Pharmacotherapy of Eating Disorders -- Jackson et al.

25 (2): 143 -- Nutrition in Clinical Practice

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Pharmacotherapy of Eating Disorders -- Jackson et al. 25 (2): 143 -- Nutrition in Clinical Practice

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 Nutrition in Clinical Practice
http://ncp.sagepub.com

Pharmacotherapy of Eating Disorders

Cherry Wyant Jackson, Marshall Cates and Raymond Lorenz
Nutr Clin Pract 2010; 25; 143
DOI: 10.1177/0884533610362239

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Invited Review
Pharmacotherapy of Eating Disorders
Cherry Wyant Jackson, PharmD1; Marshall Cates, PharmD1;
and Raymond Lorenz, PharmD2
Eating disorders are complex, chronic disorders that are difficult
to treat. In addition, the 2 primary eating disorders, anorexia ner-
vosa and bulimia nervosa, may have acute, life-threatening conse-
quences. Medication trials for eating disorders have been
hampered by high dropout rates, high placebo response, short trial
duration, insufficient doses, and difficult outcome measures. Only
1 medication has been FDA approved for any eating disorder to
E
ating disorders are complex disorders that may have
life-threatening consequences. The 3 most com-
mon eating disorders are anorexia nervosa (AN),
bulimia nervosa (BN), and binge-eating disorder (BED).
There are varying estimates of the incidence and preva-
lence of eating disorders. The lifetime estimate of AN in
women ranges from 0.3% to 3.7%, and the prevalence of
bulimia in women ranges from 1% to 4.2%.1-3 Based on
population-based research, BED prevalence has been esti-
mated at between 0.7% and 3%.4 Although eating disorders
occur more frequently in women, men may also have eat-
ing disorders at a prevalence ratio between 1:6 and 1:10.1
Antidepressants are the medications most frequently
used for the treatment of eating disorders. Although the
mechanism of action of antidepressants in the treatment
of eating disorders is unknown, it is thought that eating
disorders may be caused by the same chemical imbalance
of serotonin and norepinephrine that causes depression.
In addition, antidepressants decrease the anxiety, impul-
sivity, and obsessive behavior frequently seen in individu-
als with eating disorders. Initial adverse effects with
antidepressants, especially the second-generation agents
used for eating disorders, are nausea and headache.
Long-term adverse effects include sexual dysfunction and
weight gain.
Literature regarding the treatment of eating disorders
with medications is of highly variable quality and can be
difficult to assess. Many studies have an ambiguous
design and do not adequately describe the method of
From the 1University of AlabamaBirmingham; and the 2University
of South Alabama, Mobile.
Address correspondence to: Cherry Wyant Jackson, PharmD,
University of Alabama, Birmingham, 127 Engel, 1700 7th
Avenue South, Birmingham, AL 35294-0018; e-mail: cwj0002@
auburn.edu.
143
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Nutrition in Clinical Practice
Volume 25 Number 2
April 2010 143-159
2010 American Society for
Parenteral and Enteral Nutrition
10.1177/0884533610362239
http://ncp.sagepub.com
hosted at
http://online.sagepub.com
date, and that is for fluoxetine in the treatment of bulimia. Clearly,
new large-scale, independent studies using novel agents, and
studying the use of medications for both short- and long-term
outcomes, are needed. (Nutr Clin Pract. 2010;25:143-159)
Keywords: eating disorders, anorexia, anorexia nervosa,
bulimia, bulimia nervosa, medication therapy management
blinding, including whether the trial is single- or double-
blind. Also, some studies either use a nonplacebo control,
or they do not use a control in the study at all. We will
review literature that is clearly described as both double-
blind and placebo-controlled, as we discuss the use of
medications for the treatment of eating disorders.
Anorexia Nervosa
AN is a disorder typically beginning in early to late adoles-
cence, although it has been reported in preadolescent
children as well.5 This disorder is often precipitated by
stressful life situations in females who are high achievers
and feel that diet is an aspect of their life in which they
can exert some control when other areas of their lives
seem out of control. AN is characterized by the refusal to
maintain ones body weight over a minimal normal weight
for age and height.6 When this is the case in adolescents,
it may also limit sexual maturation and bone growth.7,8
Other characteristics include an intense fear of gaining
weight, or of becoming fat, and a distorted body image.6
Currently the Diagnostic and Statistical Manual of Mental
Disorders 4th edition Text Revised (DSM-IV-TR) lists 3
cycles of amenorrhea as being part of the diagnostic crite-
ria; however, this is not always the case in patients with
anorexia and will probably not be listed as a criterion for
diagnosis in the DSM-V.9
Patients with AN may either restrict their total food
intake or binge/purge, typically by self-inducing vomiting,
using laxatives or diuretics, and/or extensively exercising.
As long as the patient continues to be 15% below ideal
body weight (IBW) and meets other criteria for AN, the
diagnosis does not evolve to a diagnosis of BN.6
AN has a high mortality, estimated at 10% within
10 years of diagnosis, and it is the primary cause of
144 Nutrition in Clinical Practice / Vol. 25, No. 2, April 2010
Table 1. Medical Complications of Anorexia
Nervosa1,2,7,8,10-14
Bradycardia
Orthostasis
Acrocyanosis
Cognitive impairment
Anxious, depressed, or irritable mood
Possible seizures
Peripheral neuropathy
Low body temperature
Cold intolerance
Fatigue
Electrolyte abnormalities
Decreased serum T3; increase in reverse T3
Increased serum cortisol
Thiamine, folate, B12, niacin deficiency
Increased serum carotene
Delayed gastric emptying
Constipation
Bloating
Cessation of menses
Fertility problems
Point tenderness
Osteopenia or osteoporosis
death in young women between the ages of 15 and
24.10 Death typically occurs as a result of suicide,
infection, or chronic starvation.11 Refeeding the patient
may also be problematic and is associated with signifi-
cant morbidity and mortality.12,13 Medical evaluation
and stabilization of patients with AN is extremely
important. Often, by the time family and friends real-
ize the patient has a problem or they are ready to seek
help, the patient is profoundly underweight and may
be experiencing a number of physical complications
like hypothermia, bradycardia, hypotension, edema,
lanugo, and a variety of metabolic changes (Table 1).
In the case of severe weight loss (<75% of IBW), hos-
pitalization is necessary to prevent death secondary to
starvation.14
Comorbid disorders are common in AN. In patients
who restrict eating, depression, anxiety, and obsessional
behaviors such as intrusive or repetitive thoughts, perfec-
tionistic traits, and rigid cognitive styles are common and
may need treatment in addition to the eating disorder. In
patients who purge, self-harm and suicidal behaviors may
occur in addition to the comorbid disorders previously
listed.15
Medication Treatment
The initial goal of treating AN is to restore the patient
to an IBW and treat any physical complications of the
eating disorder. Following that, teaching the patient
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healthful nutrition and eating habits as well as having
the patient incorporate the new habits into his or her
daily life, and helping him or her to change cognitive
perceptions about eating, weight, and the underlying
feeling about perfection and control is imperative.
Finally, involving the family in the patients recovery
and preventing relapse are all treatment goals.16
The use of medications in the treatment of AN has
largely been disappointing. AN was first defined in DSM
III in the early 1980s, and treatments have primarily used
weight gain as a treatment outcome.17 Many of the first
trials of medications conducted for AN were of too short
a duration or used doses of medication that would now be
considered too low to achieve a response. Studies were
frequently completed without significant power, and gen-
der and ethnicity were not reported in all trials.
Table 2 includes patient demographics, study design,
duration, and outcome variables for 19 trials for the
medication treatment of AN completed between 1980
and 2009.18-36 Of those trials, 8 used either selective sero-
tonin reuptake inhibitors (SSRIs) or venlafaxine, 2 used
tricyclic antidepressants (TCAs), 2 used cisapride, 3 used
antipsychotics, 3 used hormones, and 1 used zinc. The
discussion below will focus on double-blind, placebo con-
trolled trials.
Antidepressants in the Treatment of AN
Ten studies evaluated effects of antidepressants in indi-
viduals with AN. Six studies involved fluoxetine; 1 citalo-
pram; 1 venlafaxine and fluoxetine; 1 fluoxetine,
amitriptyline, and clomipramine; and 2 amitriptyline.
Again, we will only discuss the double-blind, placebo-
controlled trials here.
Fluoxetine. Three studies compared fluoxetine vs placebo
in individuals with AN. In 1998, Attia and colleagues25
performed a double-blind, placebo-controlled trial of
fluoxetine 60 mg (n = 15) vs placebo (n = 16) in 31 inpa-
tients over a 7-week period. Patients entering the trial
weighed an average of 92 pounds (72.5% of IBW). The
primary outcome was for patients to gain 1.5 pounds per
week until 90% of IBW was achieved. Three percent of
patients dropped out of the trial. Fluoxetine was well tol-
erated. There were no significant changes between fluox-
etine and placebo in terms of weight, anxiety, or depression
scales.25
In 2001, Kaye and colleagues performed a 52-week
trial in which patients with AN were randomized to fluox-
etine (n = 19) or placebo (n = 20) prior to discharge from
inpatient hospitalization. Fluoxetine was titrated up to a
dose of 60 mg daily as tolerated. By the end of 52 weeks,
approximately 70% of patients had dropped out of
 Table 2. Anorexia Nervosa: Medication Trials
Intention to
Year Source Females Males Age (y) Location Length Design Treatment Treat Outcome
1984 Vandereycken18 18 0 13-33 Inpatient NR Double-blind, Sulpiride (300-500 mg) vs Yes No significant differences
crossover placebo
1985 Biederman et al19 25 0 11-27 Inpatient and 5 wk Double-blind, Amitriptyline (175 mg) vs No No significant differences
outpatient placebo placebo
controlled
1986 Halmi et al20 72 0 13-36 Inpatient 90 d Double-blind, Amitriptyline (160 mg) vs No Neither better than
placebo cyproheptadine (32 mg) vs placebo
controlled placebo
1994 Birmingham 54 0 >15 Inpatient NR Double-blind, Elemental zinc (14 mg) vs No Zinc improved BMI
et al21 placebo placebo (P = .03)
controlled
1995 Brambilla et al22 13 0 14-35 Outpatient 4 mo Not blinded Fluoxetine (60 mg) vs Yes No change in scores
amineptine (300 mg)
1995 Klibanski et al23 48 0 11-27 Outpatient 1.5 y No blind Estrogen (0.625 mg) progestin No No change in scores
reported, not (5 mg) vs nonmedication
placebo control
controlled
1995 Szmukler et al24 29 0 20-23 Inpatient NR Double-blind, Cisapride (10 mg tid) vs No No improvement
placebo placebo
controlled
1998 Attia et al25 33 0 16-45 Inpatient 7 wk Double-blind, Fluoxetine (60 mg) vs placebo No No change
placebo
controlled
1999 Ricca et al26 24 0 16-22 Outpatient 6 mo No blind Fluoxetine (40 mg) vs No Venlafaxine was as
reported, not venlafaxine (75 mg) effective as
placebo fluoxetine

