An Open-Label Trial of Venlafaxine in Body Dysmorphic Disorder

CME3
Original Research
An Open-Label Trial
of Venlafaxine in Body
Dysmorphic Disorder
By Andrea Allen, PhD, Sallie Jo Hadley, MD, Alicia Kaplan, MD, Daphne Simeon, MD,
Jennifer Friedberg, PhD, Lauren Priday, MA, Bryann R. Baker, BA,
Jennifer L. Greenberg, PsyM, and Eric Hollander, MD
ABSTRACT
Objective: Body dysmorphic disorder (BDD),
a preoccupation with imagined ugliness, is a disabling
condition that seems to respond preferentially
to selective serotonin reuptake inhibitors. This
open-label trial examines venlafaxine’s efficacy in
BDD and is the first known study of this serotoninnorepinephrine
reuptake inhibitor in BDD.
Methods: A total of 17 BDD patients 16–65
years of age entered and 11 completed a 12–16
week open-label trial of venlafaxine. Participants
were treated with venlafaxine until a therapeutic
dose (minimum of 150 mg/day) was reached
and then maintained at that dose for 8 weeks.
Key outcome measures were the Yale-Brown
Obsessive-Compulsive Scale Modified for
Body Dysmorphic Disorder and Clinical Global
Impressions-Improvement scale.
Results: Venlafaxine was found to be effective
in lessening the specific symptoms and global
severity of BDD. Paired t-tests were used to
compare baseline and final ratings on the Yale-
Brown Obsessive-Compulsive Scale Modified
for Body Dysmorphic Disorder total, obsessions,
Needs Assessment
Body dysmorphic disorder (BDD) is a serious, treatment-refractory disorder
for which there are few studied treatments. This article provides
the first published data on venlafaxine treatment of BDD. In addition,
this article summarizes available data on pharmacological treatments
for BDD and how treatment for BDD may differ from treatment of OCD.
Learning Objectives
At the end of this activity, the participant should be able to:
• Select a first-line pharmacologic treatment for body dysmorphic
disorder.
• Dose venlafaxine appropriately.
• Understand what treatment response to expect over the first few
months of treatment.
Target Audience: Neurologists and psychiatrists
CME Accreditation Statement
This activity has been planned and implemented in accordance with the
Essentials and Standards of the Accreditation Council for Continuing
Medical Education (ACCME) through the joint sponsorship of the Mount
Sinai School of Medicine and MBL Communications, Inc. The Mount
Sinai School of Medicine is accredited by the ACCME to provide continuing
medical education for physicians.
Credit Designation
The Mount Sinai School of Medicine designates this educational activity
for a maximum of 3 AMA PRA Category 1 Credit(s) TM . Physicians
should only claim credit commensurate with the extent of their participation
in the activity.
This activity has been peer-reviewed and approved by Joseph Zohar, MD,
professor of psychiatry at Chaim Sheba Medical Center. Review date:
January 17, 2008. Dr. Zohar does not have an affiliation with or financial
interest in any organization that might pose a conflict of interest.
To Receive Credit for This Activity
Read this article and the two CME-designated accompanying articles,
reflect on the information presented, and then complete the CME posttest
and evaluation found on page 156. To obtain credits, you should score
70% or better. Early submission of this posttest is encouraged: please
submit this posttest by February 1, 2010, to be eligible for credit. Release
date: February 1, 2008. Termination date: February 28, 2010. The estimated
time to complete all three articles and the posttest is 3 hours.
Faculty Affilations and Disclosures: Please see page 144 for biographies and disclosure information.
Off-label Usage Disclosure: The authors disclose that they will discuss off-label or investigational uses of venlafaxine for the treatment of
body dysmorphic disorder.
CNS Spectr 13:2 © MBL Communications 138
February 2008

and compulsions scores; by this measure ven-
lafaxine significantly reduced BDD symptoms
overall (P=.012), as well as obsessions (P=.034)
and compulsions specifically (P=.021). A single
sample t-test, comparing final Clinical Global
Impressions-Improvement scale ratings to “no
change” (score: 4) found significant improvement
following treatment.
