Journal of Affective Disorders 287 (2021) 34–40

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Journal of Affective Disorders

journal homepage: www.elsevier.com/locate/jad

Research paper

Predictors and moderators of symptom change during cognitive-behavioral

therapy or supportive psychotherapy for body dysmorphic disorder
Katharine A. Phillips, M.D. a, b, c, d, *, Jennifer L. Greenberg, Psy.D. e, f, Susanne S. Hoeppner, Ph.
D. e, f, Hilary Weingarden, Ph.D. e, f, Sheila O’Keefe, Ed.D. e, f, Aparna Keshaviah, Sc.M. e, f, g,
David A. Schoenfeld, Ph.D. e, f, Sabine Wilhelm, Ph.D. e, f
a
Rhode Island Hospital
b
Alpert Medical School of Brown University
c
New York-Presbyterian Hospital
d
Weill Cornell Medical College, Cornell University
e
Massachusetts General Hospital
f
Harvard Medical School
g
Mathematica Policy Research

A R T I C L E I N F O A B S T R A C T

Keywords: Background: Research on predictors of treatment outcome in body dysmorphic disorder, a common and severe
Predictors disorder, is very limited, and no prior studies have examined moderators of outcome. Because treatment is often
Moderators but not always efficacious, it is important to identify who is more likely to benefit. We examined predictors and
Body dysmorphic disorder
moderators of improvement with therapist-delivered cognitive-behavioral therapy versus supportive psycho­
Cognitive-behavioral therapy
Supportive psychotherapy
therapy in the only study of these treatments for body dysmorphic disorder. This report presents secondary
Treatment analyses from a study whose primary findings have previously been published (Wilhelm et al., 2019).
Methods: Participants (N=120) with DSM-IV body dysmorphic disorder were randomized to therapist-delivered
weekly cognitive-behavioral therapy or supportive therapy for 24 weeks. Using reliable and valid measures, we
tested baseline body dysmorphic disorder severity, insight/delusionality, and depression severity as predictors
and moderators of overall and treatment modality-specific symptom change. We explored additional variables as
predictors and moderators of outcome.
Results: Greater treatment credibility (p=0.02) and presence of obsessive-compulsive personality disorder
(p=0.03) predicted greater improvement. Serotonin-reuptake inhibitor treatment at baseline (unchanged during
the study) (p=0.01) predicted less improvement. No other variables predicted or moderated outcome (all
p>0.05).
Limitations: The study was not powered a priori to detect predictor or moderation effects, which limited our
ability to detect them unless they were strong.
Conclusions: Because greater treatment credibility predicted better outcomes, fostering credibility during therapy
may maximize gains. Improvement was not impeded by more severe body dysmorphic disorder, depressive
symptoms, or poorer insight. No variables moderated treatment-specific improvement.

Introduction
Body dysmorphic disorder (BDD), a distressing or impairing preoc­
cupation with nonexistent or slight defects in one’s physical appearance,
has a point prevalence of 1.7-2.9% and is associated with high rates of
suicidality (Hartmann and Buhlmann, 2017; Phillips et al., 2005). BDD
is characterized by significantly higher levels of suicidality than other
psychiatric disorders with high risk for suicidal thoughts and acts
(Angelakis et al., 2016; Snorrason et al., 2019). Accordingly, it is
important to identify not only efficacious treatments but also who would
benefit most from such treatments.
Cognitive-behavioral therapy (CBT) tailored to BDD’s unique
symptoms is the psychosocial treatment with the strongest empirical
support (Rasmussen et al., 2017). However, data on predictors of

* Corresponding Author
E-mail address: kap9161@med.cornell.edu (K.A. Phillips).

