Personality as a Predictor of Treatment Response to Escitalopram in Adults with Body Dysmorphic Disorder

Abstract

Objective.

Serotonin reuptake inhibitors (SRIs) are the first-line pharmacotherapy for body dysmorphic disorder (BDD), a common and severe disorder. However, predictors and correlates of treatment response are not well understood. A closer examination of baseline personality dimensions and disorders and of changes in personality during SRI treatment is needed to advance knowledge of this clinically important issue.

Method.

We conducted a secondary analysis of data from a pharmacotherapy relapse prevention trial of the SRI escitalopram in adults with BDD to examine personality dimensions and traits, as well as whether these variables predict and correlate with treatment response. A total of 65 participants with BDD completed the NEO Personality Inventory-Revised (NEO PI-R) before starting open-label treatment with escitalopram and 42 participants completed the NEO PI-R after treatment.

Results.

At baseline, participants with BDD displayed higher levels of neuroticism and lower levels of extraversion than a normed reference group. Higher baseline neuroticism was a significant predictor of nonresponse to escitalopram treatment, even when baseline depression severity was controlled for. Changes in neuroticism were not associated with treatment response.

Conclusion.

Our findings underscore the relationship between BDD and neuroticism, and they suggest a link between neuroticism and SRI treatment response.

Body dysmorphic disorder (BDD) is classified in DSM-5 in the section on “Obsessive-Compulsive and Related Disorders.” It is associated with significant functional impairment and poor quality of life.¹ In addition, rates of attempted and completed suicide in patients with BDD are markedly high.² Although cognitive-behavioral therapy (CBT) and serotonin reuptake inhibitors (SRIs) are currently considered first-line interventions for BDD, there is a dearth of research examining predictors of treatment response. Understanding who benefits from treatment, and how these individuals differ from those who do not benefit, is a critical next step to improve existing treatments for BDD.

The study of personality in healthy and clinical populations has yielded numerous well-validated measures that assess multiple aspects of personality from its broader dimensions down to its specific facets. One of the most widely studied models of personality, the Five Factor Model (FFM), assesses 5 personality dimensions: neuroticism, extraversion, openness to experience, agreeableness, and conscientiousness,³ which are conceptualized as reflecting broad, stable, and enduring dimensions of personality.⁴ The FFM dimensions encompass both normal and abnormal personality, as studies have linked these dimensions with personality disorders.^5-7 Although personality dimensions and disorders are related constructs, they are also distinct. An extreme score on one of the FFM dimensions does not necessarily equate with dysfunction, unless it is accompanied by distress and/or impairment.^5,6

Personality characteristics of people with psychiatric disorders may be informative predictors of treatment response. Theoretically, neuroticism and extraversion have been proposed as higher-order dimensions that account for significant variance in the overlap, etiology, and course of some emotional disorders, with neuroticism explaining temporal covariation between depression, social anxiety, and generalized anxiety disorder in particular.⁸ As a trait vulnerability dimension, greater neuroticism may therefore plausibly predict worse treatment outcomes across various disorders. Numerous studies have examined neuroticism (a tendency to experience negative affect across fear, sadness, embarrassment, anger, guilt, and disgust) specifically as a predictor of pharmacotherapy outcome in psychiatric samples. In depression, findings have been mixed, with some studies showing that higher levels of neuroticism led to poorer outcomes,^9,10 and some studies not finding a significant relationship.^11,12 In generalized anxiety disorder, higher neuroticism was associated with a worse treatment outcome in patients receiving various medications, including placebo,¹³ and the presence of a cluster C personality disorder was associated with worse outcomes with antidepressant medication.¹⁴ Neuroticism has also been examined as a predictor of response to nonpharmacological treatments, with studies showing that higher baseline neuroticism was associated with poorer outcomes in both CBT and acceptance and commitment therapy for anxiety disorders,¹⁵ as well as in CBT for older adults with late-life anxiety.¹⁶ It is unclear whether personality characteristics are differentially associated with response to psychotherapy versus medication. In depression, higher levels of neuroticism may be associated with better response to antidepressants than to CBT,¹⁷ although another study found that responders to combination treatment (medication and psychotherapy) exhibited lower pre-treatment neuroticism, higher extraversion, and higher openness to experience, compared with treatment nonresponders.¹⁸