Conclusion: Venlafaxine may be an effective
treatment for BDD, including both obsessive and
compulsive symptoms. Controlled research on
venlafaxine in BDD is recommended.
CNS Spectr. 2008;13(2):138-144
INTRODUCTION
Body dysmorphic disorder (BDD) is a disabling
condition in which normal-appearing individuals
are painfully preoccupied with an imagined or
slight defect in their appearance. It is a somatoform
disorder that some consider to be an obsessive-compulsive
spectrum disorder 1,2 because of
its similarities to obsessive-compulsive disorder
(OCD) in symptoms, course, age of onset, 3,4
and response to primary pharmacologic 5 and
psychological treatments. 6 BDD and OCD differ
primarily in the focus of their obsessive thinking
and compulsive behaviors and in the degree of
insight, with BDD patients having notably poorer
insight than OCD patients. 7 BDD often leads to
seriously impaired social and occupational functioning,
high rates of hospitalization, suicidal
ideation, and suicide attempts. 3,4,8-12
Research on pharmacotherapy for BDD is
limited but available reports indicate that BDD
seems to respond to the same first-line medications
as OCD, specifically the selective serotonin
reuptake inhibitors (SSRIs). Open-label
treatment studies and case series 11,13-15 suggest
that SSRIs, such as fluvoxamine, fluoxetine, and
citalopram, can reduce BDD symptoms. More
importantly, controlled studies have found that
the serotonin norepinephrine reuptake inhibitor
(SNRI) clomipramine 16 and the SSRI fluoxetine 17
can be effective in ameliorating BDD symptoms.
In a double-blind, controlled pharmacologic
treatment investigation of BDD, Hollander
and colleagues 16 concluded that the SNRI clomipramine
was significantly superior to desip-
Original Research
ramine, a selective norepinephrine reuptake
inhibitor in reducing overall BDD severity and
specific BDD symptoms; the medication was
equally effective for patients with poor insight
as those with good insight. Phillips and colleagues’
17 study of fluoxetine likewise showed
efficacy in BDD regardless of level of insight.
Venlafaxine, another SNRI, acts similarly
to clomipramine and has been shown to have
fewer side effects and a lower risk of adverse
effects than other, older antidepressants, including
clomipramine. 18-20 Venlafaxine is not associated
with the anticholinergic, antihistamine, and
α-adrenergic side effects of clomipramine. 21 Case
study and open-label data 21-26 as well as two double-blind
active comparison studies 27,28 suggest
that venlafaxine may be an effective treatment
for OCD. However, one small, placebo-controlled
trial 18,29 failed to show venlafaxine efficacy in
OCD, possibly due to the small sample size and
other methodological limitations. To date, there
are no published studies regarding the efficacy
of venlafaxine in BDD and, given the efficacy
of the SNRI clomipramine, may represent an
important option in treating BDD.
Additional research is needed on pharmacotherapy
for BDD. Recent publications have suggested
the augmentation with antipsychotics
may not be as helpful in BDD as in OCD. The
typical antipsychotic pimozide, although one
of the earliest agents shown to be effective in
monosymptomatic hypochondriasis, failed to
demonstrate any efficacy in BDD in a placebocontrolled
trial. 30 A small study of the atypical
antipsychotic olanzapine 31 showed efficacy in
only two of nine BDD patients.
We hypothesized that venlafaxine would be
an effective medication for adults with BDD
since it has a similar pharmacologic mechanism
as clomipramine, and the added advantage
of having a more favorable side-effect
profile. This open-label study is the first treatment
study to examine the efficacy of venlafaxine
in the treatment of BDD.
METHODS
Subjects
Seventeen adult outpatient subjects (20–50
years of age [mean age: 29.7±8.4 years], two
males, and 15 females) participated in this medi-
CNS Spectr 13:2 © MBL Communications 139
February 2008

cation trial; 11 completed treatment (two males,
nine females; age range: 20–50 years [mean
age: 31.2±8.8 years]). Subjects were recruited by
advertising and other media and by referral from
outside clinicians. This research was approved
by the Mount Sinai School of Medicine’s institutional
review board and written informed consent
was obtained from all participants after the
study procedure and possible side effects were
explained and prior to the psychiatric and psychological
interviews.
