Official reprint from UpToDate® www.uptodate.

com

Eating disorders: Treatment and outcome

Sara F Forman, MD

UpToDate performs a continuous review of over 375 journals and other resources.
Updates are added as important new information is published. The literature review
for version 15.1 is current through December 2006; this topic was last changed on
January 2, 2007. The next version of UpToDate (15.2) will be released in June 2007.

INTRODUCTION — Anorexia nervosa and bulimia nervosa are multidimensional

illnesses that involve complex and challenging psychological issues and can have life-
threatening medical consequences. The assessment and care of these patients is
often extremely difficult.

The treatment and outcome of anorexia nervosa and bulimia nervosa are reviewed
here. The epidemiology, pathogenesis, and clinical features of eating disorders are
discussed separately. (See "Eating disorders: Epidemiology, pathogenesis, and clinical
features").

TREATMENT — The treatment of anorexia nervosa generally involves nutritional

rehabilitation, medical monitoring, and psychological treatment. Psychological
treatment may include cognitive behavioral therapy (CBT), family therapy, or other
psychological modalities. CBT emphasizes the relationship of thoughts and feelings to
behavior and helps patients learn to recognize the thoughts and feelings that lead to
disordered eating. (See "Psychological treatment of psychiatric disorders", section on
Types of psychotherapy).

For patients with bulimia nervosa, a meta-analysis and systematic review both
concluded that cognitive behavioral therapy, other psychotherapies, antidepressant
medication, and combination treatment with an antidepressant and psychotherapy
are all likely to be beneficial [1,2]. A combination of antidepressants and
psychological treatment provided the best chance for remission. The American
Psychiatric Association (APA) Guidelines state that a combination of
psychotherapeutic intervention plus medications should be considered when initiating
treatment for patients with this disorder [3]. The Society for Adolescent Medicine has
also published specific treatment guidelines for adolescents with eating disorders [4].

For patients with binge eating disorder, dietary approaches, psychiatric therapy such
as interpersonal psychotherapy and CBT, and pharmacotherapy with
antidepressants, appetite suppressants, and antiepileptics have all been used with
encouraging results at least in the short term [5,6]. In addition to management of
the eating disorder, obese patients with binge eating disorder need to be evaluated
and treated for the physical morbidities associated with obesity (eg, diabetes, sleep
apnea, hyperlipidemia, cardiovascular disease, etc.).
Interdisciplinary care team — The most accepted treatment for eating disorders
involves an interdisciplinary team approach. This team should include a medical
provider, dietitian (with experience in treating eating disorders), and a mental health
professional.

Medical provider — The medical provider works to manage medical concerns such as
vital sign stability, electrolyte abnormalities, and hydration status, and can also act
as the coordinator of care. Often weekly weigh-in and vital sign checks are needed to
ensure weight gain and medical stability. Long-term sequelae, including issues
related to bone denisty issues, menstrual cycles, and growth issues in younger
patients, also need to be followed.

Dietitian — The dietitian plays a major role by providing nutritional education about
a healthy diet and the rationale for making changes in eating behaviors. The dietitian
also engages in concrete dialogue with the patient surrounding available meal or
dietary options and gives specific caloric or meal plan requirements. The dietitian can
help the medical provider to plan the appropriate weight goals for the patient.

Mental health provider — The third and critical part of the care team is a mental
health provider. Individual and cognitive behavioral therapy are the mainstays of
treatment for eating disorders, as is family involvement in therapy. These
approaches help the patient to work on underlying issues that may have initiated the
eating disorder. A therapist with experience and expertise in the treatment of eating
disorder patients is essential. Much of the psychological work will not focus upon the
eating behaviors per se, but on the affective issues that surround the eating
disorder. The mental health provider may also help guide the other team members
on the underlying or concurrent mental health issues, severity of the case, and the
need for psychiatric hospitalization or day treatment programs. Patients with eating
disorders appear to be at increased risk for self-injurious behavior, and this
propensity should be a part of the routine assessment of these individuals [7].

Nutritional therapy — The American Psychiatric Association (APA) Guidelines for the
treatment of patients with eating disorders state that a program of nutritional
rehabilitation should be established for all patients with anorexia nervosa who are
underweight [3]. Expected rates of controlled weight gain are 2 to 3 pounds (0.9 to
1.4 kg) per week for most inpatients and 0.5 to 1 pound (0.2 to 0.5 kg) per week for
most outpatients. Intake levels usually begin at 30 to 40 kcal/kg (1000 to 1600
kcal/day) and are advanced progressively. For patients with bulimia nervosa, the
guidelines state that nutritional counseling may be a useful adjunct to other
treatment modalities.

Patients may gain weight rapidly early in the refeeding process because of fluid
retention and a baseline low metabolic rate [8,9]. The number of calories required
increases considerably with weight gain.

In patients with binge eating disorder and obesity, dietary approaches, including very
low calorie diets, may be of benefit in reducing binge eating, but they appear to have
only limited efficacy in reducing weight [5].

Refeeding syndrome — Patients with severe anorexia nervosa (ie, less than 75
percent of ideal body weight) and those who have lost a large amount of weight
rapidly are at risk for the refeeding syndrome during the first two to three weeks of
 refeeding [9,10]. Patients with severe weight loss who are rapidly refed are at
greatest risk. Patients with recent rapid weight loss, as well as patients who have
had prolonged weight loss, may also be at increased risk.