Furthermore, there is increasing evidence of the malleability of personality with medication treatment and psychotherapy. Tang et al¹⁹ reported that paroxetine, a selective serotonin reuptake inhibitor (SSRI), compared with placebo, resulted in greater changes in neuroticism and extraversion, even when controlling for changes in depression, whereas the changes in neuroticism associated with cognitive therapy, compared with placebo, were in part attributed to changes in depression. Converging evidence investigating the unified protocol, a CBT designed to target core dimensions of neuroticism and extraversion, showed that treatment led to decreases in neuroticism and increases in extraversion, compared with a waitlist control.²⁰ As discussed below, available research on personality as a predictor of treatment outcome in BDD has focused primarily on medication trials, and no studies have examined change in neuroticism during any kind of treatment in BDD.

BDD has been found to be associated with very high levels of neuroticism, as well as low extraversion and conscientiousness, low to average agreeableness, and average openness to experience, compared with adult norms, on the NEO Five Factor Inventory (NEO-FFI),²¹ which assesses the FFM. Furthermore, BDD has been linked to high levels of behavioral inhibition, a personality dimension that reflects sensitivity to punishment and anxiety, particularly in novel situations, compared with findings in a population-based control sample,²² and it has been found to be moderately correlated with neuroticism.²³ Individuals with BDD tend to be unassertive, socially inhibited, socially anxious (both related and unrelated to appearance concerns), and sensitive to rejection, relative to normative samples.^24-26 Consistent with these findings, previous reports have indicated that 57% to 100% of adults with BDD have at least 1 personality disorder, with avoidant personality disorder most common (AVPD).^1,21,27-29 The relationship between BDD and AVPD is consistent with the high neuroticism and low extraversion scores reported in samples with BDD.²¹

Only a few studies have examined personality as a predictor of response to SRI treatment in BDD, with somewhat mixed findings. A placebo-controlled study of the SRI fluoxetine (n = 67) found that treatment response was independent of the presence of a personality disorder at baseline.³⁰ Similarly, in an open-label trial of the SRI fluvoxamine, the presence of a personality disorder at baseline did not impact treatment response relative to those who did not have a personality disorder.^21,31 However, fluvoxamine responders had significantly fewer personality disorders at baseline than nonresponders.²¹ Similarly, a double-blind crossover trial comparing the SRI clomipramine and the non-SRI desipramine in 17 patients with BDD showed that treatment responders had significantly fewer personality disorders at baseline than nonresponders.²⁷ Regarding personality traits, the fluvoxamine study discussed above found that fluvoxamine responders and nonresponders did not significantly differ in terms of baseline NEO-FFI scores, although there was a trend for responders to be more extraverted.²¹ Finally, in the open-label phase of our study of the SRI escitalopram (the study that is the focus of this report), we recently found that the presence of a personality disorder at baseline predicted poorer treatment response.³²

The main goal of the study presented in this article was to examine the relationship between personality and escitalopram treatment response by examining baseline FFM personality dimensions and individual personality disorders, as well as changes in personality during treatment. Our first objective was to characterize personality features in a sample of patients with BDD seeking escitalopram treatment. Based on earlier findings, we hypothesized that patients with BDD would show higher levels of neuroticism and lower levels of extraversion than normative samples. Although we could have generated hypotheses about each of the FFM dimensions, we selected those 2 dimensions, because we hypothesized that they would be most likely to be associated with treatment outcome in BDD, based on the literature on other disorders, and also to limit the number of predictors that would be tested in this relatively small sample. We also hypothesized that AVPD would be the most common comorbid personality disorder diagnosis, consistent with earlier findings.^1,21,27-29 Our second objective was to examine the associations between personality variables and BDD symptom severity. We hypothesized that greater neuroticism, lower extraversion, and a greater number of personality disorder diagnoses (and presence of AVPD, specifically) would be associated with greater BDD symptom severity; an earlier study had found that BDD severity was significantly greater in individuals with a personality disorder than in those without one.²¹ Third, we examined whether baseline personality variables predicted response to escitalopram treatment. We hypothesized that greater baseline neuroticism and the presence of AVPD would be significant predictors of poorer response to escitalopram. Our final objective was to examine the personality correlates of clinical improvement during escitalopram treatment. Given previous reports that SSRIs may reduce neuroticism in depression,¹⁹ we reasoned that neuroticism could at least in part be a state measure that improves with escitalopram treatment in BDD, and we hypothesized that responders would show greater reductions in neuroticism compared to nonresponders.