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controlled
2000 Hill et al27 14 1 12-18 Inpatient 28 d Double-blind, Growth hormone 15 mg/kg vs Yes Improved orthostasis only
placebo placebo no P value reported
controlled
2001 Kaye et al28 39 0 15-32 Inpatient and 52 wk Double-blind, Fluoxetine (20-60 mg) vs No No changes
outpatient placebo placebo
controlled
2001 Ruggiero et al29 35 0 19-30 Inpatient 3 mo Single-blind, Amisulpride (50 mg) vs No No significant difference
not placebo fluoxetine (28 mg) vs
controlled clomipramine (60 mg)
2002 Fassino et al30 39 0 18-32 Outpatient 12 wk No blind Citalopram (20 mg) vs waitlist No Improved depression,
reported, not obsessive-compulsive
placebo disorder, impulsiveness,
controlled and anger

(continued)

145
 146
Table 2. (continued)
Intention to
Year Source Females Males Age (y) Location Length Design Treatment Treat Outcome
31
2004 Barbarich et al 26 0 17-29 NR 6 mo Double-blind, Fluoxetine (20-60 mg) vs No No significant difference
not placebo supplements
controlled
2005 Miller et al32 38 0 18-37 Outpatient 3 wk Double-blind, Testosterone (150-300 mcg No Improved mood and spatial
placebo transdermal) vs placebo cognition (P = .002)
controlled
2005 Mondraty et al33 15 0 18-32 Inpatient 70 d Open label, Olanzapine (20 mg) vs No Possible decrease in
no placebo chlorpromazine (200 mg) ruminations
control
2006 Walsh et al34 93 0 16-45 Inpatient 52 wk Double-blind, Fluoxetine (60 mg) vs placebo Yes No benefit
placebo
controlled
2007 Brambilla et al35 30 0 18-36 Outpatient 3 mo Double-blind, Olanzapine (5 mg) vs placebo Yes No statistically significant
placebo difference
controlled