All patients met criteria for Diagnostic and
Statistical Manual of Mental Disorders-Fourth
Edition, Text Revision diagnosis of BDD or its
delusional variant as determined by a study
psychiatrist and psychologist experienced in
diagnosing BDD. The pre-admission screenings
included a psychiatric and medical evaluation
by a board-certified or board-eligible psychiatrist
and a diagnostic interview by a licensed psychologist
to determine whether the patients met
inclusion and exclusion criteria.
Exclusion criteria included comorbid psychiatric
diagnoses: schizophrenia, schizoaffective
disorder, or any other psychotic disorder not
attributable to delusional BDD; current or lifetime
bipolar disorder; current or recent (past 2 months)
substance abuse or dependence; or recent suicide
attempt or suicidal ideation that warranted
consideration of hospitalization. Patients could
not have used a psychotropic medication for the
treatment of BDD (SSRI nor SNRI) within 2 weeks
of start of the trial (6 weeks for fluoxetine). Of
the 17 subjects, 7 were SSRI naïve and 10 had
prior failed SSRI trials; one subject had tried only
one SSRI (paroxetine) and the rest had from two
to four different prior SSRI trials (an average of
2.6 prior trials), many, though not all, of the trials
would be considered adequate, while the rest
were discontinued due to adverse side effects.
Patients were also excluded if they had any significant,
unstable medical problems as were females
who were pregnant, breast feeding, or not using
adequate contraception.
Procedure
Patients who met inclusion and exclusion
criteria were entered into a 12–16 week openlabel
trial of venlafaxine. Patients were continued
past 12 weeks and up to 16 weeks if they
had not been on a minimally adequate (150 mg/
Original Research
day) dose for 8 weeks; all patients had been on
the adequate dose for 8 weeks by the 16-week
point. Both a psychiatrist and a psychologist
administered key baseline ratings, including
the Clinical Global Impressions-Severity scale
(CGI-S), 32 Yale-Brown Obsessive-Compulsive
Scale Modified for Body Dysmorphic Disorder
(BDD-YBOCS), 33 Brown Assessment of Beliefs
Scale, 34 Overvalued Idea Scale, 35 and the
Schneier Disability Scale. 36 In addition, subjects
completed the self-report version of the Body
Dysmorphic Disorder Examination (BDDE-SR), 37
the Beck Depression Inventory II (BDI-II), 38,39 and
the Beck Anxiety Inventory (BAI). 40
Subjects met with their study psychiatrist
every other week for the first 4 weeks and
monthly thereafter for medication management
and ratings. During each visit, the study
psychiatrist administered the Clinical Global
Impressions-Improvement scale (CGI-I) and
BDD-YBOCS, asked about side effects of the
medication since the last visit, and provided
venlafaxine. Patients were started at a dose of
37.5 mg/day and increased to a minimum of 150
mg/day, generally over the first 4 weeks of the
study, and then maintained at that dose for 8
weeks. Dosage and titration were tailored to
each individual subject’s current BDD symptoms
and medication side effects. The actual range
of final doses for the completers was 150–225
mg/day with a mean final dose of 164±30.34 mg/
day. Patients completed the study in an average
of 13±1.70 weeks. At the study endpoint, the
psychiatrist and psychologist each repeated the
baseline measures, including the CGI-I rather
than the CGI-S, and the patient completed the
BDDE-SR, BAI, and BDI-II.
Statistics
For most measures, pre-post analyses were
done using paired t-tests comparing baseline
ratings with endpoint ratings. In the case of the
CGI-I, a single sample t-test was conducted comparing
the endpoint ratings with no change (a
rating of 4). The key evaluative measures were
the BDD-YBOCS and CGI-I ratings by the treating
psychiatrist. For the key measures, data was
analyzed for both completers and for the intentto-treat
sample with the last observations carried
forward. Pearson correlations were used to
examine relationships between variables.