METHODS

Participants

The analyses in this study were based on a subset of treatment-seeking participants with BDD presenting to a specialty BDD outpatient program at Massachusetts General Hospital or Rhode Island Hospital (formerly Butler Hospital)/Brown University for a study on pharmacotherapy relapse prevention using escitalopram.³² The treatment trial had 2 phases: Phase I involved acute open-label escitalopram treatment (up to 30 mg/day) for 14 weeks, which was followed by Phase II, in which responders to escitalopram were randomly assigned to 6 months of additional continuation monotherapy with escitalopram or to discontinuation of escitalopram and substitution with pill placebo.³² This report examines data from the NEO PI-R. This measure was administered 3 times over the course of the study (baseline, end of Phase I, and end of Phase II), but this report includes data only from Phase I (baseline and end of Phase I) because there were significant missing data for the NEO PI-R in Phase II. Of 67 participants who completed the NEO PI-R at baseline, 2 participants had >80% missing data on the NEO PI-R, which prevented calculation of the facet and domain scores; thus, 65 participants were included in the final analyses of data for the baseline time point. By the end of Phase I, data for only 42 participants were available due to participant dropout, early withdrawal, and administrative error. A full description of inclusion and exclusion criteria for the larger trial is reported elsewhere.³² Briefly, exclusion criteria were meeting diagnostic criteria for bipolar or psychotic disorders, substance abuse/dependence in the past 3 months, clinically significant suicidality, psychotropic medication within 2 weeks of baseline (6 weeks for fluoxetine), and concomitant CBT.

Measures

The Structured Clinical Interview for DSM-IV Axis II Personality Disorders (SCID-II)³³ was used to assess for the presence of Axis II personality disorders according to DSM-IV. This interview was conducted during the screening assessment and covered the 11 DSM-IV personality disorders (including personality disorder not otherwise specified), in addition to depressive personality disorder and passive-aggressive personality disorder (which were included in the DSM-IV appendix category).

The Yale-Brown Obsessive-Compulsive Scale Modified for BDD (BDD-YBOCS)^34,35 was administered at each visit (weekly for the first month, then every 2 weeks) by an independent evaluator to assess BDD symptom severity over the past week. The BDD-YBOCS is a 12-item semi-structured clinician-administered scale, adapted from the Y-BOCS, which assesses BDD-related obsessions and compulsions, insight, and avoidance; it has been shown to have strong psychometric properties.³⁵

The Hamilton Rating Scale for Depression (HAM-D)³⁶ is a 17-item clinician-administered scale that was administered at each visit by an independent evaluator to assess depression severity over the past week. Scores on the HAM-D were used to control for depression severity in our analyses.

