Armodafinil in Binge Eating Disorder A Randomized
Armodafinil in Binge Eating Disorder A Randomized
Armodafinil in Binge Eating Disorder A Randomized
This study evaluated the efficacy, tolerability, and safety of blood pressure that resolved upon drug discontinuation.
armodafinil in the treatment of binge eating disorder (BED). The small sample size may have limited the detection of
Sixty participants with BED were randomized to receive important drug–placebo differences. As some of the
armodafinil (150–250 mg/day) (N = 30) or placebo (N = 30) observed effect sizes appeared clinically meaningful, larger
in a 10-week, prospective, parallel-group, double-blind, studies of armodafinil in the treatment of BED are
flexible-dose, single-center trial. In the primary longitudinal warranted. Int Clin Psychopharmacol 00:000–000 Copyright
analysis, armodafinil and placebo produced similar rates of © 2015 Wolters Kluwer Health, Inc. All rights reserved.
improvement in binge eating day frequency (the primary International Clinical Psychopharmacology 2015, 00:000–000
outcome measure); however, armodafinil was associated
with a statistically significantly higher rate of decrease in Keywords: armodafinil, binge eating disorder, dopamine
statistically significant reductions in obsessive–compulsive Correspondence to Susan L. McElroy, MD, Lindner Center of HOPE, Research
features of binge eating and BMI. The mean (SD) Institute, 4075 Old Western Row Road, Mason, Ohio 45040, USA
Tel: + 1 513 536 0700; fax: + 1 513 536 0709;
armodafinil daily dose at endpoint evaluation was 216.7 e-mail: susan.mcelroy@lindnercenter.org
(43.9) mg. There were no serious adverse events, although
Received 12 February 2015 Accepted 16 April 2015
one armodafinil recipient developed markedly increased
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2 International Clinical Psychopharmacology 2015, Vol 00 No 00
The Institutional Review Board at the University of package the study medication, and maintain the integrity
Cincinnati Medical Center approved the study protocol of the blinded information throughout the trial.
and the study was carried out in compliance with the
Declaration of Helsinki. All participants signed approved Outcome measures
written informed consent forms after the study proce- The primary efficacy outcome was the weekly frequency
dures had been fully explained and before any study of binge eating days (binge eating days/week), defined as
procedures were performed. Participants were enrolled the mean number of binge eating days per week in the
from 18 November 2009 to 15 August 2014. interval between visits (total number of binge eating days
in the interval divided by number of days in the interval,
Study design and then multiplied by 7). A binge eating day was
This was a prospective, randomized, parallel-group, defined as a day during which the participant had at least
double-blind, placebo-controlled, flexible-dose study one binge eating episode. Binge eating episodes were
carried out at the Lindner Center of HOPE, Mason, defined using the DSM-IV-TR criteria, and assessed by
Ohio. The trial consisted of a 2-week screening period; a clinical interview and review of participant take-home
10-week double-blind treatment period; and a 1-week diaries, on which participants recorded binge eating
treatment discontinuation period. Participants were episodes, duration of binge eating episodes, and food
evaluated at least twice during the screening period; after consumed during binge eating episodes. Secondary effi-
1, 2, 3, 4, 6, 8, and 10 weeks during the treatment period; cacy measures were weekly frequency of binge eating
and 1 week after study medication discontinuation. episodes (binge eating episodes/week); scores on the
Clinical Global Impression-Severity (CGI-S) and
Screening evaluation included the Structured Clinical Improvement Scales (CGI-I) (Guy, 1976), Yale-Brown
Interview for DSM-IV-TR (First et al., 2007) to establish Obsessive Compulsive Scale modified for Binge Eating
BED and comorbid axis I diagnoses; the Eating Disorder (YBOCS-BE) (Goodman et al., 1989), Eating Inventory
Examination-Questionnaire (Fairburn and Beglin, 1994) (EI) (Stunkard and Messick, 1985), Brief Fatigue
to confirm the diagnosis of BED; a medical history and Inventory (BFI) (Mendoza et al., 1999), Inventory of
physical examination; vital signs; height and weight; an Depressive Symptomatology (IDS) (Rush et al., 1996),
ECG; routine blood chemical and hematological tests; and Beck Anxiety Inventory (BAI) (Beck et al., 1988);
and urine drug screen. At this evaluation and at each weight (kg); and BMI (calculated by dividing body
subsequent visit, participants received take-home diaries weight in kg by height in m2). All scales were adminis-
in which to record any binge eating episodes (see out- tered at all postbaseline visits, except for the EI, IDS,
come measures). At the last visit of the screening period and BAI, which were administered at baseline and at
(the baseline assessment), participants continuing to weeks 4, 8, and 10. Weight was obtained at every visit,
fulfill entry criteria were assigned randomly to therapy assessed with the participant in light clothing without
with armodafinil or placebo. At each visit following the shoes on the same scale zeroed at each measurement.