While refeeding syndrome has been defined primarily by manifestations of severe

hypophosphatemia (including cardiovascular collapse, rhabdomyolysis, seizures, and
delirium) a number of abnormalities that occur with refeeding can produce such
symptoms:

• Malnourished patients can have depleted intracellular phosphate stores [11].

With refeeding and a shift from fat to carbohydrate metabolism, hypophosphatemia
can occur as part of glycolysis, which includes the formation of phosphorylated
carbohydrate compounds in the liver and skeletal muscle. (See "Causes of
hypophosphatemia"). Hypophosphatemia can result in impaired energy stores due to
depletion of intracellular adenosine triphosphate (ATP) and tissue hypoxia due to
reduced levels of erythrocyte 2,3 diphosphoglycerate (2,3-DPG) [9].
Hypophosphatemia can cause severe impairment of myocardial contractility. (See
"Signs and symptoms of hypophosphatemia").

• Increased oral intake leads to an increase in circulatory volume, while

myocardial function is depressed secondary to decreased myocardial mass and
secondary to hypophosphatemia. This can lead to heart failure.

• Hypokalemia and hypomagnesemia can lead to cardiac arrhythmias.

Hypokalemia results from insulin secretion in response to a caloric load, which shifts
potassium into cells. (See "Causes of hypokalemia"). The etiology of hypomagnesemia
in this setting is not known.

• Wernicke's encephalopathy can occur with refeeding in a thiamine deficient

patient and manifest as delirium.

Thus, in addition to medical monitoring of vital signs, carefully monitoring

electrolytes (including potassium and phosphate daily) and looking for signs of
edema, congestive heart failure, and mental status changes are important during
refeeding. Patients who develop hypophosphatemia should be repleted. (See
"Diagnosis and treatment of hypophosphatemia"). In patients felt to be at high risk for
refeeding syndrome (eg, less than 75 percent of ideal body weight), we suggest that
refeeding start slowly (eg, 20 kcals/kg) and increase by 100 to 200 kcals/day.

Although there are not good data to support this practice, some physicians will treat
patients with phosphorous replacement during the initial phases of refeeding. This is
acceptable management as long as the patient has adequate renal function, and it
may help to avoid the hypophosphatemia associated with refeeding. Others,
however, recommend refraining from phosphate supplementation until
hypophosphatemia is diagnosed with close laboratory surveillance [12].

Because of the risk of Wernicke's encephalopathy, we suggest that patients receive a

daily multivitamin with thiamine during refeeding. Constipation or bloating may also
occur during refeeding as a result of prolonged gastrointestinal transit.
Constipation — Gut motility is slowed in patients with anorexia nervosa and bulimia
nervosa [13,14]. Promotility agents, such as metoclopramide, can be helpful in
relieving symptoms of constipation or bloating; symptoms also may resolve with
weight gain [9]. Clinical experience also suggests that osmotic laxative agents (ie
Go-Lytely or Glycolax) can help with constipation and improve a patient's feeling of
fullness or bloating.

Psychotherapy

Cognitive behavioral therapy — Cognitive behavioral therapy (CBT) is the most

effective form of specialized psychotherapy for patients with bulimia nervosa [15,16].
(See "Psychological treatment of psychiatric disorders", section on Bulimia nervosa). CBT
emphasizes the relationship of thoughts and feelings to behavior and helps patients
learn to recognize the thoughts and feelings that lead to disordered eating. CBT
helps the patient manage the anxiety related to eating and poor body image by
developing more adaptive thoughts and coping strategies [17]. CBT is more effective
than simplified behavioral therapy or interpersonal psychotherapy for patients with
bulimia nervosa [18,19].

The evidence of efficacy of CBT for anorexia nervosa is more limited. A 20-week
randomized trial in 56 women with anorexia nervosa that compared CBT,
interpersonal therapy, and a control treatment of nonspecific supportive clinical
management found that on the primary global outcome measure, supportive clinical
management was significantly superior to interpersonal therapy and was probably
also superior to CBT [20]. These results may have important implications for the
management of anorexia nervosa but must be confirmed in other trials.

Binge eating disorder appears to respond to CBT, at least in the short term, although
the effects wane over time [5]. CBT has only limited efficacy in promoting sustained
weight loss.

Other psychotherapy — Interpersonal therapy (see "Psychological treatment of

psychiatric disorders", section on Types of psychotherapy) has been shown to be about
as effective as CBT for the treatment of binge eating disorder [21].

The Maudsley method, incorporating family therapy, has also shown promising
results [22]. This therapy encourages parents to refeed their children at home with
the support of a family therapist. Parents are placed in charge of the actual feeding
regimen of the affected child.

Medication

Anorexia nervosa — Pharmacotherapy of anorexia nervosa has been disappointing.

There have been few controlled trials, and most have demonstrated efficacy only for
treating comorbid disorders such as depression and obsessive-compulsive disorder
[23]. A systematic review identified seven small randomized controlled studies
comparing antidepressants and placebo for anorexia nervosa; four studies
demonstrated no evidence of benefit with antidepressant treatment [24].

The largest randomized trial, published subsequent to the systematic review, found
no difference in time to relapse or maintenance of BMI 18.5 comparing patients
who were randomly assigned, after completion of an in-hospital program, to receive
 fluoxetine (n = 49) or placebo (n = 44) for 52 weeks [25]. Patients in both groups
were concurrently treated with cognitive behavioral therapy, which may in part
explain why these results differ from an earlier and smaller placebo trial that did
demonstrate effectiveness of fluoxetine in weight maintenance [26]. In the latter
study, patients in the placebo arm did not receive standardized psychosocial therapy
and had a relatively high relapse rate. It should be emphasized that these studies
were designed to evaluate the effect of fluoxetine on eating behaviors and weight
maintenance; use of fluoxetine or other antidepressants to manage depression in
patients with eating disorders should not be altered, based on these results.