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2007 Brambilla et al36 20 0 19-28 Outpatient 3 mo Single-blind Olanzapine (5 mg) vs placebo Yes No statistically significant
difference

BMI, body mass index; NR, not reported.


the trial. Three patients were dropped from the study
because the blind was opened early, and 1 dropped out
because of an automobile accident. Six patients dropped
out of the fluoxetine group: 3 were dropped because of
weight loss, 1 owing to persistent depression, and 2 as a
result of persistent eating disorder. Sixteen patients were
dropped from the placebo group: 4 for substantial weight
loss, 2 for depressive symptoms, and 10 for persistent eat-
ing disorder symptoms. In the group that remained, fluox-
etine was associated with improvement in depression,
obsessive-compulsive features, and eating-disorder related
symptoms, although statistically it did not differ signifi-
cantly from placebo.28
Probably the largest and most important of the fluox-
etine trials for AN was by Walsh et al34 in 2006. In this
randomized, double-blind trial, 93 inpatient/day treat-
ment patients were randomly assigned to either fluoxet-
ine 60 mg (n = 49) or placebo (n = 44) over the course
of 1 year. The primary outcome was time to relapse and
to determine the proportion of patients completing 1 year
of treatment. Similar percentages of patients assigned to
fluoxetine (26.5%) and placebo (31.5%) maintained a
body mass index (BMI) of 18.5 and stayed in the study
for 52 weeks. There was no difference between groups in
the time to relapse (P = .64).34
Tricyclic Antidepressants. There are 2 double-blind,
placebo-controlled trials of amitriptyline for the treatment
of AN. The first trial, conducted by Biederman et al, was
a 5-week trial of patients with AN receiving either amitrip-
tyline (n = 11) in doses up to 175 mg daily or placebo
(n = 14). Eighteen additional patients served as a control
group and received only psychosocial treatment. No
patients dropped out of this trial; however, there was no
significant difference between the groups, although
patients in the amitriptyline group complained of uncom-
fortable side effects.19
Halmi and colleagues randomly assigned 72 inpa-
tients with AN to amitriptyline 160 mg, cyproheptadine
32 mg, or placebo in a 90-day trial. Although weight gain
was higher in the cyproheptadine group and time to
achieve weight gain was shorter in both medication
groups than in the placebo group, the results were not
statistically significant.20
Antipsychotics
Although there are many case reports using antipsychot-
ics to treat eating disorders, few to date have been blinded
or compared with placebo. In 1984, Vandereycken com-
pared sulpiride with placebo in a small study of 18
patients with AN. Initially, sulpiride improved weight gain
in patients; however, in the crossover phase of the study,
sulpiride did not differentiate from placebo.18 In a study
by Brambilla and colleagues, olanzapine was compared
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Pharmacotherapy of Eating Disorders / Jackson et al 147
with placebo in 30 patients. All patients also received
cognitive behavioral therapy. Although olanzapine was
associated with an increase in weight, there were no sta-
tistically significant differences between the 2 groups.35
Hormones
Both growth hormone and testosterone were compared
with placebo in the treatment of AN. In a 28-day random-
ized, double-blind, placebo-controlled trial, Hill evaluated
15 mg/kg/day of growth hormone in adolescent (age
12-18) inpatients with AN.27 The primary outcome in this
trial included time to medical stability, weight gain, and
duration of hospitalization. No patients dropped out of
the study. Although there were no significant changes in
weight, patients receiving growth hormone experienced
improvement in medical stability more rapidly than
patients taking placebo (17 vs 37 hospital days, P = .02).
In 2005, Miller and colleagues compared testosterone
transdermal patches with placebo in 38 women between
the ages of 18 and 37. They hypothesized that bone forma-
tion would increase and depressive symptoms and spatial
cognition would improve with short-term testosterone
administration. Multiple studies of testosterone in humans
have found improvement in mood with increased testoster-
one levels. Five patients (13%) dropped out of the study,
including 1 who became pregnant, 1 with multiple frac-
tures from a car accident, 2 with life-threatening weight
loss, and 1 with nausea. The researchers concluded that
patients using the transdermal patches had improvements
in mood, but no improvements in weight over placebo.32
Zinc
Open trials have suggested that zinc may cause weight
gain in patients with AN. In 1994, Birmingham and col-
leagues compared the effects of elemental zinc (n = 16)
14 mg daily with placebo (n = 19) in a double-blind,
placebo-controlled trial of 35 inpatients with AN. Patients
remained in the hospital until they achieved a 10%
increase in their BMI. Patients in the zinc group were
hospitalized for a mean of 24.5 days, whereas patients in
the placebo group were hospitalized for a mean of 31.5
days (P = .03). Nineteen patients (30%) did not complete
the study. Ten of the patients who dropped out of the
study were in the zinc group, and 9 were in the placebo
group. The reasons for patients dropping out of the study
were not reported.21
Summary of Medication Trials for AN
Eleven of 19 trials (Table 2) compared medication with
placebo in the treatment of AN.18-21,24-25,28,3234-35 Many of
the trials involving medication treatment of AN have
148 Nutrition in Clinical Practice / Vol. 25, No. 2, April 2010
significant limitations, including small trial size, lack of
adequate power, short duration, high dropout rates, and
lack of intention-to-treat analysis. Many of the trials did
not list the ethnicity of the patients involved in the trials,
and only 1 male was involved in all of the AN trials. In
addition, studies completed in inpatient units may not be
generalized to the outpatient experience. Overall, no
medication was found to be significantly better than pla-
cebo for the treatment of AN.
Bulimia Nervosa
Bulimia nervosa (BN) usually begins in adolescence or