baseline visit, participants were assessed for the number Finally, global improvement and 4-week cessation of
of binge eating episodes and binge eating days experi- binge eating were assessed; these were defined, respec-
enced since the last visit; other outcome measures; tively, as having a CGI-I of 1 or 2 (very much or much
medication compliance ascertained by capsule count; improved) at endpoint and as having no binge eating
treatment-emergent adverse events; use of nonstudy episodes in the last 4 weeks that the participant received
medications; vital signs; and weight. study medication.
All study medication was in identically appearing cap- Safety measures assessed were treatment-emergent
sules (50 mg of armodafinil or matching placebo) sup- adverse events, clinical laboratory and ECG data, and
plied in numbered containers and dispensed to vital signs. Suicidality was monitored using the Columbia-
participants according to a predetermined randomization Suicide Severity Rating Scale (Posner et al., 2011).
schedule. Study medication was started at 150 mg/day, Adherence was ascertained with returned capsule count.
taken as three capsules in the morning. If the patient had
not stopped binge eating after 4 weeks of treatment,
Statistical methods
study medication was increased to 250 mg/day, taken as
The baseline characteristics of each group were com-
five capsules in the morning. Study medication could be
pared using χ2 or Fisher’s exact test for categorical vari-
reduced back to a minimum of 150 mg/day because of
ables and independent-samples t-tests or Wilcoxon rank
side effects during the subsequent 6 weeks of treatment.
sum tests for continuous variables. SAS software (version
Participants were randomized to receive armodafinil or 9.2; SAS Institute Inc., Cary, North Carolina, USA) was
placebo in a 1 : 1 ratio according to computer-generated used to carry out all analyses. Statistical assessments of
coding. Randomization was balanced using permuted outcome variables were performed with the full analysis
blocks. Allocation concealment was achieved by having set (all randomized participants taking ≥ 1 study drug
research pharmacy personnel perform the randomization, dose and having ≥ 1 postbaseline efficacy assessment).
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Armodafinil in binge eating disorder McElroy et al. 3
Safety and tolerability assessments were performed in the the mean (SD) baseline weekly binge eating day fre-
safety analysis set (all randomized patients taking ≥ 1 quency was 4.4 (1.2) (Table 1). Lifetime depressive
study drug dose and having ≥ 1 postbaseline safety disorders were the most common comorbid psychiatric
assessment). All statistical tests and confidence intervals disorders, occurring in 12 (20%) of participants. The two
were two-sided, with a significance level of 0.05. treatment groups were well matched in demographic and
clinical variables at baseline (Table 1). Thirty-one parti-
The statistical methods used were similar to those used
cipants (16 receiving armodafinil and 15 receiving pla-
in other pharmacotherapy trials in BED (Hudson et al.,
cebo, P = 0.80) completed the 10-week treatment period
1998; McElroy et al., 2000, 2003a, 2003b, 2006, 2007a,
(Fig. 1). The mean (SD) daily dose of armodafinil at
2007b; Arnold et al., 2002; Appolinario et al., 2003;
endpoint evaluation was 216.7 (43.9) mg; for placebo, it
Guerdjikova et al., 2008, 2009, 2012; Wilfley et al., 2008).
was 208.9 (62.4) mg.
