing³³. The evidence suggests that BDD is heritable and that it might share a genetic predisposition with OCD spectrum disorders, which in turn could explain their co-occurrence. More genome-wide and transcriptomic longitudinal studies are required to better understand the genetic implications of BDD and its associated molecular pathways.

Treatment

The average age of onset is approximately 17 years and symptoms develop gradually^2,24; as such, we emphasize the importance of screening in pediatric and adolescent populations, as early interventions may prevent years of risky and unnecessary cosmetic procedures³⁵. Approaches to the treatment of BDD generally consist of some combination of selective serotonin reuptake inhibitors (SSRIs) and cognitive behavioral therapy (CBT). CBT consists of a regimen of skills-focused psychotherapy centered on addressing and altering dysfunctional thought and behavior patterns with the goals of developing patient coping mechanisms and improving quality of life^36,37. Therapy is focused on developing an understanding of the problems at hand and then responding via a tailored combination of behavioral experiments, exposure, and response prevention³⁸. Key strategies involve exposure with response prevention, which involves gradual confrontation of fear-inducing situations while intentionally resisting the urge to compensate via safety-seeking behaviors to reduce stress³⁹, and mindfulness interventions and perceptual retraining to help broaden focus and attend to aspects of appearance beyond self-perceived deficits⁴⁰. A recent meta-analysis has revealed that CBT is superior to placebo in the form of waitlist placement or other credible control treatment in the reduction of BDD symptoms with a large effect size (seven studies; d = −1.22) and is associated with improvements in insight and in delusionality with a moderate effect size (four studies; d = −0.56)⁴¹. Other control conditions used include supportive therapy, psychoeducation with weekly phone calls, anxiety management, and no treatment⁴¹. However, there are issues related to the use of waitlist controls. Additional CBT modules that address and focus on specific BDD-associated behaviors such as excoriation were developed and incorporated when appropriate. CBT administration via the internet is another promising modality of treatment. A recent pilot feasibility study of 23 subjects found that a pilot internet-based CBT program led to significant improvements as quantified by the Yale-Brown Obsessive–Compulsive Scale for Body Dysmorphic Disorder (BDD-YBOCS) (p <0.001) with a large within-group effect size (d = 2.01)⁴². These results suggest a need for additional, larger-scale trials of internet-based CBT, as the modality has the potential to substantially increase access to care.

Acceptance and commitment therapy (ACT) is a form of behavioral therapy based on the principle that patients consider internal processes aversive and thus can make ineffective attempts to change them⁴³. Difficulty in the interpersonal expression of emotion and experiential avoidance are suggested to be predictors of BDD symptom severity⁴³. ACT thus aims to demonstrate that avoidance is not effective and works with the patient to develop coping mechanisms and emotional acceptance. However, it has been suggested that the distinctions between ACT and CBT have yet to be clearly elucidated and that the differences may be more philosophical or theoretical than suggested thus far⁴⁴. A recent pilot study followed 21 subjects for 12 weeks as they received acceptance-based therapy throughout the study course. As quantified by the BDD-YBOCS, significant reductions in symptom severity before and after treatment were observed, along with a large effect size (d = 1.93)⁴⁵.

CBT has been established as the psychological treatment modality of choice in BDD, and a growing body of evidence shows that CBT is effective—both stand-alone and in combination with pharmacotherapy—in long-term maintenance therapy and relapse prevention^38,46. A recent meta-analysis found that CBT is effective in reducing symptom severity for at least 2–4 months after treatment cessation following hourly or 90-minute sessions administered over a period of 8 to 14 weeks⁴¹. SSRIs and clomipramine are favored specifically for the treatment of BDD as opposed to other serotonin and norepinephrine reuptake inhibitors (SNRIs), some of which are efficacious in conditions in which pain is the chief complaint⁴⁷. Serotonin reuptake inhibitors (SRIs) used for the treatment of this condition include fluoxetine⁴⁸, fluvoxamine⁴⁹, escitalopram⁵⁰, and clomipramine⁵¹. Dosages are typically higher than those required for depression and are similar to levels seen in the treatment of OCD; in fact, dosages required often fall outside of current manufacturer recommendations³⁹. The poor insight associated with BDD also presents challenges in treatment. A combination of frequent comorbidities such as suicidality and depressive symptoms lowers the likelihood of patient adherence to treatment⁵².