CNS Spectr 13:2 © MBL Communications 140
February 2008

RESULTS
Venlafaxine was found to be effective in lessening
the global BDD severity and specific BDD
symptoms of the 11 completers. (See the Table
for a summary of key measures.) There was a
significant decrease in overall BDD severity as
measured by the CGI-I ratings completed by the
treating psychiatrist and the study psychologist.
Original Research
BDD symptoms were reduced significantly based
on both the psychiatrist’s and the psychologist’s
ratings on the BDD-YBOCS overall, as well as
the compulsions subscale. Obsessions were
reduced significantly based on the psychiatrist’s
BDD-YBOCS ratings but did not quite reach significance
based on the psychologist’s ratings.
The findings were equally strong for the intent-
TABLE.
Clinical Ratings of Subjects with Body Dysmorphic Disorder Treated with Venlafaxine
Measure
Psychiatrist’s Ratings
BDD-YBOCS
Baseline (Mean±SD)
Completers (N=11)
Endpoint (Mean±SD) t-test Significance
Total 34.64±5.09 26.55±11.28 3.07 P=.01
Obsessions 14.73±2.20 11.45±5.03 2.45 P=.03
Compulsions 14.82±1.20 11.55±4.93 2.73 P=.02
CGI-I N/A 2.73±0.91 4.67 P

to-treat sample. Note that the 12-week ratings
by the treating psychiatrist also showed significant
improvement on the key outcome variables:
the CGI-I (t=3.634, df=10, P=.005) and total BDD-
YBOCS scores (t=2.985, df=10, P=.014). The Figure
shows the change over time in the ratings by the
psychiatrist. As indicated, the ratings for both the
CGI-I and the BDD-YBOCS are significantly different
from baseline by week 4.
Based on the treating psychiatrists’ ratings, seven
of 11 patients responded by having a CGI-I rating of
1 or 2 (four of 11 patients), indicating “very much”
or “much improved,” respectively, or a BDD-YBOCS
reduction of >33% (five of 11 patients).
Venlafaxine may have improved insight in BDD
patients when measured by the Overvalued Idea
Scale; although the psychiatrist’s ratings of insight
did not show a significant improvement after treatment,
there was a trend in that direction and there
was significant improvement based on the psychologists’
ratings. This trend was not found for
the Brown Assessment of Beliefs Scale or for the
insight question on the BDD-YBOCS (psychiatrist:
t=1.00, df=10, P=.341; psychologist: t=–.90, df=10,
P=.391). Change on the Schneier Disability Scale
also varied by rater. The ratings by the psychiatrist
did not show significant improvement but those by
the psychologist did show significant improvement
(psychiatrist: t=–1.12, df=10, P=.289;
psychologist: t=2.62, df=10, P=.026).
FIGURE.
CGI-I and BDD-YBOCS Over Time
CGI-Improvement
5
4.5
4
3.5
3
2.5
2
1.5
1
0.5
0
* Significantly different from baseline, P≤.01.
† Significantly different from baseline, P

DISCUSSION
Venlafaxine was effective in reducing the
general and specific symptoms of BDD. The
results were found for both compulsions and
obsessions. The response was relatively robust
with seven of the 11 completers (64%) rated as
responders with four rated as “much” or “very
much improved” and five having a BDD-YBOCS
score reduction of >33%.
These results are generally consistent with
the findings for venlafaxine in OCD. Additional
research is needed in both disorders to clarify
the possible advantages of SNRIs versus SSRIs.