early adulthood and is characterized by recurrent epi-
sodes of binge eating marked by rapid consumption of
large amounts of food over a distinct period of time.
These patients feel that they have lost control over their
eating behaviors during the binges and use purging meth-
ods, such as self-induced vomiting, laxatives or diuretics,
fasting, strict dieting, or excessive exercise to prevent
associated weight gain. In addition, body shape and
weight are constant concerns.6
To meet criteria for BN, patients must have an aver-
age of 2 binge-eating episodes per week for at least 3
months. Binging involves eating until the person experi-
ences abdominal discomfort. Other reasons for terminat-
ing the binge include stopping to sleep, social interruptions,
or induced vomiting. Vomiting often decreases the feeling
of discomfort associated with abdominal distention,
which may allow the person to continue with the binge or
to terminate it. Vomiting also relieves the anxiety fre-
quently associated with binging, although feelings of
depression and self-criticism frequently remain.6
BN can often remain hidden from friends and fami-
lies, since people with this eating disorder are within a
normal weight range. People with BN may feel conflicted
about eating, and fluctuations in weight are common
owing to repeated binges and fasts or purging.
There is a lower incidence of mortality with BN than
with AN. Approximately 1% of patients die within the first
10 years of diagnosis.10 This number may be artificially
low, considering that as many as 50% of people with AN
evolve into BN during the course of their illness, but they
continue to carry the diagnosis of AN.10,11 Serious medical
complications can occur from self-inducing vomiting and
use of laxatives and/or diuretics, including electrolyte
imbalances and dehydration. Other rare complications
include esophageal tears and gastric ruptures. Dental ero-
sion is commonly seen as a result of the vomiting, as are
enlarged parotid glands.11
Comorbid psychiatric disorders are seen in as many as
80% of patients with BN. Common comorbidities include
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depression, substance abuse, anxiety disorders, and per-
sonality disorders. People with BN have many of the same
personality features as do patients with AN, including per-
fectionism and rigid cognitive traits. They may also have
low self-esteem, higher impulsivity, increased novelty seek-
ing, and lower levels of cooperativeness.15,36
Medication Treatment for BN
The initial goal for treating BN is to decrease and eventu-
ally eliminate binging and purging behaviors and to treat
any medical complications. Then, as with AN, the goal is
to educate the patient on healthful eating habits and to
help the patient incorporate those habits into his or her
daily routine and correct any misperceptions about eat-
ing, weight, and other thoughts and behaviors related to
the eating disorder. It is important to treat any underlying
psychiatric conditions, including impulse control, self-
esteem issues, and unusual eating behaviors. Lastly, it is
important to get the family involved and prevent the
patient from relapsing.16
Although several antidepressants are effective for the
treatment of BN, only fluoxetine is Food and Drug
Administration (FDA) approved for the treatment for
BN.37,38 In fact, fluoxetine is the only medication to
receive FDA approval for the treatment of any eating dis-
order. There are 25 studies using medications to treat
bulimia,39-63 19 of which are double-blinded and placebo-
controlled. Although including patient demographics,
study design, duration, and outcomes for each of the 25
studies are listed in Table 3, we will review only the ones
that are double-blinded and placebo controlled.
Antidepressants
Sixteen of the 20 studies reviewed are antidepressant tri-
als.39-41,43,44,46-53,54,59,63 Seven of those trials involve fluox-
etine, 3 desipramine, 1 trazodone, 1 brofaromine, 2
fluvoxamine, 1 moclobemide, and 1 citalopram.
Selective Serotonin Reuptake Inhibitors
Fluoxetine. Fluoxetine was studied in 7 trials. Three fluox-
etine trials of between 8 and 16 weeks in length by the
Fluoxetine Collaborative Group and Goldstein and col-
leagues showed improvement in binging, purging, and
bulimia symptoms.43,46,53 Eight-week trials by Kanerva et
al, Beaumont et al, and Romano et al also showed im-
provement in symptoms of bulimia.47,49,59 Sixty milligrams
of fluoxetine was better than 20 mg in these studies. In a
4-week trial by Fichter et al, fluoxetine 60 mg did not dif-
ferentiate from placebo, although this could have been a
result of the short duration of the trial.40
 Table 3. Bulimia Nervosa: Medication Trials
Intention to
Year Source Females Males Age (y) Location Length Design Treatment Treat Outcome
39
1989 Pope et al 46 0 18-55 Outpatient 6 wks Double-blind, Trazodone (50 mg No Trazodone associated with a decrease in
placebo titrated to 400 binge and vomiting frequency (P < .05)
controlled mg) vs placebo
1991 Fichter et al40 39 1 25 mean Inpatient 35 d Double-blind, Fluoxetine (60 mg) Yes No differences on any measures
placebo vs placebo
controlled
1991 Walsh et al41 78 0 20-32 Outpatient 6 wk Double-blind, Desipramine (200- Yes Desipramine associated with fewer
placebo 300 mg) vs binging and vomiting episodes per
controlled placebo week; no P value reported
1992 Agras et al42 71 0 20-38 Outpatient 16 wk No blind Desipramine (300 Yes Desipramine and CBT better than CBT
reported, no mg) vs alone in reducing binge-and-purge
placebo desipramine (300 frequency; no P value reported
control mg) + CBT or
CBT alone
1992 Fluoxetine 387 0 19-35 Outpatient 8 wk Double-blind, Fluoxetine (20 mg) No Fluoxetine 60 mg associated with
Collaborative placebo vs fluoxetine (60 decreased binging, purging and
Study Group43 controlled mg) vs placebo bulimia; no P value reported
1993 Kennedy et al44 36 0 20-35 Outpatient 8 wk Double-blind, Brofaromine (175 No Brofaramine associated with a reduction
placebo mg) vs placebo in vomiting; no P value reported
controlled
1994 Agras et al45 71 0 20-38 Outpatient 16 wk No blind Desipramine (300 Yes See Agras et al42 1 year follow-up study;
reported, no mg) vs no P value reported
placebo desipramine (300
control mg) + CBT or