The primary efficacy analysis was a longitudinal analysis
comparing the rate of change of binge eating days/week The mean binge eating day frequency decreased over
during the treatment period between groups. The same the study period in both treatment groups, but the rate of
analysis was applied to the secondary outcomes. The reduction was similar for armodafinil recipients and pla-
difference in the rate of change was estimated by random cebo recipients (Table 2 and Fig. 2). However, compared
regression methods, as described in the study by Gibbons with placebo, armodafinil was associated with a statisti-
et al. (1993) and Fitzmaurice et al. (2004). We used a cally significantly higher rate of reduction in binge eating
model for the mean of the outcome variable that included episode frequency (Table 2 and Fig. 3). There were no
terms for treatment, time, and treatment-by-time inter- statistically significant differences between groups on
action. Time was modeled as a continuous variable, change in CGI-S, YBOCS-BE, EI, BFI, IDS, or BAI
expressed as the square root of days since randomization scores; weight; or BMI.
(baseline). For the analyses of binge eating day fre-
quency and binge eating episode frequency, we used the In the secondary analyses of baseline-to-endpoint change
logarithmic transformations log [(binge days/week) + 1] scores, armodafinil was associated with statistically sig-
and log [(binges/week + 1)], respectively, to normalize nificant decreases in YBOCS-BE total scores and in BMI
the data and stabilize the variance. In addition, log compared with placebo (Table 2). The associated stan-
transformations were used on other outcome measures dardized effect sizes were moderate in range (Cohen’s
when appropriate. To simultaneously account for indi- D = 0.60 and 0.60, respectively).
vidual differences in the initial level of the outcome, rate For categorical response, numerically more patients in
of change over time, and serial autocorrelation, we used the armodafinil group showed at least a moderate
the SAS procedure MIXED. These mixed models improvement on the CGI-I at endpoint [21 (78%)]
included random coefficients for the intercept and time compared with placebo recipients [15 (54%)], but this
variables. The best-fitting correlation structure for the difference was not statistically significant (P = 0.06).
error terms, as determined by the lowest AIC value, was Armodafinil was not associated with a statistically sig-
chosen for each model from compound symmetric, first- nificantly higher 4-week binge eating cessation rate (26
order antedependence, and first-order autoregressive vs. 21% for placebo, P = 0.69).
forms. The longitudinal analyses included all available
observations from all participants in the full analysis set. Feeling jittery and dry mouthed were significantly more
common with armodafinil than placebo (Table 3). Two
Several secondary analyses were carried out. Using the participants discontinued armodafinil and two dis-
last observation carried forward, baseline-to-endpoint continued placebo because of adverse events. For
change scores were computed for each measure and armodafinil, these were excessive fatigue and anxiety in
independent-sample t-tests or Wilcoxon rank sum tests one patient and elevated blood pressure (from
were used to compare these changes between the treat- 128/64 mmHg at baseline to 210/100 mmHg after 2 days
ment groups. Fisher’s exact tests or χ2 tests were used to of treatment) in another. The patient’s elevated blood
analyze categorical response to treatment and adverse pressure was treated successfully with intravenous labe-
events. For laboratory measures, the mean difference talol in an emergency room and by discontinuation of
between endpoint and baseline measures was computed armodafinil. Adverse events leading to placebo dis-
for each treatment group and then compared using continuation were abdominal cramping and worsening of
independent-sample t-tests or Wilcoxon rank sum tests. depressive symptoms.
Armodafinil was associated with a statistically significant
Results increase in pulse at the last visit compared with change in
Of 139 individuals assessed for eligibility, 60 fulfilled the the placebo group (5.5 vs. − 2.6 beats/min, respectively,
entry criteria and were randomized to armodafinil P = 0.02). Two patients developed tachycardia (each
(N = 30) or placebo (N = 30) (Fig. 1). Of these 60 parti- 105 bpm). In both cases, the tachycardia was asympto-
cipants, 51 (85%) were women, 46 (77%) were White, and matic and transient. There were no significant differences
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4 International Clinical Psychopharmacology 2015, Vol 00 No 00
Fig. 1
14 discontinued 15 discontinued
(a) Adverse event (2) (a) Adverse event (2)
(b) Personal reasons (1) (b) Personal reasons (3)
(c) Lost to follow-up (8) (c) Lost to follow-up (3)
(d) Lack of efficacy (1) (d) Lack of efficacy (2)
(e) Study nonadherence (2) (e) Study nonadherence (3)
(f) Onset of new medical condition (2)
Participants who entered a 10-week, randomized, placebo-controlled trial of armodafinil in binge eating disorder. aFull analysis set defined as all
randomized participants who received at least study medication dose and had at least postbaseline efficacy assessment. bSafety population defined
as all randomized participants who received at least one dose of study medication and for whom at least one postbaseline safety measure was
available.