Anxiolytic medications may be helpful before meals for the anorexic patient who is
having anxiety before eating. There are case reports in the literature of the
successful use of olanzapine in patients with severe anorexia nervosa. The APA
guidelines state that psychotropic medications should not be used as the sole or
primary treatment for anorexia nervosa, but they can be considered for the
prevention of relapse in weight restored patients or to treat depression or obsessive
compulsive disorder [3].

Bulimia nervosa — Pharmacotherapy of bulimia nervosa has been much more

successful, with antidepressant drugs having been best studied [27]. A number of
trials have shown an improved course in patients with bulimia nervosa who have
been treated with fluoxetine [28-30]. As an example, in one double-blind, placebo-
controlled study, 382 patients were randomly assigned to receive fluoxetine at a
dose of 20 mg or 60 mg daily for eight weeks, or placebo [30]. Treatment with the
lower dose of fluoxetine resulted in reductions in binge eating and vomiting
compared with placebo (45 versus 33 percent and 29 versus 5 percent,
respectively). Those receiving 60 mg of fluoxetine had even greater improvement: a
67 percent reduction in binge eating and a 56 percent reduction in vomiting. The
United States Food and Drug Administration has approved fluoxetine for the
treatment of bulimia nervosa.

The tricyclic antidepressants, such as desipramine [31], imipramine [32], and

amitriptyline [33], monoamine oxidase inhibitors [34], and buspirone [35] are also
more effective than placebo at decreasing binging and vomiting in patients with
bulimia nervosa. However, the better safety and side-effect profile of the selective
serotonin reuptake inhibitors like fluoxetine make these drugs more attractive for
first-line therapy. (See "Antidepressant medication in adults: SSRIs and heterocyclics" and
see "Antidepressant medications in adults: MAO inhibitors and others").

Two other drugs that may be useful in patients with bulimia nervosa are the
antiepileptic agent topiramate and the selective serotonin antagonist ondansetron:

• Topiramate at a dose of 25 to 600 mg/day (median dose 212 mg/day) in a

randomized study of 61 outpatients (53 women, 8 men) with binge eating disorder
(not bulimia nervosa) significantly reduced binge frequency and weight compared
with placebo (94 versus 46 percent reduction, 5.9 kg versus 1.2 kg weight loss,
respectively) [36]. However, a large percentage of patients in both the topiramate
and placebo groups did not complete the entire 14 weeks of treatment (46.7 and
38.7 percent, respectively).
• Ondansetron (24 mg/day) was reported to reduce binge eating and self-
induced vomiting in a small placebo-controlled study of 29 patients with bulimia
nervosa [37].

Further study of both of these agents is necessary before they can be considered
treatment options in patients with bulimia nervosa.

Other drugs that have been investigated for the treatment of bulimia nervosa include
lithium and naltrexone; neither has shown to be of significant benefit [35,38].

Binge eating disorder — A number of pharmacological treatments including SSRI

antidepressants [39], antiepileptics [36], and appetite suppressants [40], improve
the symptoms of binge eating disorder [6].

As discussed above, one study of the antiepileptic medication topiramate suggested

that it may be particularly promising for the treatment of binge eating disorder [36].

Hospitalization — There have been no controlled trials that have evaluated criteria
for hospitalization in patients with eating disorders. The Society for Adolescent
Medicine (SAM) has published guidelines for hospitalization; one or more of the
following justify hospitalization [4]:

• Severe malnutrition (weight less than 75 percent of average body weight for
age, sex, and height)
• Dehydration
• Electrolyte disturbances (hypokalemia, hyponatremia, hypophosphatemia)
• Cardiac dysrhythmia
• Physiologic instability (severe bradycardia [heart rate less than 50 beats per
minute during the day or less than 45 at night], hypotension [less than 80/50
mmHg], hypothermia [less than 96ºF], orthostatic changes in pulse [more than 20
beats per minute] or blood pressure [more than 10 mmHg])
• Arrested growth and development
• Failure of outpatient treatment
• Acute food refusal
• Uncontrollable binging and purging
• Acute medical complication of malnutrition (eg, syncope, seizures, cardiac
failure, pancreatitis, etc.)
• Acute psychiatric emergencies (eg, suicidal ideation, acute psychosis)
• Comorbid diagnosis that interferes with the treatment of eating disorders (eg,
severe depression, obsessive compulsive disorder, severe family dysfunction)

More recent APA guidelines present other criteria for hospitalization (show table 1).
[3]. The APA emphasizes that the decision to hospitalize should be based upon
psychiatric, behavioral, and general medical factors, and provides the following
indications, with specific parameters for adults and children/adolescents:

• Medical instability (significant bradycardia, hypotension, metabolic

abnormality: glucose or electrolytes, dehydration, or evidence of organ compromise)
• Suicidality with high lethality plan or attempt
• Weight <85 percent normal body weight or rapid decline with food refusal
despite outpatient or partial hospitalization treatment
• Comorbid psychiatric conditions
• Poorly motivated patient needing assistance to eat or cooperative only in a
highly structured environment

Recovery is difficult without an added level of support when in a low weight range.
Hospitalization can be on either a medical or psychiatric ward, depending upon the
age and medical status of the patient and local resources. The hospital unit must be
experienced with the care and refeeding of the anorexic patient and have guidelines
or a protocol. Patients may be resistant to being refed. Thus, nurses who are
sensitive yet able to set limits and enforce eating requirements are a key in the
success of the hospitalization.