The Revised NEO Personality Inventory (NEO PI-R)⁴ was administered to assess the 5 factors of personality (neuroticism, extraversion, openness, agreeableness, conscientiousness). It was given at baseline and post-treatment time points during the open-label phase (Phase I). The NEO PI-R is a self-report measure designed to operationalize the 5-factor model of personality.³ It includes 240 self-statements, such as “I am easily frightened” (neuroticism) and “I really like most people I meet” (extraversion), and participants are asked to rate the degree to which these statements are true of themselves on a 5-point scale of strongly disagree to strongly agree. For each of the 5 personality domains, there are 6 sub-scales that measure facets of that domain. For example, neuroticism facets include anxiety, angry hostility, depression, self-consciousness, impulsiveness, and vulnerability to stress. Facet scores range from 0 to 32, and domain scores range from 0 to 192. Mean domain scores are compared to T scores (with a mean of 50 and standard deviation of 10) derived from normative data based on a group of 1000 healthy individuals (500 men and 500 women) who ranged in age from 21 to 96 years and represented a distribution of age and race groups that matched U.S. census projections for 1995.^4,37 Mean domain scores are also compared to ranges based on these normative data that correspond to 5 levels along the distribution for each domain: very low (T ≤ 34), low (T = 35 to 44), average (T = 45 to 55), high (T = 56 to 65), and very high (T ≥ 66).⁴

Procedure

This report examines pre-to-post treatment data only from Phase I of the original treatment trial, corresponding to the open-label phase. In Phase I, participants received open-label escitalopram monotherapy for 14 weeks (except for 2 patients who received 16 weeks of open-label treatment), starting at 10 mg/day during weeks 1–3, 20 mg/day during weeks 4–6, and 30 mg/day thereafter, with dosing adjusted as needed to improve tolerability. This study was approved by the institutional review boards at both study sites and registered through Clinicaltrials.gov (). Written informed consent was obtained from all participants before the study procedures.

Analytic Approach

We calculated the means and standard deviations of the FFM personality dimensions from the NEO PI-R, as well as the proportion of participants with personality disorders as assessed by the SCID-II (Hypothesis 1). We then examined associations between neuroticism, extraversion, and the presence of AVPD, and BDD symptom severity, using Pearson’s correlations for continuous measures and point-biserial correlations between continuous and dichotomous measures (Hypothesis 2). To test whether baseline neuroticism and AVPD predicted response to escitalopram treatment (Hypothesis 3), we conducted a series of logistic and linear regressions (to examine predictors of treatment response as dichotomous and continuous outcomes, respectively). We tested whether neuroticism and AVPD were predictive of treatment response in separate, univariate models, as there was considerable multicollinearity between these predictors (r = 0.534, P < 0.001). To test whether responders showed greater reductions in neuroticism than nonresponders (Hypothesis 4), we conducted logistic and linear regressions to examine associations between changes in neuroticism and treatment response as dichotomous and continuous measures. Analyses for Hypotheses 3 and 4 controlled for baseline depression and changes in depression, respectively, given that personality characteristics may be related to depression severity, which may have an impact on treatment outcome.³⁸ Treatment response was defined in 2 ways: a) as a dichotomous outcome measure: meeting a cutoff of ≥ 30% reduction in the BDD-YBOCS from baseline that persisted for at least 2 consecutive assessments and through post-treatment (or through the last visit, for early terminators), and b) as a continuous outcome measure: reflecting a change in BDD-YBOCS scores from baseline to post-treatment. The definition of ≥ 30% reduction in the BDD-YBOCS is the standard that is used in treatment studies of BDD; previous research indicates that this criterion for responder status corresponds to “much” or “very much improved” on the Clinical Global Impressions Scale, with very high sensitivity and specificity.^34,35 As reported in the original outcome paper,³² 67.0% of treated participants and 81.1% of participants who completed the phase of the trial relevant for this analysis (Phase I) responded to escitalopram.

All NEO PI-R variables were checked for normality and outliers. Outliers were defined as +/− 3 SD of the sample mean. We assessed missingness and found that nearly 80% of those cases with missing data were missing only 1 value on the NEO PI-R (range of missing values = 0–13 items). As such, we employed multiple imputation to generate 5 datasets containing values for missing baseline NEO data, and conducted all analyses based on imputed values. Regarding dropout, a total of 23 participants did not complete the NEO PI-R at post-treatment due to the following reasons: dropped due to medication side effects (n = 2) or unknown reasons (n = 11), withdrawn due to missing too many appointments (n = 6) or missing more than 5 days of medication (n = 1), and completed the study but missing data at post-treatment due to administrative error (n = 3). A majority of the dropouts/withdrawals occurred within the first 8 weeks of the study (n = 16/20, 80%). For our prediction analyses, we used multiple imputation to generate 5 datasets containing values for missing BDD-YBOCS and HAMD-D scores for every assessment time point in the trial (baseline, weeks 1, 2, 3, 4, 6, 8, 10, 12, and 14), and determined responder status based on week 12 and week 14 BDD-YBOCS scores to conform with our definition of response as a dichotomous measure. For Hypothesis 4, rather than using multiple imputation to impute missing values on the NEO PI-R at week 14, we assessed neuroticism change using available NEO PI-R data at week 14 due to the amount of missing data and dropout rate.