BAI, Beck Anxiety Inventory; BED, binge eating disorder; BFI, Brief Fatigue Inventory; CGI, Clinical Global Impression; EI, Eating Inventory; IDS, Inventory of Depressive
Symptomatology; NA, not applicable; YBOCS-BE, Yale-Brown Obsessive Compulsive Scale modified for Binge Eating.
a
Mean (SD) or n (%) shown.
b
Fisher’s exact tests, t-tests, or Wilcoxon rank sum tests.
between armodafinil-treated patients and those adminis- n = 35), except that armodafinil was associated with
tered placebo in mean change from baseline to final visit decreased glucose (− 2.5 vs. 13.5 mg/dl, P = 0.02) and
for blood pressure and laboratory values (laboratory data, increased sodium (0.88 vs. − 0.35 mmol/l, P = 0.02)
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Armodafinil in binge eating disorder McElroy et al. 5
Table 2 Primary (longitudinal) and secondary (endpoint) analyses of each outcome measure
Estimated difference between groups at 10 weeks (n = 55)
Change (endpoint − baseline) Armodafinil change from BL − placebo change from BL [95% CI]
Armodafinil (n = 27) Placebo (n = 28) Longitudinal analysis P-value Endpoint analysis P-value da
Binge days per week − 3.1 (2.1) − 2.4 (1.6) 0.78 [0.55–1.10]b 0.15 − 0.7 [ − 1.7 to 0.3] 0.16 0.38
Binge episodes per week − 4.2 (3.1) − 2.8 (1.8) 0.71 [0.51–1.00]b 0.05 − 1.3 [ − 2.7 to 0.0] 0.06 0.52
CGI-severity − 2.3 (1.7) − 1.5 (1.5) − 0.7 [ − 1.6 to 0.2] 0.14 − 0.8 [ − 1.7 to 0.1] 0.07 0.51
YBOCS-BE total − 12.5 (6.9) − 8.5 (6.4) − 3.1 [ − 6.6 to 0.5] 0.09 − 4.0 [ − 7.6 to − 0.4] 0.03 0.60
EI-restraint 2.7 (5.2) 2.4 (4.6) 0.5 [ − 2.5 to 3.5] 0.76 0.3 [ − 2.6 to 3.2] 0.84 − 0.06
EI-disinhibition − 2.9 (4.6) − 1.8 (3.9) − 1.3 [ − 4.0 to 1.5] 0.36 − 1.1 [ − 3.6 to 1.4] 0.37 0.26
EI-hunger − 3.7 (3.4) − 2.7 (3.8) − 1.4 [ − 3.6 to 0.9] 0.23 − 1.0 [ − 3.1 to 1.1] 0.35 0.28
BFI − 16.7 (24.3) − 15.9 (17.2) 0.66 [0.34–1.30]b 0.35 − 0.8 [ − 12.1 to 10.6] 0.89 0.04
IDS − 5.4 (6.9) − 5.5 (7.9) 0.99 [0.64–1.52]b 0.95 0.1 [ − 4.2 to 4.4] 0.96 − 0.01
BAI − 1.1 (6.0) − 1.1 (5.9) 1.18 [0.63–2.2]b 0.60 − 0.1 [ − 3.5 to 3.4] 0.97 0.02
Weight (kg) − 1.6 (2.4) 0.0 (3.6) 0.98 [0.97–1.0]b 0.08 − 1.6 [ − 3.3 to 0.0] 0.06 0.52
BMI (kg/m2) − 0.6 (0.8) 0.1 (1.2) 0.98 [0.97–1.0]b 0.07 − 0.6 [ − 1.2 to − 0.1] 0.03 0.58
BAI, Beck Anxiety Inventory; BFI, Brief Fatigue Inventory; BL, baseline; CGI, Clinical Global Impression; CI, confidence interval; EI, Eating Inventory; IDS, Inventory of
Depressive Symptomatology; YBOCS-BE, Yale-Brown Obsessive Compulsive Scale modified for Binge Eating.
a
Cohen’s effect size; positive values indicate a greater reduction in the armodafinil group.
b
Log transformation used; estimate equals ratio of (Armweek 10/Armbaseline) to (Placeboweek10/Placebobaseline).