https://doi.org/10.1016/j.jad.2021.03.011
Received 24 November 2020; Received in revised form 28 February 2021; Accepted 2 March 2021
Available online 11 March 2021
0165-0327/© 2021 Elsevier B.V. All rights reserved.
K.A. Phillips et al.
post-treatment outcome with CBT for BDD are limited to a few studies.
In one study, greater treatment credibility and working alliance (Fly­
gare et al., 2020), and in another study greater expectancy of
improvement (Greenberg et al., 2019), predicted better CBT outcome.
Worse CBT outcome at post-treatment was predicted by poorer
BDD-related insight in two of four studies (Flygare et al., 2020; Green­
berg et al., 2019; Neziroglu et al., 2001; Veale et al., 2014), greater BDD
severity in one of two studies (Flygare et al., 2020; Greenberg et al.,
2019), greater depression severity in one of three studies (Flygare et al.,
2020; Greenberg et al., 2019; Veale et al., 2014), and longer duration of
BDD in one of two studies (Flygare et al., 2020; Veale et al., 2014). A
meta-analysis of seven randomized controlled trials of CBT for BDD did
not identify any reliable predictors of CBT outcome (Harrison et al.,
2016).
Data on predictors of improvement with therapy for BDD are limited
to these studies. Most of the data on predictors of BDD improvement
come from studies with fairly small sample sizes and limited statistical
power. Also, no studies have examined predictors of improvement with
supportive psychotherapy, the most commonly received therapy for
BDD (Phillips et al., 2013b). And no therapy studies for BDD have
examined moderators of treatment outcome.
In this report we examine predictors and moderators of improvement
with therapist-delivered CBT versus enhanced supportive therapy; this is
the first study to examine the relative efficacy of these in-person treat­
ments and the largest study of predictors of treatment outcomes in BDD
to date, which enhances statistical power. The primary findings from
this study have previously been published (Wilhelm et al., 2019); the
present report presents secondary analyses from this study. Identifying
factors that predict or moderate improvement is important for choosing
or tailoring treatment to patients.
Our a priori hypotheses were that more severe BDD and depressive
symptoms, as well as poorer BDD-related insight/delusionality, would
predict poorer treatment outcome. When we began this study, data on
predictors of psychosocial treatment outcome were available from only
one small study (N=30), which examined only BDD-related insight
(Neziroglu et al., 2001). We additionally based our hypotheses on our
clinical experience and studies of obsessive-compulsive disorder (OCD)
(Keeley et al., 2008), which has similarities to BDD (Phillips et al.,
2007). We also explored a range of additional demographic and clinical
variables as possible predictors and moderators of treatment outcome.
Methods
Participants
Massachusetts General Hospital/Harvard Medical School and Rhode
Island Hospital/Brown University were the two sites for this randomized
controlled trial of therapist-delivered CBT versus enhanced supportive
psychotherapy for BDD (N=120). Inclusion criteria were: 1) primary
diagnosis of DSM-IV BDD for ≥6 months; 2) age 18 or older; 3) at least
moderate BDD symptoms (score ≥24 on the Yale-Brown Obsessive
Compulsive Scale Modified for BDD); and 4) appropriate for outpatient
treatment. Exclusion criteria were: 1) current, clinically significant
suicidality; 2) intellectual disability, dementia, brain damage, or other
cognitive impairment that would interfere with ability to engage in CBT;
3) meeting DSM-IV criteria for substance abuse or dependence within
the past 3 months or a positive urine toxicology screen for illicit,
unprescribed drugs; 4) meeting DSM-IV criteria for a current manic
episode, lifetime psychotic disorder, or borderline personality disorder;
5) body image concerns better accounted for by an eating disorder; 6)
previous completion of ≥10 sessions of CBT for BDD; 7) current psy­
chotherapy; or 8) behavioral or medical illness that was likely to inter­
fere with study participation. Psychotropic medications had to be stable
for at least 2 months before enrollment, medication could not change
during the study, and new medication or psychotherapy could not be
initiated during study treatment. Of the 120 enrolled participants, 92
35
Journal of Affective Disorders 287 (2021) 34–40
completed clinical assessments at week 24 (end of treatment; CBT: 44/
61, enhanced supportive psychotherapy: 48/59).
Procedures
Study procedures are described in detail in Wilhelm et al. (2019).
Procedures were approved by both sites’ Institutional Review Boards,
the study conformed to recognized standards, and participants provided
written informed consent. An independent Data and Safety Monitoring
Board oversaw study procedures.
Participants completed assessments with a master’s- or doctoral-
level independent evaluator at screening, baseline, mid-treatment
(week 12), and post-treatment (week 24). The independent evaluators
also administered briefer assessments monthly during treatment. Inde­
pendent evaluators were blind to treatment received, were extensively
trained and supervised, and attained strong inter-rater reliability on
primary diagnostic and outcome assessments (Wilhelm et al., 2019).
Participants also completed self-report questionnaires at each
assessment.
Participants were randomly assigned at the baseline visit (50/50,
stratified by treatment site) to therapist-administered CBT for BDD or to
therapist-administered enhanced supportive therapy. See Wilhelm et al.