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CBT alone
1995 Goldstein et al46 393 5 17-63 Outpatient 16 wk Double-blind, Fluoxetine (20 mg) No Fluoxetine associated with greater
placebo vs fluoxetine (60 decline in vomiting (P < .001) and
controlled mg) vs placebo binge eating (.002) and a decrease in
overall bulimia symptoms
1995 Kanerva et al47 50 0 >15 Outpatient 8 wk Double-blind, Fluoxetine (60 mg) No Fluoxetine associated with a greater
placebo vs placebo decline in symptoms of bulimia and
controlled preoccupation with food; no P value
reported
1996 Fichter et al48 257 0 19-30 Inpatient 3 wk Double-blind, Fluvoxamine (182 Yes Fluvoxamine associated with higher
placebo mg average) vs binge abstinence, lower relapse rates,
controlled placebo and a decreased urge to binge; no P
value reported
(continued)

149
 150
Table 3. (continued)
Intention to
Year Source Females Males Age (y) Location Length Design Treatment Treat Outcome
49
1997 Beaumont et al 67 0 19-31 Outpatient 8 wk Double-blind, Fluoxetine (20 mg Yes Improvement in concern about shape
placebo tid) vs placebo and weight at week 8
controlled
1997 Fichter et al50 257 0 19-30 Outpatient 12 wk Double-blind, Fluvoxamine (182 Yes See Fichter et al42; continuation of
placebo mg) vs placebo 3-week study; no P value reported
controlled
1997 Goldbloom et al51 76 0 20-31 Outpatient 6 wk No blind Fluvoxamine (300 Yes CBT alone and CBT + fluvoxamine
reported, no mg) vs CBT vs associated with a greater reduction
placebo Fluvoxamine (300 than fluvoxamine alone; no P value
control mg) + CBT reported
1997 Walsh et al52 120 0 20-33 Outpatient 16 wk Double-blind, CBT + DMI (300 Yes CBT better than supportive therapy;
placebo mg) vs CBT + CBT + meds was better than CBT
controlled placebo vs DMI alone; meds alone was better than
(300 mg) vs CBT alone for decreasing BMI and
supportive care + weight; meds alone was better for
DMI (300 mg) vs binging and vomiting frequency
supportive care + (P = .03)
placebo
1999 Goldstein et al53 393 5 17-63 Outpatient 16 wk Double-blind, Fluoxetine (20 mg) Yes See Goldstein et al40; same study,
placebo vs fluoxetine (60 reported additional measures
controlled mg) vs placebo (P = .05)
1999 Wilson et al54 120 0 20-33 Outpatient 16 wk Double-blind, CBT + DMI (300 Yes See Walsh et al52; same study, reported
placebo mg) vs CBT + additional domains, therapeutic
controlled placebo vs DMI alliance (P = .03), predictive factors

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(300 mg) vs (P = .03), and time course to change
supportive care + (P = .03)
(DMI 300 mg) vs
supportive care +
placebo
2000 Faris et al55 29 0 23-35 Outpatient 4 wk Double-blind, Ondansetron (4 mg Yes Ondansetron associated with lower
placebo up to 6 doses a binge/purge frequency at week 4
controlled day) vs placebo (P < .001)
2001 Carruba et al56 78 0 19-40 Inpatient 6 wk Double-blind, Moclobemide (600 No Moclobemide is not effective
placebo mg) vs placebo
controlled

(continued)
 Table 3. (continued)
Intention to
Year Source Females Males Age (y) Location Length Design Treatment Treat Outcome
57
2001 Mitchell et al 48 0 18-46 Outpatient 16 wk Single-blind Placebo vs self- Yes Fluoxetine alone and fluoxetine with
help vs fluoxetine self-help is better than self-help or
(60 mg) vs placebo as far as decrease in vomiting;
fluoxetine (60 no P value reported
mg) + self-help
2002 Mitchell et al58 62 0 20-35 Outpatient 16 wk No blind Fluoxetine (60 mg) Yes No difference
reported, no vs IPT
placebo
control
2002 Romano et al59 155 5 21-40 Outpatient 8 wk Double-blind, Fluoxetine (60 mg) Yes Fluoxetine is associated with smaller
placebo vs placebo increase in eating disorder behavior
controlled (P < .02)
2003 Hoopes et al60 68 1 19-40 Outpatient 10 wk Double-blind, Topiramate (100 Yes Topiramate associated with greater
placebo mg) vs placebo percent reduction in binging and
controlled purging days, carb craving, 50%-75%
improvement in binging and purging
(P = .015)
2003 Hedges et al61 68 1 19-40 Outpatient 10 wk Double-blind, Topiramate (100 Yes Same as Hoopes e al60; reported
placebo mg) vs placebo psychiatric measures
controlled
2004 Walsh et al62 91 0 22-39 Outpatient 4 mo No blind Fluoxetine (60 mg) Yes Fluoxetine and placebo are better than
reported, vs placebo vs self- self-help; no P value reported

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placebo help vs fluoxetine
controlled (60 mg) + self-
help
2005 Sundblad et al63 46 0 NR Outpatient 12 wk Double-blind, Flutamide (500 Yes Decrease binding with flutamide but not
placebo mg) vs citalopram citalopram, increase in transaminases
controlled (40 mg) vs in flutamide patients
placebo or
flutamide (500
mg) + citalopram
(40 mg)

BMI, body mass index; NR, not reported; CBT, Cognitive Behavioral Therapy; DMI, desipramine.