Fig. 2 Fig. 3
7 5
4.5
6 Armodafinil Armodaf inil
Placebo
4
Placebo
5
Binge eating episodes
3.5
Binge eating days
3
4
2.5
3
2
2 1.5
1
1
0.5
0 0
0 1 2 3 4 5 6 7 8 9 10 0 1 2 3 4 5 6 7 8 9 10
Study week Study week
Weekly mean binge eating episodes by treatment group. Weekly mean binge eating days by treatment group.
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6 International Clinical Psychopharmacology 2015, Vol 00 No 00
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Armodafinil in binge eating disorder McElroy et al. 7
Fitzmaurice GM, Laird NM, Ware JH (2004). Applied longitudinal analysis. McElroy SL, Kotwal R, Guerdjikova AI, Welge JA, Nelson EB, Lake KA, et al.
Hoboken, NJ: John Wiley & Sons. (2006). Zonisamide in the treatment of binge eating disorder with obesity: a
Gibbons RD, Hedeker D, Elkin I, Waternaux C, Kraemer HC, Greenhouse JB, randomized controlled trial. J Clin Psychiatry 67:1897–1906.
et al. (1993). Some conceptual and statistical issues in analysis of longitudinal McElroy SL, Guerdjikova A, Kotwal R, Welge JA, Nelson EB, Lake KA, et al.
psychiatric data. Application to the NIMH treatment of Depression (2007a). Atomoxetine in the treatment of binge-eating disorder: a randomized
Collaborative Research Program dataset. Arch Gen Psychiatry 50:739–750. placebo-controlled trial. J Clin Psychiatry 68:390–398.
Goodman WK, Price LH, Rasmussen SA, Mazure C, Fleischmann RL, Hill CL, McElroy SL, Hudson JI, Capece JA, Beyers K, Fisher AC, Rosenthal NR,
et al. (1989). The Yale-Brown Obsessive Compulsive Scale. I. Development, Topiramate Binge Eating Disorder Research Group (2007b). Topiramate for
use, and reliability. Arch Gen Psychiatry 46:1006–1011. the treatment of binge eating disorder associated with obesity: a placebo-
Guerdjikova AI, McElroy SL, Kotwal R, Welge JA, Nelson E, Lake K, et al. (2008).
controlled study. Biol Psychiatry 61:1039–1048.
High-dose escitalopram in the treatment of binge-eating disorder with obesity:
McElroy SL, Hudson JI, Mitchell JE, Wilfley D, Ferreira-Cornwell MC, Gao J, et al.
a placebo-controlled monotherapy trial. Hum Psychopharmacol 23:1–11.
(2015). Efficacy and safety of lisdexamfetamine for treatment of adults with
Guerdjikova AI, McElroy SL, Welge JA, Nelson E, Keck PE, Hudson JI (2009).
moderate to severe binge-eating disorder: a randomized clinical trial. JAMA
Lamotrigine in the treatment of binge-eating disorder with obesity: a rando-
mized, placebo-controlled monotherapy trial. Int Clin Psychopharmacol Psychiatry 72:235–246.
24:150–158. Mendoza TR, Wang XS, Cleeland CS, Morrissey M, Johnson BA, Wendt JK,
Guerdjikova AI, McElroy SL, Winstanley EL, Nelson EB, Mori N, McCoy J, et al. Huber SL (1999). The rapid assessment of fatigue severity in cancer patients:
(2012). Duloxetine in the treatment of binge eating disorder with depressive use of the Brief Fatigue Inventory. Cancer 85:1186–1196.
disorders: a placebo-controlled trial. Int J Eat Disord 45:281–289. Posner K, Brown GK, Stanley B, Brent DA, Yershova KV, Oquendo MA, et al.
Guy W (1976). Clinical Global Improvement Scale ECDEU Assessment Manual (2011). The Columbia-Suicide Severity Rating Scale: initial validity and
for Psychopharmacology – Revised (DHEW Publ No ADM 76-338). internal consistency findings from three multisite studies with adolescents
Rockville, MD: US Department of Health, Education, and Welfare. and adults. Am J Psychiatry 168:1266–1277.