(2013, 2019) for a detailed description of treatments. Both treatments
consisted of 22 1-hour individual weekly sessions; the final two sessions
occurred every two weeks. Treatments were manualized and adminis­
tered by therapists who had a master’s or doctoral degree, had received
training in BDD, and were experienced in delivering CBT or supportive
therapy. Therapists provided treatment for only one condition, to
maintain treatment fidelity, and obtained weekly supervision from
expert clinicians in their respective treatment modality. Therapy ses­
sions were taped, and adherence to the treatment manual was assessed
by a doctoral-level rater for 15% of randomly selected sessions.
Measures
Structured Clinical Interview for DSM-IV, Patient Version (SCID-
I/P and SCID-II): This gold-standard, reliable semi-structured, clini­
cian-administered diagnostic measure (First et al., 1997; First et al.,
2002) assessed DSM-IV mental disorders. Avoidant (45.0%) and obses­
sive compulsive personality disorder (OCPD) (19.2%) were the most
common personality disorders; given statistical power considerations,
these were the only individual personality disorders examined in this
report.
Yale-Brown Obsessive-Compulsive Scale Modified for BDD
(BDD-YBOCS): This 12-item gold-standard, semi-structured, clinician-
administered measure of current (past-week) BDD severity was the
primary outcome measure. Higher scores indicate greater severity. The
BDD-YBOCS has excellent internal consistency, construct validity,
sensitivity to change, inter-rater reliability, and test-retest reliability
(Phillips et al., 2014; Phillips et al., 1997).
Brown Assessment of Beliefs Scale (BABS): This semi-structured,
clinician-administered measure assesses insight/delusionality across a
range of mental disorders, including BDD. “I look ugly and hideous” is an
example of a BDD belief assessed by the BABS.
Higher scores indicate poorer insight; a score of ≥18 plus a score of 4
on item 1 indicates delusional beliefs. The BABS has strong internal
consistency, construct validity, sensitivity to change, inter-rater reli­
ability, and test-retest reliability (Eisen et al., 1998; Phillips et al.,
2013a).
Beck Depression Inventory (BDI-II): This widely used, well-
validated 21-item Likert-style self-report questionnaire assesses
depression severity during the past two weeks. Higher scores reflect
more severe depressive symptoms (Beck et al., 1996).
Credibility/Expectancy Questionnaire (CEQ): The six-item self-
report CEQ is widely used in clinical outcome studies to assess the
credibility of the treatment rationale (items 1-3) and expectations for
K.A. Phillips et al.
change due to treatment (items 4-6) at baseline or early in treatment.
Higher scores indicate greater treatment credibility and expectancy,
respectively. In this study, we specified the treatment target symptoms
as “appearance concerns, avoidance behaviors, and compulsions” in
items 2 and 3 for credibility, and used only a single item (”By the end of
therapy, how much improvement in your anxiety do you think will
occur?”) to assess treatment expectancy. The CEQ has good internal
consistency, test–retest reliability, and predictive validity for treatment
outcomes (Devilly and Borkovec, 2000). In our sample, the internal
consistency of the credibility factor was good (Cronbach’s α=0.78), and
credibility and expectancy showed a moderate to strong positive cor­
relation (r=.73).
BDD Data Form: The frequently used BDD Data Form (Phillips et al.,
2013b) obtained data on demographics and clinical variables, such as
age of BDD onset, BDD duration, past course of BDD (continuous [i.e.,
less than 1 month of remission excluding treatment response] vs
episodic), and medication and prior therapy received. Psychosocial
treatment histories varied greatly among participants in terms of treat­
ment type, length of treatment, and reason for treatment; we oper­
ationalized treatment history into a binary variable differentiating
between participants with five or more sessions of psychosocial treat­
ment vs. those with little to no exposure to prior treatment.
Statistical Approach
Baseline site differences in the potential predictors examined were
assessed using Barnard’s exact tests for categorical outcomes and 2-sam­
ple t-tests for continuous outcomes. Correlations between the potential
predictors were calculated as Pearson correlations for correlations be­
tween two continuous variables (i.e., age, BDD-YBOCS total scores,
BABS total scores, BDI-II total scores, BDD duration, treatment credi­
bility, and treatment expectancy), point-biserial correlations for corre­
lations between continuous variables and truly binary variables (i.e.,
gender), biserial correlations between continuous and dichotomized
binary variables (i.e., racial-ethnic minority status, both education
variables, unemployment status, marital status variables, living situa­
tion variables, BABS delusionality, major depressive disorder diagnosis,
current comorbid SCID-I or SCID-II diagnosis (yes/no), current OCPD,
current avoidant personality disorder, and current use of psychotropic
medications, including use of a serotonin-reuptake inhibitor (SRI),
another type of antidepressant, or a benzodiazepine, and tetrachoric
correlations between any binary variables.
For each predictor variable, we then used a separate linear latent
growth curve model with BDD-YBOCS total scores (during weeks 0-24)
as the outcome and specifying the following model effects: site but not
treatment differences at baseline (Twisk et al., 2018), site effects over
time, treatment-by-site interactions over time, the predictor as a base­