RESULTS

Descriptive Results

Descriptive characteristics of the sample are shown in Table 1. Table 2 displays descriptive data of the FFM personality dimensions from the NEO PI-R, as well as frequencies of personality disorder diagnoses based on the SCID-II. A majority of participants (n = 41, 64.1%) met diagnostic criteria for at least 1 personality disorder at intake. As expected, the most common personality disorder was AVPD (n = 31, 48.4%), followed by depressive personality disorder (n = 13, 20.3%) and paranoid personality disorder (n = 11, 17.2%). Compared with the normative reference group, descriptive results from the NEO PI-R revealed mean domain scores for patients with BDD that fell in the high range on neuroticism, low range on extraversion and conscientiousness, the average to low range on openness to experience, and the low to very low range on agreeableness. Participants who completed the NEO PI-R at baseline did not differ from those in the larger trial who did not complete the measure on baseline BDD severity, depression severity, or neuroticism (all Ps > 0.05).

Table 1.

Demographic Characteristics (n = 65)

Demographic variable
Age (yr), mean (SD)	34.60 (13.88)
Sex (female), n (%)	44 (67.7%)
Ethnicity, n (%)
Hispanic or Latino	7 (10.8%)
Not Hispanic or Latino	56 (86.2%)
Unknown	2 (3.1%)
Race, n (%)
Caucasian	57 (87.7%)
African American	5 (7.7%)
American Indian	3 (4.6%)
Asian	2 (3.1%)
Alaskan Native	1 (1.5%)
Marital Status, n (%)
Single	43 (66.2%)
Married	9 (13.9%)
Divorced	9 (13.9%)
Separated	2 (3.1%)
Other	2 (3.1%)

Table 2.

Descriptive Data from the NEO PI-R and the SCID-II

	BDD (n = 65)
NEO PI-R Personality Domain	M	SD
Neuroticism	100.79**	11.09
Extraversion	98.85**	13.27
Openness	101.35**	10.10
Agreeableness	100.46**	9.60
Conscientiousness	109.04**	11.79
SCID-II Personality Disordera	%	n
Avoidant	48.4	31
Depressive	20.3	13
Paranoid	17.2	11
Obsessive-Compulsive	12.5	8
Passive-Aggressive	9.4	6
Dependent	4.7	3
Borderline	4.7	3
Narcissistic	1.6	1
Schizoid	0.00	0
Schizotypal	0.00	0
Histrionic	0.00	0
Antisocial	0.00	0
Personality disorder NOS	0.00	0
Total number of personality disordersa	%	n
None	35.9	23
1	34.4	22
2	14.1	9
3	9.4	6
4	4.7	3
6	1.6	1
Any personality disordera	64.1	41

NEO PI-R indicates Revised NEO Personality Inventory; SCID-II, Structured Clinical Interview for DSM-IV Axis II Personality Disorders.

NEO PI-R personality domains were compared with data from a normative group of 1000 healthy individuals (500 men and 500 women) whose age ranged from 21 to 96 years and who represented a distribution of age and race that matched U.S. census projections for 1995.^{4, 37}

^***Reflects significant differences from normative group, P < 0.001.