One study examined outcomes after hospitalization and found that those eating
disordered patients who were allowed to remain in the hospital until they had
regained their necessary weight (90 to 92 percent of ideal body weight) had a much
improved outcome compared with those who did not regain their weight and were
discharged earlier [40]. As well, longer initial hospitalization has been shown to be
cost-effective [41]. These findings suggest that prolonged initial hospitalizations may
provide the support necessary to successfully treat patients with eating disorders.

When referring patients for inpatient treatment, providers should be aware that the
range of treatments is quite varied with some programs using oral liquid nutrition,
nasogastric tube feedings, or gradual caloric increase with "regular" food. Parenteral
nutrition is almost never indicated. Providers should become familiar with the
treatment options available in their area.

Management of osteopenia — Osteopenia is one of the most severe complications of

anorexia nervosa. (See "Eating disorders: Epidemiology, pathogenesis, and clinical
features", section on Osteopenia). The primary therapy is weight gain. Estrogen
replacement therapy has been used in women with anorexia nervosa with variable
success. (See "Overview of the management of osteoporosis in postmenopausal women",
section on Estrogen/progestin therapy). Other potential treatments that have been
or are being investigated include:

• Growth factors such as IGF-I may have short-term effects upon bone
formation in women with anorexia nervosa [42]; the long-term effects of this therapy
are unknown.

• Bisphosphonates such as alendronate are not recommended for use in patients

with anorexia in the APA guidelines [3]. In a randomized, controlled study of 32
adolescents with anorexia nervosa, treatment with alendronate for one year resulted
only in a nonsignificant increase in bone mineral density compared with placebo [43].
Additionally, long-term side effects of bisphosphonates in young people are
unknown.

• DHEA is a naturally occurring adrenal hormone that is decreased in women

with anorexia nervosa. Preliminary studies of urinary and serum bone markers have
suggested increases in bone formation and reductions in bone resorption in short-
term follow-up of patients with anorexia nervosa treated with this agent [44,45].

In the above study of DHEA, patients with a higher level of activity/exercise at

baseline had a higher bone density [46]. Although this suggests that exercise might
 be beneficial, recommending appropriate levels of activity may be difficult in this
group of patients that often has problems with excessive exercise.

Recommendations from the Society for Adolescent Medicine include weight gain,
1200 to 1500 mg/day of elemental calcium, and a multivitamin providing 400 IU of
vitamin D [4]. Individual assessments for estrogen/progestin replacement in women
may be considered. Dual emission X-Ray Absorptiometry (DEXA) scan at the initial
medical assessment of a patient with an eating disorder and at varying intervals
every 6 to 12 months can assist in counseling those at high risk for fractures and
bone loss. Care should be taken in counseling regarding exercise recommendations.
(See "Clinical manifestations and diagnosis of osteoporosis").

Reimbursement — It may be difficult for patients in the United States to access

health care benefits for the treatment of eating disorders. In many cases, benefits
for mental health services are limited or have separate "carve outs" for treatment
and require particular approvals separate from the primary care physician's.
Nevertheless, one study found no association between the severity of illness, as
indicated by hospitalization at intake to a referral center, and whether the patient's
insurance was an indemnity or managed care plan [47]. Often the most difficult
challenge is convincing insurance programs that hospitalization or day treatment
programs are necessary for optimal treatment of the patient; there may be
additional costs due to medical complications when the diagnosis is delayed or
ignored and adequate treatment is not obtained. Eating disorders organizations have
advocated for appropriate insurance coverage for patients with eating disorders [48].
A number of national organizations provide referral services and information for
these patients (show table 2).

Summary

• Patients with eating disorders should generally be cared for by an

interdisciplinary team consisting of a medical provider, dietitian, and mental health
provider.

• Cognitive behavioral therapy (CBT) is the psychotherapeutic treatment of

choice for bulimia nervosa. CBT along with other forms of psychotherapy should be
used in the treatment of anorexia nervosa.

• Patients with bulimia nervosa may also benefit from pharmacologic therapy,
particularly with the selective serotonin reuptake inhibitors such as fluoxetine.

• Patients with severe medical or psychological manifestations of anorexia and

bulimia nervosa may require hospitalization (See "Hospitalization" above).

• Patients with anorexia nervosa are at risk for osteopenia. Treatment includes
weight gain and daily supplementation with 1200 to 1500 mg of elemental calcium
plus a multivitamin containing 400 IU of vitamin D. Estrogen/progestin replacement
may be appropriate in selected women.

• A reasonable approach to the treatment of binge eating disorder is to start

with psychological interventions (cognitive behavioral or interpersonal therapy) and
consider the addition of medications such as SSRIs, topiramate, or an appetite
suppressant. Medical evaluation for the complications of obesity and counseling on
dietary modification may also be of benefit.

OUTCOME — Outcome studies in patients with eating disorders have looked

predominantly at those with anorexia nervosa [4,49]. A review of published studies
found that approximately 50 percent of patients have good outcomes as defined by
return of menses and weight gain, 25 percent have intermediate outcomes with
some weight regain and some relapse, and 25 percent have a poor outcome [49].
However, the component studies often had high drop-out rates and the duration of
follow-up was variable.