Hudson JI, McElroy SL, Raymond NC, Crow S, Keck PE Jr, Carter WP, et al. Reas DL, Grilo CM (2008). Review and meta-analysis of pharmacotherapy for
(1998). Fluvoxamine in the treatment of binge-eating disorder: a multicenter binge-eating disorder. Obesity (Silver Spring) 16:2024–2038.
placebo-controlled, double-blind trial. Am J Psychiatry 155:1756–1762. Reas DL, Grilo CM (2014). Current and emerging drug treatments for binge
Hudson JI, Hiripi E, Pope HG Jr, Kessler RC (2007). The prevalence and corre- eating disorder. Expert Opin Emerg Drugs 19:99–142.
lates of eating disorders in the National Comorbidity Survey Replication. Biol Rush AJ, Gullion CM, Basco MR, Jarrett RB, Trivedi MH (1996). The Inventory of
Psychiatry 61:348–358. Depressive Symptomatology (IDS): psychometric properties. Psychol Med
Hudson JI, Lalonde JK, Coit CE, Tsuang MT, McElroy SL, Crow SJ, et al. (2010). 26:477–486.
Longitudinal study of the diagnosis of components of the metabolic syndrome Spencer TJ, Madras BK, Bonab AA, Dougherty DD, Clarke A, Mirto T, et al.
in individuals with binge-eating disorder. Am J Clin Nutr 91:1568–1573. (2010). A positron emission tomography study examining the dopaminergic
Kessler RC, Berglund PA, Chiu WT, Deitz AC, Hudson JI, Shahly V, et al. (2013). activity of armodafinil in adults using [(1)(1)C]altropane and [(1)(1)C]raclo-
The prevalence and correlates of binge eating disorder in the World Health pride. Biol Psychiatry 68:964–970.
Organization World Mental Health Surveys. Biol Psychiatry 73:904–914. Striegel-Moore RH, Dohm FA, Wilfley DE, Pike KM, Bray NL, Kraemer HC,
Loland CJ, Mereu M, Okunola OM, Cao J, Prisinzano TE, Mazier S, et al. (2012). Fairburn CG (2004). Toward an understanding of health services use in
R-modafinil (armodafinil): a unique dopamine uptake inhibitor and potential
women with binge eating disorder. Obes Res 12:799–806.
medication for psychostimulant abuse. Biol Psychiatry 72:405–413.
Stunkard AJ, Messick S (1985). The three-factor eating questionnaire to measure
Masheb RM, Grilo CM (2004). Quality of life in patients with binge eating dis-
dietary restraint, disinhibition and hunger. J Psychosom Res 29:71–83.
order. Eat Weight Disord 9:194–199.
Wang GJ, Geliebter A, Volkow ND, Telang FW, Logan J, Jayne MC, et al. (2011).
Mathes WF, Brownley KA, Mo X, Bulik CM (2009). The biology of binge eating.
Enhanced striatal dopamine release during food stimulation in binge eating
Appetite 52:545–553.
McElroy SL, Casuto LS, Nelson EB, Lake KA, Soutullo CA, Keck PE Jr, Hudson JI disorder. Obesity (Silver Spring) 19:1601–1608.
(2000). Placebo-controlled trial of sertraline in the treatment of binge eating Wilfley DE, Crow SJ, Hudson JI, Mitchell JE, Berkowitz RI, Blakesley V, Walsh BT
disorder. Am J Psychiatry 157:1004–1006. (2008). Efficacy of sibutramine for the treatment of binge eating disorder: a
McElroy SL, Arnold LM, Shapira NA, Keck PE Jr, Rosenthal NR, Karim MR, et al. randomized multicenter placebo-controlled double-blind study. Am J
(2003a). Topiramate in the treatment of binge eating disorder associated with Psychiatry 165:51–58.
obesity: a randomized, placebo-controlled trial. Am J Psychiatry Wilson GT, Wilfley DE, Agras WS, Bryson SW (2010). Psychological treatments
160:255–261. of binge eating disorder. Arch Gen Psychiatry 67:94–101.
McElroy SL, Hudson JI, Malhotra S, Welge JA, Nelson EB, Keck PE Jr (2003b). Wonderlich SA, Gordon KH, Mitchell JE, Crosby RD, Engel SG (2009). The
Citalopram in the treatment of binge-eating disorder: a placebo- validity and clinical utility of binge eating disorder. Int J Eat Disord
controlled trial. J Clin Psychiatry 64:807–813. 42:687–705.
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