151
152 Nutrition in Clinical Practice / Vol. 25, No. 2, April 2010
Citalopram. Sundblad and colleagues (2005) compared
flutamide 500 mg to citalopram 40 mg and to placebo vs
a combination of flutamide 500 mg vs citalopram 40 mg
in a double-blind, placebo-controlled trial of 46 female
outpatients over a period of 12 weeks. Flutamide appeared
to decrease binging, but also to increased serum liver
transaminases. At a dose of 40 mg, citalopram did not
have any significant effect on symptoms of bulimia.63
Fluvoxamine. Fichter et al (1996, 1997) compared fluvox-
amine 182 mg (mean dose per day) with placebo in 257
inpatients for 3 weeks and found no improvements in
symptoms of bulimia, but they then extended the trial to
12 weeks post-discharge to evaluate the role of fluvox-
amine in relapse prevention. They found that patients
who received fluvoxamine had fewer binge episodes, less
of an urge to binge, and fewer episodes of vomiting than
patients receiving placebo.48,50
Tricyclic Antidepressants
Walsh (1991) and coauthors published results of a trial
using desipramine vs placebo for 6 weeks and found
desipramine was associated with reduced binging and
vomiting episodes each week.41 Another study by Walsh,
Wilson, and colleagues in 1997 randomized patients to 1
of 4 groups: cognitive behavioral therapy (CBT) and
desipramine, CBT and placebo, desipramine and support-
ive therapy, or supportive therapy and placebo. They
found that CBT was better than supportive therapy, and
CBT and desipramine was better than CBT alone.
According to the authors, desipramine was significantly
superior for reducing BMI as well as binging and vomit-
ing frequency.52 Wilson and Walsh published the results
of the 1997 trial again in 1999 along with additional
domains not reported in the original trial.54
Trazodone. In a 6-week double-blind, placebo-controlled
trial of 42 females, Pope and colleagues found that trazo-
done, in doses titrated up to 400 mg daily, was associated
with a decrease in frequency of binging and purging (P <
.05). There were no improvements in patient depression
and anxiety scores at the end of the trial.39
Monoamine Oxidase Inhibitors (MAOIs)
In 1993, Kennedy et al conducted an 8-week trial of bro-
faromine at a mean dose of 175 mg daily vs placebo and
found that it was associated with a reduction in vomiting.44
In 2001, Carruba et al randomized patients to moclobemide
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600 mg or placebo for 6 weeks and found that moclobe-
mide was not effective for symptoms of bulimia.56 Patients
did not have difficulty adhering to the MAOI diet in either
trial.
Anticonvulsants
Topiramate. In 2003, Hoopes performed a 10-week trial
comparing effects of topiramate 100 mg with placebo.
Compared with placebo, topiramate was associated with
a greater decline in binging and purging days, a decline
in patient carbohydrate craving, and a 50%-75% improve-
ment in binge purge days.60 Hedges reported the results
of the psychological measures (Eating Disorder Inven-
tory [EDI], Eating Attitudes Test [EAT], Hamilton Rating
Scale for Anxiety [HAM-A], Hamilton Rating Scale for
Depression [HAM-D] and Patient Global Improvement
[PGI]) from this same study.61
5HT 3 Antagonist
Ondansetron. Faris and colleagues performed a 4-week,
double-blind, placebo-controlled trial in 29 female pa-
tients comparing ondansetron (n = 14) to placebo (n =
12). Ondansetron was dosed 4 mg up to 6 times daily dur-
ing the 4 weeks. The authors found that ondansetron was
associated with a lower binge/purge frequency (6.5 times
per week) vs placebo (13.2 times per week) at the comple-
tion of the study.55
Summary of Medication Trials for BN
Antidepressant medications have shown significant ben-
efit in the treatment of BN. To date, fluoxetine is the only
medication that is FDA-approved for this indication.
Studies have shown that at a dose of 60 mg daily, fluox-
etine administered for at least 6 weeks can improve symp-
toms of BN, as well as prevent relapse for up to 52 weeks.
Trazodone, fluvoxamine, desipramine, brofaromine, topi-
ramate, and ondansetron have shown similar benefits to
fluoxetine, but larger studies are needed to replicate these
findings.
Binge-eating Disorder
Currently, binge-eating disorder (BED) belongs to the
DSM-IV-TR diagnostic criteria of Eating Disorders Not
Otherwise Specified (EDNOS). Eating disorders in the
diagnostic category of EDNOS may be similar to the pre-
viously discussed eating disorders, but they do not meet
the full diagnostic criteria. EDNOS are treated in much
the same way as the disorders that meet full criteria. Of

the eating disorders in the EDNOS category, provisional
diagnostic criteria were established for BED, and it will
likely be a stand-alone eating disorder when DSM V is
published in 2012.9
Like BN, BED is marked by binge eating, but without
the compensatory behaviors such as purging, excessive
exercise, or laxative or diuretic abuse. BED appears to
have an older age at onset, similar male-to-female ratio of
occurrence, and more ethnic diversity. BED is character-
ized by low self-esteem, depression, and dissatisfaction
with body shape and image. In addition to depression,
another common comorbidity of BED includes obesity.6
Medication Treatment for BED
With BED, there are typically 2 primary goals of treat-
ment. The first is to decrease binging behaviors with a
goal of eliminating them, and the other goal is to work
with the patient to help him or her lose weight.16
Antidepressants used at higher doses than are typi-
cally used for depression are effective in decreasing bing-
ing behaviors, but they are not effective for any significant
weight loss. Appetite suppressants and topiramate have
also been studied in BED and may have promising roles.
Thirteen medication-related studies were conducted for
the treatment of BED (see Table 4).64-76 Eleven of these
are double-blind, placebo-controlled trials.65-68,70-76
Antidepressants
Seven of the 11 trials reviewed are antidepressant tri-
als.66-68,70,72,74-75 Two involved fluoxetine, 2 involve fluvox-
amine, and 1 each for sertraline, citalopram, and
imipramine.
Selective Serotonin Reuptake Inhibitors
Fluoxetine. Fluoxetine was studied in 2 trials for BED.
The first trial, by Arnold and colleagues in 2002, was a
6-week outpatient trial of fluoxetine (n = 30) in doses of
60-80 mg daily compared with placebo (n = 30).70 In this
trial, fluoxetine was associated with a decrease in the se-
verity of BED, reduced weight gain, and increased con-
trol over the patients BMI over the course of 6 weeks.
In a second 16-week trial of 108 patients by Grilo and
coworkers in 2005, patients received fluoxetine 60 mg
or placebo alone, fluoxetine 60 mg plus CBT, or placebo
plus CBT. The primary outcome was based on remission
rates, which were defined as no binges occurring within a
28-day period. Eighty-six patients (80%) completed treat-
ment. Remission, as defined, occurred in 29% of fluox-
etine patients, 30% of placebo patients, 55% of patients on
CBT and fluoxetine, and 73% of patients on a combination
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Pharmacotherapy of Eating Disorders / Jackson et al 153
of CBT and placebo. The authors found that CBT was su-
perior to fluoxetine alone or placebo alone in decreasing
eating behaviors and binging and in decreasing concerns
over shape. Although the combination of CBT and fluox-
etine was better than placebo alone, the combination was
not found to be better than CBT alone.75
Fluvoxamine. In 1998, Hudson and coworkers66 com-
pared fluvoxamine, at an average dose of 300 mg, with
placebo in a 9-week trial involving 85 patients. The inves-
tigators found that fluvoxamine decreased binge fre-
quency, decreased binge severity, and improved BMI over
the course of the trial.66 In a second 12-week study of 20
patients in which fluvoxamine was compared with pla-
cebo,74 no differences emerged for binge frequency, shape
and weight concerns, or weight changes. This study by
Pearlstein et al, completed in 2003, used an average flu-
voxamine dose of 239 mg daily.74 It is possible that the
lower average fluvoxamine doses used in the Pearlstein
trial are responsible for the lack of efficacy, but because
there is no long-term follow-up, findings of both studies
should be viewed with caution.
Sertraline. In a 6-week trial of sertraline at an average dose
of 187 mg/day, McElroy and colleagues (2000)68 found
that compared with placebo, sertraline decreased binge
frequency and improved body weight. The authors also
suggested that illness severity declined, but there were no
changes in depressed mood compared with placebo.
Twenty-eight percent of the patients in the sertraline group
and 19% of the patients in the placebo group dropped out
of the study.68
Citalopram. McElroys group also compared citalopram
40 mg with 60 mg and with placebo in 38 patients in
2003. Citalopram caused a decline in binge eating and
binge-eating days, and also caused a decrease in BMI. In
this 6-week study, patients lost 2.7 kg, whereas patients in
the placebo group gained 5.2 kg. The dropout rate in this
study was 16% in the citalopram group (1 for worsening
depression, 1 for sexual dysfunction, 1 for a personal
conflict) and 21% for the placebo group (3 for worsening
depression, 1 for noncompliance).72
Tricyclic Antidepressants
Imipramine. In a trial by Laederach-Hoffman and colleagues
in 1999, imipramine 25 mg three times daily or placebo
was added to a treatment regimen of diet counseling and
 154
Table 4. Binge Eating Disorder: Medication Trials
Intention to
Year Source Females Males Age (y) Location Length Design Treatment Treat Outcome
1994 Agras et al64 109 0 22-65 Outpatient 9 mos Additive design, Weight loss No CBT was better than weight loss
no blind treatment vs weight alone in decreasing binge
reported, not loss + CBT vs frequency; CBT + desipramine
placebo- weight loss + CBT was better at decreasing weight;
controlled + desipramine (300 no p value reported
mg)
1996 Stunkard et al65 28 0 NR Outpatient 8 weeks Double-blind, d-fenfluramine (15 NR d-fenfluramine decreased the
placebo- mg) vs placebo frequency of binge eating
controlled
1998 Hudson et al66 77 8 31-52 Outpatient 9 weeks Double-blind, Fluvoxamine (300 Yes Fluvoxamine decreased binge
placebo- mg) vs placebo frequency (P < .006), severity
controlled (p < .04) and BMI (P< .002)
over 9 weeks
1999 Laederach- 27 4 25-50 Outpatient 32 weeks Double-blind, Imipramine (25 mg No Imipramine decreased binge
Hoffman et al67 placebo- tid) vs placebo frequency, illness severity, BMI
controlled and weight over 14 weeks
(P< .001)
2000 McElroy et al68 32 2 29-53 Outpatient 6 weeks Double-blind, Sertraline (187 mg Yes Sertraline was superior in
placebo- mean) vs placebo decreasing binge frequency (P<
controlled .008), illness severity (P< 0.01),
and BMI (P< .01)
2001 Ricca et al69 64 44 19-33 Outpatient 18 mos Parallel series, CBT vs CBT + Yes CBT was more effective than
open label, not fluoxetine (60 mg) fluoxetine or fluvoxamine;