A number of patients with anorexia nervosa have a bulimic phase during their
recoveries. Poor outcomes are associated with later age of onset of the eating
disorder, longer duration of the illness, and lower minimal weight [4]. Overall, 32 to
70 percent recover fully at 20 years of follow-up; those who do not may have
increased psychiatric comorbidity [50-52].

Other studies have found psychological variables to be important predictors of

outcome. In one four-year follow-up study, for example, strong fears of maturing
predicted a poor outcome in patients with restricting anorexia nervosa, while low
self-esteem was associated with a poor outcome in those with bulimia nervosa [53].
In another report, the most significant items predicting outcome in patients with
anorexia nervosa were insight, sexual, familial, and social relationships, and mental
state; negative prognostic indicators included mood and personality disorders [54].

A focus only on treating weight issues may leave many anorexia nervosa patients
with persisting psychological problems. This was illustrated in a case-control study of
70 women with this disorder [55]. A minority of the patients (10 percent) continued
to meet the criteria for anorexia nervosa at a mean of 12 years after initial referral to
an eating disorders service. Even among those who no longer met these criteria,
relatively low body weight and cognitive features characteristic of anorexia nervosa
(perfectionism and cognitive restraint) persisted. The rates of lifetime comorbid
major depression, alcohol dependence, and a number of anxiety disorders were very
high.

One study that examined the follow-up of bulimia patients found that the number of
women who continued to meet the full criteria for bulimia nervosa declined as the
duration of follow-up increased [56]. However, 30 percent continued to engage in
recurrent binging and purging behaviors over approximately 10 years of follow-up.
Substance abuse and long duration of the disorder were poor prognostic signs.

Mortality — There is significant mortality associated with anorexia nervosa. One 10-
year follow-up study found an overall mortality rate of 6.6 percent [57]. Similar
findings were noted in a meta-analysis that examined 42 outcome studies between
1920 and 1980: the overall mortality rate was 0.56 percent per year [58]. Young
women with anorexia nervosa had a 10-fold increase in mortality compared with
women who were unaffected. Causes of death in the meta-analysis included
complications of the eating disorder (54 percent), suicide (27 percent), and unknown
or other causes (19 percent).

Most of the follow-up studies that assessed mortality were for referral-based care to
an eating disorders center or hospital; as a result, they may reflect a sicker
population of cases. In contrast, a population-based study of 208 patients (193
women and 15 men, median follow-up 22 years) diagnosed with anorexia nervosa in
Minnesota found a trend toward a decrease in mortality (standardized mortality ratio
0.71, 95% CI 0.42-1.09) [59]. Although the numbers are small, a decrease in deaths
from cardiovascular disease may have offset deaths due to anorexia and related
comorbidities (such as depression, alcoholism, and pneumonia) [60].

PREVENTION — Many studies of interventions to prevent eating disorders in high risk

groups are significantly limited by lack of randomization or control groups. A meta-
analysis acknowledged study limitations but found cumulative evidence suggesting
that interventions were more successful if they selected specific high risk groups,
were interactive rather than instructional, and were multisession [61]. However,
effect size was marginal for any intervention. Interventions included written
brochures, videos, didactic or interactive psychoeducational sessions, self-esteem
exercises, and media literacy programs promoting critical evaluation.

A randomized control trial of an internet-based psychosocial intervention targeted at

500 college women with weight or body image concerns had no effect on the primary
outcome of time to onset of subclinical or clinical eating disorder [62]. A subset of
women with BMI >25 (n = 68) did demonstrate a significant reduction in the two-
year incidence of eating disorders, comparing the treatment group with control (0
versus 12 percent, 95% CI 2.7 -21.1).

Use of UpToDate is subject to the Subscription and License Agreement.