line covariate, predictor effects over time (predictor-by-time interac­
tion), and moderator of the treatment effect over time
(predictor-by-treatment-by-time interaction). The growth models used
random intercepts and slopes with an unstructured covariance matrix to
account for repeated measures. Degrees of freedom were estimated
using the Kenward-Roger method. Continuous predictors were
mean-centered and standardized before adding them to the growth
models. Model residuals did not indicate any departures from normality
and showed homogeneity of variance. Effect sizes of slopes over time
were calculated as dgrowth-modeling analysis change = βtx/(τ)1/2, in which βtx
was the difference between treatment-specific slope estimates and τ was
the model-specific variance of the slopes (Feingold, 2009); effect sizes
for baseline differences were calculated analogously with model-specific
intercept variances. These effect sizes can be interpreted in the same way
as Cohen d.
In a follow-up analysis to investigate features associated with SRI
medication use at baseline, we used a logistic regression model with five
predictors, allowing for ~5 events per variable (Vittinghoff and
McCulloch, 2007). The predictors selected included baseline BDD
36
Journal of Affective Disorders 287 (2021) 34–40
symptom severity (BDD-YBOCS total score) to adjust for anticipated
effects of the severity of the disorder; the other four predictors chosen
were depression severity (BDI-II total scores), BDD duration, course of
BDD, and prior exposure to five or more sessions of therapy, all of which
were significant univariate predictors of baseline SRI use in exploratory
univariate models at p<.10.
Statistical significance was evaluated at a 2-tailed p<.05 unless
otherwise noted. Effect estimates of slopes and slope differences are
presented as model-adjusted estimates with 95% confidence intervals.
All analyses were performed using SAS System for Windows, version 9.4
(IBM).
Results
Participants had a mean (SD) age of 34 (13.1); 83% were Caucasian,
and 77% were female. See the primary manuscript for detailed de­
mographic and clinical characteristics of the sample and a CONSORT
diagram describing participant recruitment and retention (Wilhelm
et al., 2019). The key study outcome (previously reported) was that BDD
severity decreased significantly more with CBT than with supportive
psychotherapy by the end of treatment; however, the treatment differ­
ence was significant at only one of the two treatment sites. Regarding
response rates for assessment completers at week 24, at one site they
were 84.6% for CBT versus 69.2% for supportive psychotherapy; at the
other site they were 83.3% for CBT versus 45.5% for supportive psy­
chotherapy (Wilhelm et al., 2019).
Key Correlations at Baseline
Of the 23 baseline characteristics examined in the longitudinal
mixed models, nine were significantly associated with BDD severity at
baseline. Seven baseline characteristics were associated with greater
BDD severity: high school degree or less (raw r=.39; model b=3.09, 95%
CI: [0.34, 5.84], dGMA-intercept =0.72), poorer BDD-related insight (raw
r=.46; model b=2.53, 95%CI: [1.68, 3.37], dGMA-intercept =0.70), BDD-
related delusionality (raw r=.50; model b=3.94, 95%CI: [2.04, 5.84],
dGMA-intercept =0.99), greater depression severity (raw r=.39; model
b=2.27, 95%CI: [1.39, 3.14], dGMA-intercept =0.61), one or more current
Axis I comorbidities (raw r=.27; model b=2.37, 95%CI: [0.16, 4.58],
dGMA-intercept =0.56), current major depressive disorder (raw r=.42;
model b=3.48, 95%CI: [1.52, 5.45], dGMA-intercept =0.85), and current
OCPD (raw r=.27; model b=2.45, 95%CI: [0.07, 4.83], dGMA-intercept
=0.57). Two baseline characteristics were associated with less severe
BDD: having a college degree or more (raw r=-.15; model b=-2.24, 95%
CI: [-4.20, -0.28], dGMA-intercept =-0.53) and longer BDD duration (raw
r=-.23; model b=-1.00, 95%CI: [-1.94, -0.05], dGMA-intercept =-0.23).
Supplemental Table 1 shows these correlations and additional correla­
tions among the baseline characteristics.
Baseline Predictors of Treatment Outcome
Only three examined baseline characteristics predicted treatment
outcome over time: greater treatment credibility, current comorbid
OCPD, and baseline use of an SRI (Table 1 and Supplemental Table 2).
Participants who at baseline reported higher credibility ratings for their
assigned treatment type experienced greater improvement in BDD
severity during the course of treatment (weekly slope difference for
+1SD: b=-0.12, 95% CI: [-0.21, -0.02], dGMA-slope =-0.33) (Figure 1). We
were unable to detect a significant correlation between baseline BDD
severity and treatment credibility (raw r=.16; model b=0.12, 95% CI:
[-0.87, 1.11], dGMA-intercept =0.03) or between baseline insight and
treatment credibility (raw r= -0.02; see Supplemental Table 1). Our
previously reported (Wilhelm et al, 2019) significant 3-way interaction
of treatment type by site over time became non-significant (p=.13) after
including treatment credibility in the model.
Participants with current OCPD also experienced greater reduction
 K.A. Phillips et al.
Table 1
Effect estimates for baseline covariates, predictor effects, and treatment moderation effects of predictors on BDD symptom severity over time (baseline to post-treatment [week 24]) in a sample of people with primary BDD
(n=120) randomized to 24 weeks of treatment with either cognitive behavioral therapy or enhanced supportive psychotherapy for BDD.
Predictors and moderators effecta Baseline difference Predictor effect a Treatment moderator effect a