^aReflects n = 64 due to 1 subject with missing data on the SCID

Association Between Personality Variables and BDD Symptom Severity

Table 3 provides the full correlation matrix for all variables examined. As predicted, neuroticism was significantly positively correlated with baseline BDD symptom severity (r = 0.279, P = 0.024). In addition, the total number of personality disorder diagnoses at baseline was correlated with BDD symptom severity (r = 0.314, P = 0.011). Paranoid personality disorder was the individual personality disorder that was most strongly associated with BDD symptom severity (r = 0.349, P = 0.004), followed by AVPD (r = 0.333, P = 0.007). However, contrary to our hypothesis, extraversion was not associated with BDD symptom severity, nor was any other FFM personality dimension.

Table 3.

Correlations Between BDD Severity, FFM Dimensions, and Total Personality Disorder Diagnoses

		1	2	3	4	5	6	7
1	BDD-YBOCS total at baseline	1
2	NEO PI-R Neuroticism	0.279*	1
3	NEO PI-R Extraversion	−0.211	0.135	1				.
4	NEO PI-R Openness	−0.126	0.349**	0.588***	1
5	NEO PI-R Agreeableness	−0.101	0.303*	0.677**	0.598***	1
6	NEO PI-R Conscientiousness	−0.200	0.204	0.594**	0.640***	0.530***	1
7	Total Number PDs	0.314*	0.518***	0.122	0.246*	0.224	0.054	1

BDD-YBOCS indicates Yale-Brown Obsessive-Compulsive Scale Modified for BDD; NEO PI-R, Revised NEO Personality Inventory; PDs, personality disorders

^***P ≤ 0.001 (2-tailed)

^**P ≤ 0.01 (2-tailed)

^*P ≤ 0.05 (2-tailed)

Prediction of Response to Escitalopram Treatment

Consistent with our hypothesis, when examining treatment response as a dichotomous outcome, neuroticism significantly predicted treatment response (B = −0.032, P = 0.008, OR = 0.968, CI = 0.946 to 0.992). The odds ratio of 0.97 indicated that patients were 0.97 times less likely to respond to escitalopram for every unit increase in baseline neuroticism. When we controlled for baseline depression severity, this effect was still significant (B = −0.030, P = 0.017, OR = 0.971, CI = 0.948 to 0.995). We explored whether any specific neuroticism facets were predictive of treatment response. With all neuroticism facets included in the model (anxiety, angry hostility, depression, self-consciousness, impulsiveness, and vulnerability), greater anxiety (B = −0.152, P = 0.010, OR = 0.859, CI = 0.765 to 0.964), and greater vulnerability (B = −0.108, P = 0.021, OR = 0.897, CI = 0.818 to 0.984) were associated with a lower likelihood of responding to escitalopram. Contrary to our hypothesis, AVPD was not a significant predictor of treatment response (B = −0.281, P = 0.273, OR = 0.755, CI = 0.456 to 1.249, % responders with/without AVPD = 46.3%/53.7%, Ps ranging from 0.306 to 0.885 across multiple imputation datasets). Controlling for baseline depression severity did not alter this effect. Interestingly, the presence of obsessive-compulsive personality disorder was associated with lower odds of responding to escitalopram (B = −0.894, P = 0.011, OR = 0.409, CI = 0.206 to 0.812), and the presence of depressive personality disorder was associated with better odds of responding to escitalopram (B = 0.772, P = 0.037, OR = 2.164, CI = 1.046 to 4.476). No other personality disorders were significant predictors of treatment outcome.

Using a continuous measure of treatment response (defined as a change in BDD-YBOCS scores from baseline to post-treatment), there were no significant associations between personality variables and treatment response. When testing for whether neuroticism predicted responder status while controlling for baseline depression severity, neuroticism was not associated with treatment response, whereas depression severity was (B = −0.166, P = 0.043, CI = −0.327 to 0.005), with more severe depressive symptoms associated with worse treatment response.