REFERENCES
1. Whittal, ML, Agras, WS, Gould, RA. Bulimia nervosa: A meta-analysis of
psychosocial and pharmacological treatments. Behav Ther 1999; 30:117.
2. Bacaltchuk, J, Hay, P, Trefiglio, R. Antidepressants versus psychological treatments
and their combination for bulimia nervosa. Cochrane Database Syst Rev 2001;
:CD003385.
3. American Psychiatric Association. Practice guideline for the treatment of patients
with eating disorders, third edition. Am J Psychiatry 2006; 163 Suppl 1:1.
4. Golden, NH, Katzman, DK, Kreipe, RE, et al. Eating disorders in adolescents:
position paper of the Society for Adolescent Medicine. J Adolesc Health 2003;
33:496.
5. Wonderlich, SA, de Zwaan, M, Mitchell, JE, et al. Psychological and dietary
treatments of binge eating disorder: conceptual implications. Int J Eat Disord 2003;
34 Suppl:S58.
6. Carter, WP, Hudson, JI, Lalonde, JK, et al. Pharmacologic treatment of binge eating
disorder. Int J Eat Disord 2003; 34 Suppl:S74.
7. Paul, T, Schroeter, K, Dahme, B, Nutzinger, DO. Self-injurious behavior in women
with eating disorders. Am J Psychiatry 2002; 159:408.
8. Platte, P, Pirke, KM, Trimborn, P, et al. Resting metabolic rate and total energy
expenditure in acute and weight recovered patients with anorexia nervosa and in
healthy young women. Int J Eat Disord 1994; 16:45.
9. Mehler, PS. Diagnosis and Care of Patients with Anorexia Nervosa in Primary Care
Settings. Ann Intern Med 2001; 134:1048.
10. Solomon, SM, Kirby, DF. The refeeding syndrome: a review. JPEN J Parenter Enteral
Nutr 1990; 14:90.
11. Hearing, SD. Refeeding syndrome. BMJ 2004; 328:908.
12. Ornstein, RM, Golden, NH, Jacobson, MS, Shenker, IR. Hypophosphatemia during
nutritional rehabilitation in anorexia nervosa: implications for refeeding and
monitoring. J Adolesc Health 2003; 32:83.
13. Kamal, N, Chami, T, Andersen, A, et al. Delayed gastrointestinal transit times in
anorexia nervosa and bulimia nervosa. Gastroenterology 1991; 101:1320.
14. Stacher, G. Gut function in anorexia nervosa and bulimia nervosa. Scand J
Gastroenterol 2003; 38:573.
15. Lewandowski, LM, Geging, TA, Anthony, JL, O'Brien, WH. Meta-analysis of cognitive-
behavioral treatment studies for bulimia. Clin Psychol Rev 1997; 17:703.
16. Garner, DM, Garfinkel, PE. Handbook of treatment for eating disorders, 2nd ed,
Guilford Press, New York 1997.
17. Fairburn, CG, Norman, PA, Welch, SL, et al. A prospective study of outcome in
bulimia nervosa and the long-term effects of three psychological treatments. Arch
Gen Psychiatry 1995; 52:304.
18. Agras, WS, Walsh, T, Fairburn, CG, et al. A multicenter comparison of cognitive-
behavioral therapy and interpersonal psychotherapy for bulimia nervosa. Arch Gen
Psychiatry 2000; 57:459.
19. McIntosh, VV, Jordan, J, Carter, FA, et al. Three psychotherapies for anorexia
nervosa: a randomized, controlled trial. Am J Psychiatry 2005; 162:741.
20. Wilfley, DE, Welch, RR, Stein, RI, et al. A randomized comparison of group
cognitive-behavioral therapy and group interpersonal psychotherapy for the
treatment of overweight individuals with binge-eating disorder. Arch Gen Psychiatry
2002; 59:713.
21. J Am Acad Child Adolesc Psychiatry 2005; 44:632.
22. Jimerson, DC, Wolfe, BE, Brotman, AW, Metzger, ED. Medications in the treatment
of eating disorders. Psychiatr Clin North Am 1996; 19:739.
23. Claudino, A, Hay, P, Lima, M, et al. Antidepressants for anorexia nervosa. Cochrane
Database Syst Rev 2006; :CD004365.
24. Walsh, BT, Kaplan, AS, Attia, E, et al. Fluoxetine after weight restoration in anorexia
nervosa: a randomized controlled trial. JAMA 2006; 295:2605.
25. Kaye, WH, Nagata, T, Weltzin, TE, et al. Double-blind placebo-controlled
administration of fluoxetine in restricting- and restricting-purging-type anorexia
nervosa. Biol Psychiatry 2001; 49:644.
26. Bacaltchuk, J, Hay, P. Antidepressants versus placebo for people with bulimia
nervosa (Cochrane Review). Cochrane Database Syst Rev 2001; 4:CD003391.
27. Goldstein, DJ, Wilson, MG, Thompson, VL, et al. Long-term fluoxetine treatment of
bulimia nervosa. Br J Psychiatry 1995; 166:660.
28. Walsh, BT, Wilson, GT, Loeb, KL, et al. Medication and psychotherapy in the
treatment of bulimia nervosa. Am J Psychiatry 1997; 154:523.
29. Fluoxetine in the treatment of bulimia nervosa. A multicenter, placebo-controlled,
double-blind trial. Fluoxetine Bulimia Nervosa Collaborative Study Group. Arch Gen
Psychiatry 1992; 49:139.
30. Hughes, PL, Wells, LA, Cunningham, CJ, Ilstrup, DM. Treating bulimia with
desipramine. A double-blind, placebo-controlled study. Arch Gen Psychiatry 1986;
43:182.
31. Pope, HG Jr, Hudson, JI, Jonas, JM, Yurgelun-Todd, D. Bulimia treated with
imipramine: A placebo-controlled, double-blind study. Am J Psychiatry 1983;
140:554.