Est. 95% CL Pr > F ES Est. 95% CL Pr > F ES Est. 95% CL Pr > F ES

Demographics
Age (years) -0.76 [-1.71, 0.20] 0.12 -0.17 -0.03 [-0.11, 0.05] 0.41 -0.10 0.15 [-0.01, 0.31] 0.06 0.44
Gender (male) -0.13 [-2.43, 2.16] 0.91 -0.03 0.09 [-0.11, 0.29] 0.37 0.26 -0.25 [-0.65, 0.15] 0.21 -0.71
Racial/ethnic minority (y/n) 1.67 [-0.90, 4.24] 0.20 0.38 -0.11 [-0.34, 0.12] 0.33 -0.32 0.30 [-0.16, 0.75] 0.19 0.85
High school degree or less (y/n) 3.09 [0.34, 5.84] 0.03 0.72 -0.10 [-0.36, 0.15] 0.42 -0.29 -0.15 [-0.66, 0.36] 0.57 -0.41
College degree or more (y/n) -2.24 [-4.20, -0.28] 0.03 -0.53 0.13 [-0.05, 0.30] 0.15 0.36 -0.02 [-0.37, 0.33] 0.92 -0.05
Unemployed (y/n) 2.00 [-0.43, 4.42] 0.11 0.46 0.09 [-0.13, 0.30] 0.44 0.24 0.09 [-0.35, 0.53] 0.68 0.25
Never married (y/n) 1.73 [-0.22, 3.68] 0.08 0.40 0.08 [-0.09, 0.25] 0.34 0.23 -0.05 [-0.39, 0.28] 0.75 -0.15
Clinical characteristics
BDD-YBOCS (bsl. total score) n/a -0.07 [-0.16, 0.01] 0.08 -0.21 -0.07 [-0.24, 0.10] 0.40 -0.20
Lack of insight (BABS bsl. total score) 2.53 [1.68, 3.37] <.0001 0.70 -0.04 [-0.12, 0.05] 0.42 -0.10 0.13 [-0.04, 0.30] 0.12 0.38
Delusionality (BABS, y/n) 3.94 [2.04, 5.84] <.0001 0.99 -0.02 [-0.20, 0.16] 0.82 -0.06 0.08 [-0.28, 0.44] 0.68 0.21
Depression severity (BDI-II, bsl. score) 2.27 [1.39, 3.14] <.0001 0.61 0.02 [-0.07, 0.11] 0.64 0.06 0.04 [-0.14, 0.21] 0.68 0.10
Current Axis-I comorbidity (y/n) 2.37 [0.16, 4.58] 0.04 0.56 0.05 [-0.16, 0.25] 0.65 0.13 0.04 [-0.36, 0.45] 0.83 0.12
37