Patients should remain on medication for relatively long periods following symptom remission to reduce the likelihood of relapse^50,53. A recent prospective study showed that patients who responded to a 14-week treatment of escitalopram significantly lengthened time to relapse with continued treatment for 6 months relative to placebo⁵⁰. Upon demonstrated reduction of BDD symptoms as quantified by the BDD-YBOCS, 18% of patients who continued treatment for 6 months relapsed, in contrast to 40% with placebo⁵⁰. Thus, SSRI treatment was significantly better than placebo, but a high risk of relapse remained^50,53. The side effects that can be associated with SSRIs, the often-extended or even indefinite duration of treatment, a desire to discontinue medication, or the lack of access to medication are all reasons why SSRIs can be an imperfect approach to therapy. A questionnaire-based study demonstrated that depression, specifically in the forms of thwarted belonging and perceived burdensomeness, is the primary mediator of suicide risk in BDD. It is important to note the cyclical nature of these symptoms and thus the value of treating comorbid depression when treating BDD⁵⁴. In treatment-resistant cases, changing the SSRI used or adding a second medication may be helpful. Such augmentation medications can include second-generation antipsychotics, including olanzapine, quetiapine, and risperidone; among these, risperidone has the best demonstrated efficacy⁵⁵. Other options, including buspirone, administration of CBT in tandem, or switching to clomipramine, may also be beneficial⁵⁶. Additionally, a case study found that the addition of antipsychotics was associated with increased adherence to treatment⁵⁷.

A recent pilot study in adolescents developed a novel approach to CBT for adolescents that incorporated the family in exposure exercises, decreased family participation in BDD-related compulsions, and introduced mindfulness techniques and attentional/perceptual retraining⁵⁸. Patients who completed treatment experienced an average symptom reduction of 68%⁵⁸. Another case study targeted shame and anger in treatment-resistant BDD with a focused form of regular CBT⁵⁹. The subject of the study reported a preoccupation with facial skin associated with a history of sexual abuse and bullying⁵⁹. Administered CBT was enhanced with a form of imagery re-scripting, incorporation of family or support network participation, and compassion-oriented therapy⁵⁹. Symptom severity per the BDD-YBOCS assessment dropped by 94% throughout treatment relative to baseline, and these gains were maintained at an 18-month follow-up visit⁵⁹. Patients with BDD often report a history of appearance- or competency-related bullying; emotional, physical, or sexual abuse; and neglect. These patients typically retain such memories with greater detail and experience them as particularly traumatic^22,60,61. The specific goal of imagery re-scripting in this context is to restructure these memories⁶¹. Imagery re-scripting involves cognitive restructuring, in which the patient explores the central negative meaning of an image and memory, and image re-scripting, which changes the nature of the relevance of the experience to the present⁶¹. One case in which imagery re-scripting was used led to a 26% decrease in symptom severity, as quantified by the BDD-YBOCS, at the follow-up at 2 weeks⁶¹. Another study compared imagery re-scripting with more traditional talk therapy and found that symptoms improved within the first week post-treatment, and gains were maintained for months relative to CBT alone⁶². A key finding was that patients shifted their perception of their symptoms from the perceived physical flaw to a psychiatric condition; the discovery of insight in a condition characterized by its lack is of considerable interest^61,62.

However, one issue with these techniques as proposed is the significant time and financial commitment required in adherence to a prolonged, tailored treatment with a specialist. Computerized treatment programs have been proposed and explored as an alternative modality for therapy. A computerized four-session treatment regimen that focused on interpretation bias modification was found to result in a significant increase in benign biases and reduction in threat biases post-treatment in comparison with placebo control treatment⁶³. Therapist-guided CBT provided via the internet has been found to be superior to online supportive therapy and has been found to significantly reduce symptom severity⁴². The demonstration of a modality by which CBT can be administered via the internet has tremendous potential in increasing the access to care and in removing many significant obstacles to patient adherence⁴².

Classification

The Diagnostic and Statistical Manual of Mental Disorders (DSM) first included BDD, then called “dysmorphophobia”, in the DSM-III as an atypical somatoform disorder and did not include diagnostic criteria³. It was eventually classified as a somatoform disorder in the DSM-IV, and its delusional variant was listed as a psychotic disorder^3,64. In the DSM-IV, OCD was grouped in with anxiety disorders. Research since has led to a distinction between these conditions, and the DSM-V now classifies OCD and related disorders as being distinct within the category of “Obsessive–Compulsive and Related Disorders”. This new category includes BDD, excoriation disorder, hoarding disorder, and trichotillomania. Patients with BDD and patients with OCD share certain biases, which include a tendency toward perfectionism, a preference for symmetry, and repetitive compulsions^65,66. There is also a basis for linking autism spectrum disorder (ASD) and BDD. The two disorders have a similar neurocognitive profile that is marked by a detail-oriented processing bias and a focus on the self⁶⁷. These comparisons raise the question, then, of whether treatment options have translational value. ASD and OCD have been extensively studied and characterized, and promising new treatments in these overlapping fields may provide future directions for research in BDD-specific treatment and pathophysiology.