32. Mitchell, JE, Groat, R. A placebo-controlled, double-blind trial of amitriptyline in
bulimia. J Clin Psychopharmacol 1984; 4:186.
33. Horne, RL, Ferguson, JM, Pope, HG Jr, et al. Treatment of bulimia with bupropion: A
multicenter controlled trial. J Clin Psychiatry 1988; 49:262.
34. Hsu, LK, Clement, L, Santhouse, R, Ju, ES. Treatment of bulimia nervosa with
lithium carbonate. A controlled study. J Nerv Ment Dis 1991; 179:351.
35. McElroy, SL, Arnold, LM, Shapira, NA, et al. Topiramate in the treatment of binge
eating disorder associated with obesity: a randomized, placebo-controlled trial. Am J
Psychiatry 2003; 160:255.
36. Faris, PL, Kim, SW, Meller, WH, et al. Effect of decreasing afferent vagal activity with
ondansetron on symptoms of bulimia nervosa: a randomised, double-blind trial.
Lancet 2000; 355:792.
37. Mitchell, JE, Christenson, G, Jennings, J, et al. A placebo-controlled, double-blind,
crossover study of naltrexone hydrochloride in outpatients with normal weight
bulimia. J Clin Psychopharmacol 1989; 9:94.
38. Arnold, LM, McElroy, SL, Hudson, JI, et al. A placebo-controlled, randomized trial of
fluoxetine in the treatment of binge-eating disorder. J Clin Psychiatry 2002;
63:1028.
39. Appolinario, JC, Bacaltchuk, J, Sichieri, R, et al. A randomized, double-blind,
placebo-controlled study of sibutramine in the treatment of binge-eating disorder.
Arch Gen Psychiatry 2003; 60:1109.
40. Baran, SA, Weltzin, TE, Kaye, WH. Low discharge weight and outcome in anorexia
nervosa. Am J Psychiatry 1995; 152:1070.
41. Crow, SJ, Nyman, JA. The cost-effectiveness of anorexia nervosa treatment. Int J
Eat Disord 2004; 35:155.
42. Grinspoon, S, Herzog, D, Klibanski, A. Mechanisms and treatment options for bone
loss in anorexia nervosa. Psychopharmacol Bull 1997; 33:399.
43. Golden, NH, Iglesias, EA, Jacobson, MS, et al. Alendronate for the treatment of
osteopenia in anorexia nervosa: a randomized, double-blind, placebo-controlled
trial. J Clin Endocrinol Metab 2005; 90:3179.
44. Gordon, C, Grace, E, Jean Emans, S, et al. Changes in bone turnover markers and
menstrual function after short-term oral DHEA in young women with anorexia
nervosa. J Bone Miner Res 1999; 14:136.
45. Gordon, CM, Grace, E, Emans, SJ, et al. Effects of oral dehydroepiandrosterone on
bone density in young women with anorexia nervosa: a randomized trial. J Clin
Endocrinol Metab 2002; 87:4935.
46. Gordon, CM, Goodman, E, Emans, SJ, et al. Physiologic regulators of bone turnover
in young women with anorexia nervosa. J Pediatr 2002; 141:64.
47. Bravender, T, Robertson, L, et al. Managed care and outpatient eating disorder
program referral patterns: 1996 vs 1991 (abstract). J Adolesc Health 1998; 22.
48. International Academy of Eating Disorders. Position statement on equity in
insurance coverage for eating disorders. www.aedweb.org/disorders.html#healthins.
49. Steinhausen, HC. The outcome of anorexia nervosa in the 20th century. Am J
Psychiatry 2002; 159:1284.
50. Theander, S. Outcome and prognosis in anorexia nervosa and bulimia. J Psychiatr
Res 1985; 19:493.
51. Russell, GF. The prognosis of eating disorders, Springer-Verlag, New York 1991.
p.198.
52. Strober, M, Freeman, R, Morrell, W. The long-term course of severe anorexia
nervosa in adolescents: Survival analysis of recovery, relapse, and outcome
predictors over 10-15 years in a prospective study. Int J Eat Disord 1997; 22:339.
53. van der Ham, T, van Strien, DC, van Engeland, H. Personality characteristics predict
outcome of eating disorders in adolescents: A 4-year prospective study. Eur Child
Adolesc Psychiatry 1998; 7:79.
54. Saccomani, L, Savoini, M, Cirrincione, M, et al. Long-term outcome of children and
adolescents with anorexia nervosa: Study of comorbidity. J Psychosom Res 1998;
44:565.
55. Sullivan, PF, Bulik, CM, Fear, JL, Pickering, A. Outcome of anorexia nervosa: A case-
control study. Am J Psychiatry 1998; 155:939.
56. Keel, PK, Mitchell, JE, Miller, KB, et al. Long-term outcome of bulimia nervosa. Arch
Gen Psychiatry 1999; 56:63.
57. Eckert, ED, Halmi, KA, Marchi, P, et al. Ten-year follow-up of anorexia nervosa:
Clinical course and outcome. Psychol Med 1995; 25:143.
58. Sullivan, PF. Mortality in anorexia nervosa. Am J Psychiatry 1995; 152:1073.
59. Korndorfer, SR, Lucas, AR, Suman, VJ, et al. Long-term survival of patients with
anorexia nervosa: a population-based study in Rochester, Minn. Mayo Clin Proc
2003; 78:278.
60. Sullivan, PF. Discrepant results regarding long-term survival of patients with
anorexia nervosa?. Mayo Clin Proc 2003; 78:273.
61. Stice, E, Shaw, H. Eating disorder prevention programs: a meta-analytic review.
Psychol Bull 2004; 130:206.
62. Taylor, CB, Bryson, S, Luce, KH, et al. Prevention of eating disorders in at-risk
college-age women. Arch Gen Psychiatry 2006; 63:881.