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placebo- vs CBT vs fluoxetine did not enhance the
controlled fluvoxamine (300 CBT while fluvoxamine did
mg) vs fluoxetine seem to enhance CBT
(60 mg) vs (P< .01)
fluovoxamine (300
mg)
2002 Arnold et al70 56 4 31-55 Outpatient 6 weeks Double-blind, Fluoxetine Yes Fluoxetine was associated with a
placebo- (60-80 mg) vs decrease in illness severity (P=
controlled placebo 0.32), less weight gain (P<
.001), and controlled BMI over
6 weeks
(continued)
 Table 4. (continued)
Intention to
Year Source Females Males Age (y) Location Length Design Treatment Treat Outcome
2003 Appolinario 53 7 26-46 Outpatient 12 weeks Double-blind, Sibutramine (15 mg) Yes Sibutramine decreased binge
et al71 placebo- vs placebo frequency and severity (P< .03),
controlled weight decline in sibutramine
group (P< .001)
2003 McElroy et al72 36 2 38-52 Outpatient 6 weeks Double-blind, Citalopram (60 mg) Yes Citalopram decreased binge days
placebo- vs placebo (P< .001), BMI (P< .001) and
controlled weight (P< .005)
2003 McElroy et al73 61 0 31-50 Outpatient 16 weeks Double-blind, Topiramate (212 mg) Yes Topiramate superior in decreasing
placebo- vs placebo binge frequency (P< .0004),
controlled illness severity (P< .02), BMI,
and weight over the length of the
study (P< .005)
2003 Pearlstein et al74 17 3 41 mean Outpatient 12 weeks Double-blind, Fluvoxamine (239 NR No difference between
placebo- mg) vs placebo fluvoxamine and placebo; no
controlled weight change over time
2005 Grilo et al75 84 24 21-59 Outpatient 16 weeks Double-blind, Fluoxetine (60 mg) Yes CBT superior to fluoxetine alone
placebo- vs placebo vs and placebo alone in decreasing
controlled CBT + placebo vs eating shape concerns and
CBT + fluoxetine binging; CBT + fluoxetine better

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60 mg) than placebo alone; CBT and
fluoxetine not better than CBT
alone; no P values given
2005 Grilo et al76 44 6 35-58 Outpatient 12 weeks Double-blind, CBT + orlistat (120 Yes CBT + orlistat was superior in
placebo- mg) vs CBT + total weight loss over 12 weeks;
controlled placebo no P values given

BMI, body mass index; NR, not reported; CBT, cognitive behavioral therapy.