The improvement was found as early as 4 weeks
and was found even with relatively moderate
doses of venlafaxine. These are both notable findings
given that the assumption, supported by most
of the existing literature, is that SSRI treatment
of BDD requires high doses and a relatively long
trial. The current findings are, however, consistent
with the findings for clomipramine 16 : we found clomipramine
to be significantly more effective than
desipramine at a mean dose of 138±87 mg/day
(the mean dose of desipramine was 147±80 mg/
day); the clomipramine dose is comparable with or
slightly lower than the mean dose of venlafaxine
used in the current study. A reanalysis of the data
shows that the effect in the clomipramine versus
desipramine study was approaching significance
at 4 weeks for both the BDD-YBOCS (t=2.01, df=20,
P=.058) and the CGI-I (t=1.87, df=21, P=.075). Our
current findings are also consistent with a recent
open-label citalopram trial that found significant
improvement at 4.6±2.6 weeks, which preceded
the increase in dose to 60 mg/day. 14
Venlafaxine also seems to improve the general
distress felt by BDD patients as shown by
the change in those measures on the BDDE-SR.
Other aspects of BDD symptoms measured by
this instrument were not found to change significantly
though it is not clear whether this was
due to insensitivity of the instrument, a lack of
change in the behaviors that are asked about,
or the small sample size. Likewise, there was
no change in functioning as measured by the
Schneier Disability Scale.
Evidence for a change in insight was weak
and further research is required to clarify the
efficacy of venlafaxine in improving insight and
relationship between insight and response to
venlafaxine. Past research has suggested that
Original Research
SSRIs in BDD are as effective in patients with
poor insight as with good insight 16,17 and may
actually improve insight. 14,16
The primary limitations of this study are the
small sample size (n=17, 11 completers), the
open-label design, and the primarily female sample.
Most of the patients in this study received
only venlafaxine 150 mg/day, which was what
we established as our minimally acceptable dose
because it is considered the minimal adequate
dose in OCD. We would expect higher doses to
be more effective in BDD as in OCD. However,
even this relatively low dose was effective in
these patients.
CONCLUSION
Venlafaxine may be an effective treatment
for BDD, including both obsessive and compulsive
symptoms, even at relatively low doses.
Further research should be conducted using a
placebo control and a larger sample in order to
establish the efficacy of venlafaxine more conclusively
and to allow further investigation of
other more subtle effects, such as the impact of
venlafaxine on insight. CNS
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Original Research
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Dr. Allen is assistant professor of psychiatry in the Department of Psychiatry at the Mount Sinai School of Medicine (MSSM) in New York City. Dr. Hadley
is assistant clinical professor of psychiatry in the Department of Psychiatry at MSSM. Dr. Kaplan is assistant professor of psychiatry at Drexel University
College of Medicine, Allegheny General Hospital’s Department of Psychiatry in Pittsburgh, Pennsylvania. Dr. Simeon is associate professor of psychiatry in
the Department of Psychiatry at MSSM. Dr. Friedberg is health science specialist at the Veterans Administration New York Harbor Healthcare System in New
York City. Ms. Priday is intern in the Department of Psychiatry at MSSM. Ms. Baker is doctoral student in clinical psychology in the Department of Psychology
at the University of Maryland in College Park. Ms. Greenberg is clinical fellow in psychology (psychiatry) in the Body Dysmorphic Disorder Clinic & Research
Unit at Massachusetts General Hospital and Harvard Medical School in Boston, Massachusetts. Dr. Hollander is the editor of this journal, Esther and Joseph
Klingenstein Professor and Chairman of Psychiatry at MSSM, and director of the Seaver and New York Autism Center of Excellence in New York City.
Faculty Disclosures: Drs. Allen, Hadley, Kaplan, Simeon, and Friedberg and Mses. Priday, Baker, and Greenberg do not have an affiliation with or financial
interest in any organization that might pose a conflict of interest. Dr. Hollander is a consultant to Wyeth. Data were presented as a poster at the sixth annual
International Obsessive Compulsive Disorder Conference in Lanzarote, Canary Islands, Spain from November 14–16, 2003.
Submitted for publication: August 24, 2007; Accepted for publication: January 20, 2008.
Please direct all correspondence to: Andrea Allen, PhD, The Mount Sinai School of Medicine, Department of Psychiatry, One Gustave L. Levy Place, Box
1230, New York, NY 10029-6574; Tel: 212-241-3176, Fax: 212-987-4031; E-mail: andrea.allen@mssm.edu.
CNS Spectr 13:2 © MBL Communications 144
February 2008