GRAPHICS

Level of care

Level of care guidelines for patients with eating disorders

Level 3:
Partial Level 4:
Level 2:
Level 1: hospitalizatio Residential Level 5: Inpatient
Intensive
Outpatient n (full-day treatment hospitalization
outpatient
outpatient center
care)*
Medical status Medically stable to the extent that Medically For adults: Heart
more extensive medical monitoring, stable to rate <40 bpm;
as defined in levels 4 and 5, is not the blood pressure
<90/60 mmHg;
required extent
glucose <60
that
mg/dl;
intraveno potassium <3
us fluids, mEq/L;
nasogastr electrolyte
ic tube imbalance;
feedings, temperature
or <97.0°F;
multiple dehydration;
hepatic, renal, or
daily
cardiovascular
laborator
organ
y tests compromise
are not requiring acute
needed. treatment;
poorly controlled
diabetes

For children and

 adolescents:
Heart rate near
40 bpm,
orthostatic blood
pressure
changes (>20
bpm increase in
heart rate or
>10 mmHg to 20
mmHg drop),
blood pressure
<80/50 mmHg,
hypokalemia ,
hypophosphatem
ia, or
hypomagnesemi
a

Suicidality If suicidality is present, inpatient monitoring Specific plan

and treatment may be needed depending on with high
the estimated level of risk lethality or
intent;
admission may
also be
indicated in
patient with
suicidal ideas
or after a
suicide attempt
or aborted
attempt,
depending on
the presence or
absence of
other factors
modulating
suicide risk

Weight as Generall Generall Generally Generally Generally <85

percentage of y >85 y >80 >80 <85 percent; acute
healthy body percent percent percent percent weight decline
weight with food
refusal even if
not <85
percent of
healthy body
weight

Motivation to Fair-to- Fair Partial Poor-to- Very poor to

recover, good motivati motivatio fair poor
including motivati on n; motivatio motivation;
cooperativen on cooperati n; patient patient
ess, insight, ve; preoccupi preoccupied
 and ability to patient ed with with intrusive
control preoccupi intrusive repetitive
obsessive ed with repetitive thoughts§;
thoughts intrusive, thoughts patient
repetitive § 4 to 6 uncooperative
thoughts§ hours a with treatment
>3 day; or cooperative
hours/day patient only in highly
cooperati structured
ve with environment
highly
structure
d
treatmen
t

Co-occurring Presence of comorbid condition may influence Any existing

disorders choice of level of care psychiatric
(substance disorder that
use, would require
depression, hospitalization
anxiety)

Structure Self- Self- Needs Needs Needs

needed for sufficient sufficien some supervisi supervision
eating/gainin t structure on at all during and
g weight to gain meals or after all meals
weight will or
restrict nasogastric/sp
eating ecial feeding
modality

Ability to Can Some degree of external structure beyond self-

control manage control required to prevent patient from compulsive
compulsive compulsi exercising; rarely a sole indication for increasing the
exercising ve level of care
exercisin
g
through
self-
control

Purging Can greatly reduce incidents of Can ask Needs

behavior purging in an unstructured setting; for and supervision
(laxatives and no significant medical complications, use during and
diuretics) such as electrocardiographic or other support after all meals
abnormalities, suggesting the need from and in
for hospitalization others or bathrooms;
use unable to
cognitive control multiple
and daily episodes
behaviora of purging that
 l skills to are severe,
inhibit persistent, and
purging disabling,
despite
appropriate
trials of
outpatient
care, even if
routine
laboratory test
results reveal
no obvious
metabolic
abnormalities

Environmental Others able to provide Others Severe family conflict or

stress adequate emotional able to problems or absence of
and practical support provide at family so patient is unable
and structure least to receive structured
limited treatment in home; patient
support lives alone without
and adequate support system
structure

Geographic Patient lives near treatment Treatment program is too

availability of setting distant for patient to
treatment participate from home
program

In general, a given level of care should be considered for patients who meet
one or more criteria under a particular level. These guidelines are not
absolutes, however, and their application requires physician judgment.
* This level of care is most effective if administered for at least 8 hours/day,
5 days/week; less intensive care is demonstrably less effective (101).
If the patient is dehydrated, whole-body potassium values may be low even
if the serum potassium value is in the normal range; determine concurrent
urine specific gravity to assess dehydration.
Determining suicide risk is a complex clinical judgment, as is determining
the most appropriate treatment setting for patients at risk for suicide.
Relevant factors to consider are the patient's concurrent medical conditions,
psychosis, substance abuse, other psychiatric symptoms or syndromes,
psychosocial supports, past suicidal behaviors, and treatment adherence and
the quality of existing physician-patient relationships. These factors are
described in greater detail in the APA's Practice Guideline for the Assessment
and Treatment of Patients With Suicidal Behaviors (84).
Although this table lists percentages of expected healthy body weight in
relation to suggested levels of care, these are only approximations and do
not correspond to percentages based on standardized values for the
population as a whole. For any given individual, differences in body build,
body composition, and other physiological variables may result in
considerable differences as to what constitutes a healthy body weight in
relation to "norms." For example, for some patients, a healthy body weight
may be 110 percent of the standardized value for the population, whereas for
other individuals it may be 98 percent. Each individual's physiological
differences must be assessed and appreciated. For children, also consider the
rate of weight loss. Finally, weight level per se should never be used as the
sole criterion for discharge from inpatient care. Many patients require
inpatient admission at higher weights and should not be automatically
discharged just because they have achieved a certain weight level unless all
other factors are appropriately considered. See text for further discussion
regarding weight.
§ Individuals may experience these thoughts as consistent with their own
deeply held beliefs (in which case they seem to be ego-syntonic and
"overvalued") or as unwanted and ego-alien repetitive thoughts, consistent
with classic obsessive-compulsive disorder phenomenology.
Reproduced with permission from Practice guideline for the treatment of
patients with eating disorders, Third Edition. Am J Psychiatry 2006; 163
Suppl 1:1. Copyright © 2006 American Psychiatric Association.

Organizations eating disorders

National organizations for eating disorders

National Eating Disorders Association
603 Steward Street, Suite 803
Seattle, WA 98101
206-382-3587; 800-931-2237
www.nationaleatingdisorders.org
Anorexia Nervosa and Related Eating Disorders, Inc
P.O. box 5102
Eugene, OR 97405
541-344-1144
www.anred.com
National Association of Anorexia Nervosa and Associated Disorders
P.O. box 7
Highland Park, IL 60035
847-831-3438
www.anad.org
New Search Contents My UpToDate Feedback Help Log Out
©2007 UpToDate® • www.uptodate.com
SupportTag: [WEB005-201.211.168.58-0D0329ACFF-2579]