155
156 Nutrition in Clinical Practice / Vol. 25, No. 2, April 2010
sychological support in 31 patients. Patients were assessed
p percent of patients in the orlistat group and 20% in the
at 8 weeks and again at 32 weeks. Patients in the imipramine
group experienced reductions in depressed mood, binges,
and body weight at both 8 and 32 weeks, whereas those in
the placebo group had an increase in weight. Dropout rates
were relatively low: 6% for imipramine and 7% for placebo.67
Anticonvulsants
Topiramate. Topiramate, at an average dose of 212 mg
daily, was studied in 61 females in a 16-week trial by
McElroy and colleagues in 2003. Patients receiving topi-
ramate had a greater decline in binge frequency, illness se-
verity, and BMI vs patients receiving placebo. The dropout
rate in this trial was high (topiramate 47%, placebo 39%).
Reasons for dropping out of the study included patient
choice (11 topiramate, 21 placebo), adverse effects (28
topiramate, 15 placebo), lack of efficacy (1 topiramate, 3
placebo), lost to follow-up (13 topiramate, 17 placebo),
and other reasons (2 topiramate, 3 placebo). The high
dropout rate makes it difficult to evaluate the significance
of the results.73
Appetite Suppressants
Sibutramine. Sibutramine (n = 23) 15 mg daily, was com-
pared with placebo (n = 30) in a 12-week trial by Appoli-
nario in 2003.71 The primary outcome was binge frequen-
cy. In this trial, sibutramine caused a significant decrease
in binge frequency and severity. Patients also reported im-
provement in feelings of depression. At the end of the trial,
the sibutramine group lost 7.4 kg, whereas the placebo
group gained weight (1.4 kg). Twelve (52%) of 23 sibutra-
mine and 8 (32%) of 25 placebo patients attained remis-
sion at week 12. Eighteen patients (78%) of 23 sibutra-
mine and 13 (52%) of 25 placebo patients showed a 50%
reduction in binge frequency. The dropout rate in this trial
was 23% for sibutramine and 17% for placebo. Four pa-
tients withdrew from the study because of adverse effects.
In the sibutramine group, 1 patient withdrew for insomnia
and 1 for appendicitis. In the placebo group, 1 withdrew
because of nausea, and 1 because of headache.71
Orlistat. In 2005, Grilo and colleagues compared CBT
and orlistat with CBT and placebo in 50 obese BED
patients in a 12-week trial. Orlistat was used at a dose of
120 mg three times daily. The primary outcome was for
no binges to occur over the course of 28 days. In this
study, the authors reported that a combination of CBT
and orlistat was associated with a more significant weight
loss (64%) than CBT and placebo (36%) at the end of the
study; however, at a 3-month follow-up, there was no dif-
ference in weight loss in either group (52%). Twenty-four
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placebo group dropped out of the study.76
D-fenfluramine. In an 8-week trial of 28 patients by
Stunkard and colleagues in 1996, d-fenfluramine at a
dose of 15 mg daily was found to decrease the frequency
of binge eating when compared with treatment with pla-
cebo.65 Because of concerns about pulmonary hyperten-
sion and deformities in heart valves when taken in
combination with phenteramine, d-fenfluramine is no
longer available in the United States or in global markets.
Summary of Medication Trials for BED
There is good evidence that antidepressants, especially
SSRIs, can improve BED in terms of reducing binge-eat-
ing behaviors, at least in the short term. The antidepres-
sants do not appear to be associated with long-term
significant weight loss. The case for the appetite suppres-
sant sibutramine is better in terms of both reducing
binge-eating behaviors and causing weight loss.
Topiramate may lead to improvements with binging and
weight loss as well, although more studies are necessary
to confirm these results.
Conclusion
The eating disorders AN, BN, and BED are important,
complex, and potentially life-threatening disorders. The
first of these, AN, was not recognized as an official disor-
der until the mid-1980s. BED has not yet been classified
as an official disorder, but there is a high likelihood that
it will be in the near future.
Medication trials for the treatment of these disorders
are highly variable, and the literature is especially weak in
the area of medication use in the treatment of AN.
Managing patients with AN using medications alone is
not appropriate. No study to date has shown efficacy for
medications alone, and the medical complications of AN
and the mortality associated with it demand more effica-
cious treatment. There is some evidence that the use of
CBT in AN appears to decrease the incidence of relapse
after weight restoration, and should be considered in
addition to medical stabilization. In addition, the use of
medications in the treatment of AN is associated with a
high dropout rate, suggesting that patients do not find
medications acceptable.
Binging and purging, the core physiologic symptoms
of BN, respond to higher doses of fluoxetine (60 mg/
day). Lower doses do not appear to work, and in fact they

may contribute to a relapse in symptomatology. There is
some evidence that other antidepressants (trazodone,
fluvoxamine, desipramine, MAOIs) and the anticonvul-
sant topiramate may also decrease the physiological
symptoms of BN. To date, only 1 medication has been
FDA approved to treat an eating disorder, and that is
fluoxetine for the treatment of BN.
There is good evidence that CBT is effective for BN.
There is some preliminary evidence that the combination
of CBT and medication may be effective, but more
research is needed in this area. Compliance with CBT in
BN tends to be greater than with medications. Many
patients treated with medications for BN are noncompli-
ant in the long term, owing to adverse effects such as
sexual dysfunction and weight gain.
To date, most of the trials for BED have been short-
term trials. There is initial evidence that SSRIs, tricyclic
antidepressants, and sibutramine may be effective. CBT
appears to decrease the primary target symptom of BED,
binging, but it does not help with weight loss. Initial evi-
dence using combination treatments of CBT and medica-
tion appear to improve both binge eating and weight loss.
Patients with BED tend to have lower study dropout rates
and better compliance with medications than do the
other 2 eating disorders.
The studies that have been completed for the treat-
ment of the eating disorders have multiple limitations.
Studies do not distinguish between what is statistically
and clinically significant. In addition, multiple assess-
ment tools make comparing trials difficult. Not having a
consistent definition of stage of illness, remission, recov-
ery, and relapse also limit the ability to compare outcome
data from trials.
There is a tendency for lack of rigor in the scientific
design and statistical analysis in these trials. Lack of
attention to baseline characteristics of subgroups, poorly
designed and/or reported randomization designs, insuffi-
cient sample sizes, lack of sufficient power and reporting
of degrees of freedom, as well as lack of intention-to-treat
analysis are all problems with many of the current studies
that may bias results.
The high dropout rate inherent in psychiatric research
also has a negative effect on study outcomes. Initial
power analyses often did not take the high dropout rates
into account. There were multiple reasons for dropouts in
these trials. The highest dropout rates occurred in the AN
trials. Patients with AN often fear taking medication and
the weight gain associated with it. These dropouts have
an effect on the integrity of outcome data.
Eating disorders create a life-long challenge for
patients, and long-term follow-up is important in eating
disorder trials. Most trials that have been completed are
of short duration, and it is inappropriate to expect that
these results can be extrapolated to long-term results. In
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Pharmacotherapy of Eating Disorders / Jackson et al 157
addition, studies do not give enough attention to medical
issues and the long-term sequelae of the eating disorders.
It is clear that more research is needed in this area.
Large-scale, independent studies using appropriate doses
and duration of therapy, in addition to delineation of sex,
age, and ethnicity, need to be undertaken. Studies using
appropriate statistical analysis, power, research design, and
outcome measures are needed. For all 3 disorders, use of
novel therapeutic agents and comparison of medications to
psychotherapy would be important.
There is a paucity of outcome studies in the area of
eating disorders. Recovery, remission, and relapse need to
be defined and adequately researched to give eating dis-
order patients and their caregivers information on treat-
ment for these life-long illnesses.
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