Current MDD (y/n) 3.48 [1.52, 5.45] 0.00 0.85 -0.04 [-0.22, 0.14] 0.69 -0.10 -0.04 [-0.40, 0.32] 0.84 -0.10
BDD duration (years) -1.00 [-1.94, -0.05] 0.04 -0.23 0.00 [-0.08, 0.08] 0.95 0.01 0.13 [-0.03, 0.29] 0.12 0.36
Current Axis-II comorbidity (y/n) 1.93 [-0.03, 3.90] 0.05 0.45 -0.11 [-0.28, 0.06] 0.21 -0.30 -0.06 [-0.41, 0.28] 0.71 -0.18
Current OCPD (y/n) 2.45 [0.07, 4.83] 0.04 0.57 -0.22 [-0.41, -0.03] 0.02 -0.64 -0.02 [-0.41, 0.37] 0.92 -0.06
Current Avoidant PD (y/n) 1.92 [-0.09, 3.92] 0.06 0.45 -0.08 [-0.26, 0.09] 0.35 -0.23 -0.11 [-0.46, 0.24] 0.53 -0.31
Psychotropic medication use
Psychotropic med. use at baseline (y/n) 0.05 [-1.90, 2.00] 0.96 0.01 0.15 [-0.02, 0.32] 0.09 0.41 0.11 [-0.22, 0.45] 0.50 0.33
SRI use at baseline (y/n) 0.27 [-1.92, 2.46] 0.81 0.06 0.24 [0.06, 0.43] 0.01 0.71 0.11 [-0.26, 0.48] 0.55 0.33
Benzodiazepine use at baseline (y/n) 2.29 [-0.36, 4.94] 0.09 0.53 0.01 [-0.22, 0.24] 0.95 0.02 -0.22 [-0.67, 0.24] 0.34 -0.60
Antidepressant use at baseline (y/n) -1.24 [-4.01, 1.53] 0.38 -0.28 -0.06 [-0.30, 0.18] 0.61 -0.17 -0.01 [-0.49, 0.48] 0.98 -0.01
Treatment credibility/expectancy
Treatment credibility (bsl. score) 0.12 [-0.87, 1.11] 0.81 0.03 -0.12 [-0.21, -0.02] 0.02 -0.33 -0.13 [-0.32, 0.06] 0.18 -0.36
Treatment expectancy (bsl. score) -0.24 [-1.22, 0.75] 0.63 -0.06 -0.09 [-0.18, 0.01] 0.07 -0.24 -0.08 [-0.27, 0.11] 0.38 -0.23
a
For continuous variables, effect estimates are based on a 1 standard deviation increase from the mean.Est. = effect estimate; 95% CL = estimated 95% confidence limits; Pr > F = p-value based on Type 3 tests of fixed
effects; ES = effect size; bsl = baseline; BDD = body dysmorphic disorder; BDD-YBOCS = Yale-Brown Obsessive Compulsive Scale Modified for Body Dysmorphic Disorder; BABS = Brown Assessment of Beliefs Scale; BDI-