Change in Neuroticism During Open-Label Escitalopram Treatment

We examined the hypothesis that responders would show greater change in neuroticism compared with nonresponders. This hypothesis was not supported, as change in neuroticism was not associated with responder status (B = −0.015, P = 0.488, OR = 0.985, CI = 0.943 to 1.028). However, after we controlled for changes in depression severity during treatment, changes in neuroticism were significantly associated with responder status (B = −0.140, P = 0.000, OR = 0.869, CI = 0.805 to 0.938), and changes in depression were also significantly associated with responder status (B = 0.483, P = 0.000, OR = 1.621, CI = 1.382 to 1.900): less change in neuroticism and greater change in depression severity were associated with a greater likelihood of treatment response.

When examining treatment response as a continuous measure, the pattern of results was similar. Change in neuroticism was not associated with treatment response when examined as the only predictor in the model; when we controlled for change in depression severity, change in neuroticism was still not associated with treatment response, but change in depression was (B = 0.682, P = 0.000, CI = 0.517 to 0.846).

DISCUSSION

The results of this study confirmed our hypothesis that BDD is associated with high levels of neuroticism and low levels of extraversion. Our hypothesis that AVPD would be the most common personality disorder was also supported, and, consistent with earlier studies, we found that paranoid personality disorder was also common.²⁹ Also, as predicted, a greater number of personality disorder diagnoses at baseline was associated with greater BDD symptom severity. Our findings for conscientiousness and openness to experience were generally similar to earlier findings, although we found lower average levels of agreeableness (low to very low) than in an earlier report,²¹ which is consistent with previous findings of high mean levels of anger/hostility in individuals with BDD.³⁹ Taken together, these findings are largely consistent with findings from earlier research on personality characteristics in BDD, which reflects a personality profile marked by high levels of negative affect, introversion, fears of negative evaluation by others, and social avoidance.^21,27 These personality characteristics, particularly low extraversion, may also be present in social anxiety,⁴⁰ and this finding supports a broader literature on similarities between BDD and social anxiety.²⁵

Contrary to our hypothesis, AVPD was not predictive of poorer treatment response to escitalopram; however, this finding aligns with previous studies showing that having at least 1 baseline personality disorder diagnosis did not predict response to fluoxetine³⁰ or to fluvoxamine^21,31 in those with BDD, although these studies did not examine AVPD in particular as a predictor of treatment outcome. Notably, in this study, the presence of a personality disorder diagnosis at baseline was significantly associated with poorer treatment response, although the current analyses did not find that AVPD specifically was associated with poorer treatment response. The latter negative finding may, in part, reflect limited statistical power, as fewer participants met diagnostic criteria for AVPD than for any personality disorder, and because personality disorders were assessed as dichotomous, rather than continuous, variables. With regard to the version of the SCID used in the current study, diagnostic criteria for personality disorders are the same in DSM-IV and DSM-5, and thus our findings should also apply to DSM-5 personality disorders; however, because some of the wording of questions in the SCID was changed for DSM-5, it is possible (but seems unlikely) that our findings might have been different if the SCID-5-PD had been used. We also note that our study included depressive and passive-aggressive personality disorders, which were included in the DSM-IV appendix but have been removed from DSM-5.

Interestingly, the only predictor of escitalopram treatment response in the current study was neuroticism. This finding is inconsistent with the previously cited fluvoxamine study, which found that responders and nonresponders did not significantly differ in terms of baseline NEO-FFI scores on any domain, although statistical power was limited. Our finding that neuroticism predicted treatment response even when baseline depression severity was controlled for is consistent with previously reported findings from this study that baseline depression severity did not predict response to escitalopram.³² It is also consistent with other studies of SRIs in BDD, none of which have found an association between presence of major depression at baseline and treatment outcome.^30,31,41 It is interesting that, although baseline depression severity did not predict escitalopram response, the presence of depressive personality disorder was associated with response to escitalopram, and in an unexpected direction (having depressive personality disorder at baseline was associated with better response to escitalopram). Although the different findings for depressive symptoms and depressive personality may seem inconsistent, depressive symptoms have been noted to differ in important ways from those of depressive personality disorder.⁴² In the depression literature, mixed findings have been reported with regard to whether depressive personality disorder predicts treatment outcome,^43,44 which may be due to methodological differences (for example, the continuous versus dichotomous assessment of personality disorder features).