Journal of Affective Disorders 287 (2021) 34–40

II = Beck Depression Inventory-II; MDD = major depressive disorder; OCPD = obsessive-compulsive personality disorder; SRI = serotonin reuptake inhibitor; baseline predictor data was missing for the following variables,
resulting in a lower sample size for the affected models: depression severity (n=1); current MDD (n=1); SRI use at baseline (n=1); benzodiazepine use at baseline (n=1); antidepressant use at baseline (n=1); treatment
credibility (n=11); treatment expectancy (n=11). All models also included site but not treatment differences at baseline, site effects over time, treatment effects over time, and treatment-by-site interactions over time in
accordance with the main outcome analysis reported previously (effect estimates shown in Supplementary Table 2).
K.A. Phillips et al.
Figure 1. BDD severity over the course of therapy by baseline treatment
credibility
in BDD symptoms over the 24 weeks of treatment than participants
without current OCPD (weekly slope difference: b=-0.22, 95% CI:
[-0.41, -0.03], dGMA-slope =-0.64) (Figure 2). Those with OCPD had more
severe BDD symptoms at baseline (Figure 2). In addition, participants
with current OCPD attended more therapy sessions than those without
OCPD: M (SD) 22.8 (2.3) with OCPD vs. 17.8 (7.8) without OCPD, t
(df=111.58)=-5.27, p<.0001). However, there was no group difference
in terms of the percentage of CBT homework completion: M (SD) 74.2
(13.8) with OCPD vs. 74.0 (21.2) without OCPD, t(df=54)=-0.03,
p=0.98).
Participants who reported SRI use at baseline experienced smaller
reductions in BDD severity than those not taking an SRI (weekly slope
difference: b=0.24, 95% CI: [0.06, 0.43], dGMA-slope =0.71) (Figure 3). In
the follow-up analysis to investigate features associated with SRI
medication use at baseline (Vittinghoff and McCulloch, 2007), BDD
symptom severity was not a significant predictor of baseline SRI use (OR
[95% CI] for a 1 SD increase: 0.68 [0.38, 1.20]; p=.1854). However,
baseline SRI use was significantly associated with greater depression
severity (OR [95% CI] for a 1 SD increase: 2.13 [1.18, 3.86]; p=.0123),
longer BDD duration (OR [95% CI] for a 10-year increase: 1.48 [1.06,
2.05]; p=.0203), past continuous course of BDD (episodic course OR
[95% CI]: 0.16 [0.04, 0.68]; p=.0134), and five or more sessions of prior
CBT for any reason, including BDD (OR [95% CI]: 10.79 [2.06, 56.43];
p=.0048).
Treatment expectancy, BDD duration, and our hypothesized vari­
ables of BDD-related insight, BDD severity, and depression severity did
not significantly predict change in BDD outcome over 24 weeks of
treatment (Table 1).
Figure 2. BDD severity over the course of therapy by the presence or absence
of baseline comorbid obsessive-compulsive personality disorder (OCPD)
38
Journal of Affective Disorders 287 (2021) 34–40
Figure 3. BDD severity over the course of therapy by baseline use of a sero­
tonin reuptake inhibitor (SRI)
Baseline Moderators of Treatment-Specific Outcome
No baseline demographic, clinical, medication use, or treatment
credibility/expectancy characteristics moderated the effect of treatment
(i.e., the rate of BDD-symptom improvement in CBT versus supportive
therapy) on BDD severity over the course of treatment (all p values >.05;
Table 1).
Discussion
We found that greater treatment credibility and OCPD at baseline
predicted greater BDD improvement, whereas baseline SRI use (un­
changed during treatment) predicted less improvement. Improvement
was not impeded by poorer BDD-related insight, more severe BDD or
depressive symptoms, comorbid Axis I or II disorders, or other examined
variables. No examined variables moderated treatment outcome (i.e.,
predicted better or worse outcome with CBT or supportive psychother­
apy specifically).
One prior study found that treatment credibility predicted better
outcome with internet-based CBT for BDD (Flygare et al., 2020),
whereas our prior study of therapist-delivered CBT found this at only a
trend level (p=0.07; n=48) (Greenberg et al., 2019). However, statistical
power in the latter study was limited, and the odds ratio was 1.66 (95%
CI: [0.95-2.91]); treatment credibility became a significant predictor in
that study when assuming all missing outcomes were treatment
non-responders, but not when missing outcomes were assumed to be
responders. The latter study found that treatment expectancy signifi­
cantly predicted better CBT outcome, which the present study found at
only a trend level (p=0.07). In other disorders, greater therapy credi­
bility and expectancy of improvement with treatment predict symptom
improvement (Chambless et al., 2017; Mooney et al., 2014), although
some OCD CBT studies have not found this for expectancy (Steketee
et al., 2011; Vogel et al., 2006). The reason for these somewhat varying
results regarding treatment credibility and expectancy as predictors of
treatment outcome are unclear, although in some studies limited sta­
tistical power may play a role. Further research is needed to examine
treatment credibility and expectancy as possible predictors of therapy
outcomes in BDD. In the meantime, findings regarding treatment cred­
ibility from the present study and the above-noted study of Flygare and
colleagues suggest that it may be helpful to attempt to strengthen
treatment credibility by discussing with patients research results that
show that therapy for BDD can be effective. CBT’s credibility can also be
enhanced by developing a personalized CBT treatment model early in
treatment that explains how specific CBT strategies may improve the
patient’s BDD symptoms.
No prior BDD studies have examined OCPD as a predictor of treat­
ment outcome. A possible explanation for our result that comorbid
K.A. Phillips et al.
OCPD predicted better therapy outcomes is the general tendency of in­
dividuals with OCPD to follow guidelines and meet expectations, which
may have positively influenced their participation in therapy. This is
consistent with our finding that participants with OCPD attended more
therapy sessions. Although the average amount of CBT homework
completion was not significantly associated with OCPD (homework was
not assigned for supportive psychotherapy), the variance was limited,
due to overall high completion rates. It is possible that participants with
OCPD did higher-quality CBT homework, but our study did not measure
this. In a meta-analysis of CBT for various disorders, both quantity and
quality of homework completion were associated with better outcome
(Kazantzis et al., 2016). In OCD, comorbid OCPD has been variably re­
ported to predict a worse outcome (Pinto et al., 2011) (with more
behaviorally based treatment) or a better outcome (with cognitively
focused therapy) (Gordon et al., 2016).
We found that SRI use at study baseline – which was not changed for
at least two months before, or during, the study – predicted less