Our findings raise interesting questions about the etiology and maintenance of BDD. As personality is generally conceptualized as stable, it may constitute a vulnerability factor for the development of BDD, which usually has its onset in early adolescence.¹ Given that neuroticism is highly heritable, it remains plausible that one may inherit a genetic predisposition to experience negative affect, which then predisposes toward the development of rejection sensitivity and the development of avoidant personality traits. One hypothesis is that these factors may then lay the groundwork for the development of BDD. Conversely, it is also plausible that BDD may cause rejection sensitivity, social avoidance, and other characteristics of AVPD, as noted by Phillips and McElroy.²¹ In other words, what appear to be stable personality traits, such as social anxiety and rejection sensitivity, might in fact reflect a “state” that is due to BDD. In support of this possibility, evidence suggests that antidepressant medication, relative to placebo, may change neuroticism and extraversion in people with depression even after accounting for improvement in depression.¹⁹ Similarly, in the study of the SRI fluvoxamine in BDD discussed above,²¹ there was a significant decrease in the total number of personality disorders from baseline to treatment endpoint among fluvoxamine responders. These findings raise the question whether these broader FFM personality dimensions of neuroticism and extraversion may actually be somewhat malleable and have dynamic interactions with the manifestation of BDD symptoms.

Our results indicated that changes in neuroticism were not associated with treatment response, but it is unclear whether this is because personality dimensions overall did not change in our study (mean difference score range = −1.72 to 3.06), or because neuroticism is a stable dimension resistant to change. If neuroticism were a “state” due to BDD, we might expect changes in neuroticism to correlate with changes in BDD or even depression (called the “state effect hypothesis,”^11,19) which we did not observe in our study. Changes in depression would be expected to correlate with treatment response because escitalopram is an antidepressant medication. It is also possible that what appear to be personality disorders or traits actually reflect, to some degree, the confounding of personality traits by state (eg, BDD and/or depressive symptoms). Indeed, it can be difficult to differentiate certain personality traits from Axis I states (such as BDD symptoms), especially when the Axis I condition has an early onset and is chronic, as is usually the case with BDD.¹

LIMITATIONS

Our study was limited by the study design, which was observational and correlational in nature. Future research should move beyond observational approaches that show relationships between personality and treatment outcome toward causal models, to examine whether changes in what appears to be personality have specifically been caused by treatment with SRIs or instead are due to a change in anxiety, depression, or BDD, all of which have been shown to be SRI responsive. While our data show that certain personality features may predict escitalopram treatment response, these data are preliminary and require replication in a controlled treatment trial. A placebo-controlled trial could more robustly test our hypothesis that neuroticism specifically predicts SRI treatment response (and not just changes in BDD symptoms over time). We were also limited by the post-hoc nature of our research question, as our study represents a secondary analysis of a larger clinical trial. Accordingly, it may not have been adequately powered to detect differences in personality factors between treatment responders and nonresponders. In addition, as our sample included individuals who were primarily non-Hispanic Caucasian, results may not generalize to more diverse populations. Finally, because the second phase of our study involved treatment with an SRI and pill placebo, some individuals were excluded from participation (for example, those with bipolar disorder, current substance use disorder, and higher degrees of suicidality), which may limit the generalizability of our findings.

CONCLUSIONS

The clinical implications of our findings are numerous. Our study replicates previous findings showing that individuals with BDD display, on average, low levels of extraversion and high neuroticism, a personality dimension linked to adverse public health outcomes, such as mental and physical disorders, and mental and general health service use.⁴⁵ The high prevalence of personality disorder impairment, particularly AVPD, in our sample is consistent with previous research on the overlapping features between BDD and social anxiety, such as introversion, rejection sensitivity, and social avoidance.²¹ Our finding that treatment response is correlated with baseline neuroticism suggests a possible role of personality in escitalopram treatment response separate from the role of depression. Future studies are needed to examine these and other predictors of treatment response in BDD, an important topic that has clinical implications yet has received little research attention.