improvement. It is highly unlikely that SRIs – the first-line medication
treatment for BDD, which numerous studies have shown are efficacious
for BDD (Phillips, 2017) – would interfere with therapy. A possible
explanation for our result is that baseline SRI use was associated with
several variables that might reflect greater treatment resistance. Such
patients might possibly benefit from more intensive therapy. It is
possible that if these individuals had not received an SRI before study
entry, they might have been even more severely ill at baseline and then
had greater gains with study treatment. Additional research is needed to
examine whether SRI use at the beginning of therapy (which has been at
a stable dose for at least 2 months before starting therapy and also
during therapy) predicts therapy outcomes in BDD and may be a marker
of treatment resistance.
Our a priori hypotheses that greater BDD and depression severity and
poorer BDD-related insight/delusionality would predict poorer treat­
ment outcome were not supported. Prior studies are mixed regarding
these characteristics as predictors of CBT outcome (Flygare et al., 2020;
Greenberg et al., 2019; Neziroglu et al., 2001; Veale et al., 2014). In our
clinical experience, poor or absent BDD-related insight may increase
reluctance to initiate mental health treatment, but our results suggest
that once patients participate in therapy, poorer insight does not impede
improvement.
Limitations: Our study was not powered a priori to detect predictor or
moderation effects, which limited our ability to detect them unless they
were strong; this may have limited our findings. Another study limita­
tion is potential for Type I error due to multiple testing; thus, our find­
ings regarding significant predictors should be considered exploratory
and hypothesis generating, rather than hypothesis testing, and a guide
for future studies. Because this was an efficacy trial at two academic U.S.
sites, the results may not be generalizable to all clinical settings. We
attempted to include types of patients often seen in clinical settings (for
example, those with more severe depression and suicidal ideation, poor
or absent BDD-related insight), but our exclusion criteria excluded
certain symptoms and diagnoses; thus our findings may not apply to
excluded groups (for example, those with severe suicidality).
In conclusion, therapy for BDD appears efficacious even for patients
with comorbid disorders, poor or absent BDD-related insight, or more
severe BDD or depressive symptoms. Because greater treatment credi­
bility predicted better outcomes, fostering credibility during therapy
may maximize gains. While many patients benefit from therapy for BDD,
not everyone responds. To maximize treatment outcomes and ensure
that patients are given the intervention that best meets their needs,
additional studies are needed to further examine predictors and mod­
erators of outcome.
Contributors
All authors have materially participated in the research and/or
article preparation. Dr. Phillips conceptualized the study, obtained
39
Journal of Affective Disorders 287 (2021) 34–40
funding for the study, oversaw all aspects of the conduct of the study,
reviewed and interpreted study results, provided supervision to study
personnel, drafted portions of the manuscript, and wrote the final
manuscript. Dr. Greenberg participated in obtaining funding, overseeing
the conduct of the study, and reviewing and interpreting study results.
Dr. Weingarden drafted portions of the manuscript. Dr. O’Keefe partic­
ipated in conceptualizing the study and provided therapist supervision.
Dr. Keshaviah participated in obtaining funding for the study and
reviewing and interpreting study results. Dr. Hoeppner conducted sta­
tistical analyses and interpreted study results. Dr. Schoenfeld partici­
pated in obtaining funding for the study, contributed to statistical
analyses, and interpreted study results. Dr. Wilhelm conceptualized the
study, obtained funding for the study, oversaw all aspects of the conduct
of the study, reviewed and interpreted study results, and provided su­
pervision to study personnel. All authors have reviewed and approved
the final article.
Declaration of Competing Interest
Dr. Phillips reports grants from the National Institute of Mental
Health and a grant from the David Judah Fund during the conduct of the
study; personal fees from Oxford University Press/International Creative
Management Inc, personal fees from Merck Manual, personal fees from
UpToDate/Wolter’s Kluwer, personal fees from Guilford Press, personal
fees from Oakstone Publishing, personal fees from the International OCD
Foundation, personal fees from the New York Times, personal fees from
Wheeler, Trigg, O’Donnell, and personal fees from Aesculap Academia
(B. Braun Medical Limited) outside the submitted work. Dr. Greenberg
reports salary support from Telefonica Alpha Innovacion and is a pre­
senter for the Massachusetts General Hospital Psychiatry Academy in
educational programs supported through independent medical educa­
tion grants from pharmaceutical companies. Dr. Weingarden reports
salary support from Telefonica Alpha Innovacion, is a presenter for the
Massachusetts General Hospital Psychiatry Academy in educational
programs supported through independent medical education grants
from pharmaceutical companies, and a grant from the National Institute
of Mental Health (K23MH119372) outside the submitted work. Drs.
O’Keefe, Keshaviah, and Schoenfeld have no declarations of interest. Dr.
Hoeppner reports salary support through a research project sponsored
by Telefonica Alpha Innovacion outside the submitted work. Dr. Wil­
helm reports grants from the National Institute of Mental Health and
grants from Telefonica Alpha, Inc., (now Koa Health) and a grant from
the David Judah Fund during the conduct of the study; personal fees
from New Harbinger Publications, personal fees from Guilford Publi­
cations, personal fees from Oxford University Press, personal fees from
Springer, personal fees from the International OCD Foundation, personal
fees from Elsevier, personal fees from the Tourette Association of
America, and and personal fees from One-Mind PsyberGuide outside the
submitted work.
Role of the Funding Sources
This work was supported by the National Institute of Mental Health
(grant numbers R01MH091078 and R01MH091023) and the David
Judah fund, Boston, MA. The funding sources had no role in the prep­
aration of the article; in the study design; in the collection, analysis, or
interpretation of data; in writing of the report; or in the decision to
submit the article for publication.
Acknowledgements
None
Supplementary materials
Supplementary material associated with this article can be found, in
K.A. Phillips et al.
the online version, at doi:10.1016/j.jad.2021.03.011.
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