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Reviewed
December 22, 2003

Rashmi
Deshmukh, MD

Rashmi Deshmukh, MD

Departments of
Psychiatry and
Psychology

Kathleen
Franco, MD

Kathleen Franco, MD

Departments of
Psychiatry and
Psychology

Print Chapter

Copyright 2003
The Cleveland Clinic Foundation

   The eating disorders are classified in the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) on the basis of the clusters of symptoms with which they present.1 They are syndromes, characterized by severe disturbances in eating behavior and by distress or excessive concern about body shape or weight. They have a varied presentation and severe medical and psychiatric comorbidity. These factors combined with patients denial of symptoms and reluctance to seek treatment make treatment of eating disorders a real challenge. This chapter presents a summary of the diagnosis of eating disorders, the comorbidities and treatment options available.

 

Chapter Outline

Classification

Prevalence

Pathophysiology

Signs and
Symptoms

Representative
Instruments

Psychiatric
Comorbidity
of Eating
Disorders

Medical
Comorbidity
of Eating
Disorders

Differential
Diagnosis

Treatment

Course and
Prognosis

References

 

National Guidelines

Practice guideline for the treatment of patients with eating disorders
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 

 
CLASSIFICATION

Eating disorders can be classified as anorexia nervosa (AN) (Table 1), bulimia nervosa (BN) (Table 2) and eating disorder not otherwise specified (ED-NOS) (Table 3). Although DSM-IV criteria allow clinicians to diagnose patients with a specific eating disorder, many patients demonstrate a mixture of both anorexic and bulimic behaviors. Up to 50% of patients with AN develop bulimic symptoms, and some patients who are initially bulimic develop anorexic symptoms.2

AN has two subtypes: (a) restrictive eating and (b) alternating between restrictive eating and binge-eating/purging, at different periods of their illness. Patients with BN can be subclassified into (a) purging and (b) nonpurging. Many patients, particularly in younger age groups, have a combination of eating disorder symptoms that cannot be strictly categorized as either AN or BN and are technically diagnosed as ED-NOS.

PREVALENCE

Eating disorders have been reported in up to 4% of adolescents and young adults. The most common age of onset for AN is the midteens although in 5% of the patients, the onset of the disorder is in the early twenties. The onset of BN is usually in adolescence but may be as late as early adulthood.

Gender Prevalence
Both AN and BN are more commonly seen in females with estimates of male-to-female ratio ranging from 1:6 to 1:10.3-5

Lifetime Prevalence
The reported lifetime prevalence of AN among women has ranged from 0.5% when narrowly defined to 3.7% for more broadly defined anorexia nervosa.6,7 With regards to BN, estimates of lifetime prevalence among women range from 1.1 to 4.2%.8,9 Prevalence of eating disorders in young children is unknown. However, children as young as five have reported awareness of dieting and know that "sticking fingers" down one's throat can produce weight loss.10

Cultural Considerations
Eating disorders are more frequent in industrialized societies, where there is an abundance of food and being thin, especially for females, is considered attractive. Eating disorders are most common in the United States, Canada, Europe, Australia, New Zealand and South Africa. The rates are increasing, especially in nonwestern countries like Japan and China, where women are exposed to cultural change and modernization.11,12 In the United States, eating disorders are common in young Hispanic, Native American and African-American women but the rates are still lower than in Caucasian women.13 African-American women are more likely to develop bulimia and more likely to purge.14 Female athletes involved in running and gymnastics, ballet dancers, male body builders and wrestlers are also at increased risk.15-17
PATHOPHYSIOLOGY

Biological and psychosocial factors are implicated in the pathophysiology, but the causes and mechanisms underlying eating disorders remain unknown.18-23

Biological
Endogenous opioids may contribute to denial of hunger in patients with AN. Increased endorphin levels have been described in patients with BN after purging and may be likely to induce feelings of well-being. Diminished norepinephrine turnover and activity are suggested by reduced 3-methoxy-4-hydroxyphenylglycol in the urine and cerebrospinal fluid of some patients with AN. Antidepressants often benefit patients with BN and implicate a role for serotonin and norepinephrine. Starvation results in many biochemical changes such as hypercortisolemia, nonsuppression of dexamethasone, suppression of thyroid function and amenorrhea. Several computerized tomographic (CT) studies of the brain have revealed enlarged sulci and ventricles, a finding that is reversed with weight gain. In one positron-emission tomography (PET) scan study, metabolism was higher in the caudate nucleus during the anorectic state than after hyperalimentation.

First-degree female relatives and monozygotic twins of patients with AN have higher rates of AN and BN. Children of patients with AN have a lifetime risk for AN which is ten-fold that of the general population (5%). Families of patients with BN have higher rates of substance abuse, particularly alcoholism, affective disorders and obesity.

Psychosocial Factors
High levels of hostility, chaos, and isolation and low levels of nurturance and empathy are reported in families of children presenting with eating disorders. Anorexia has been formulated as a reaction to demands on adolescents to behave more independently or to respond to societal pressures to be slender. AN patients are usually high achievers. Many experience their bodies to be under the control of their parents. Self-starvation may be an effort to gain validation as a unique individual. Patients with BN have been described as having difficulties with impulse regulation.

SIGNS AND SYMPTOMS

Anorexia Nervosa
The essential features of AN are refusal to maintain a minimally normal body weight, intense fear of gaining weight and significant disturbance in the perception of the shape or size of one's body.1,18 Individuals frequently lack insight into the problem and are brought to professional attention by a family member after marked weight loss. DSM-IV identifies two types of AN: restricting type and binge eating/purging type. Comorbid psychiatric symptoms include depressive symptoms such as depressed mood, social withdrawal, irritability, insomnia and decreased sexual interest. Many depressive features may be secondary to the physiological sequelae of semistarvation. Symptoms of mood disturbances need to be reassessed after partial or complete weight restoration. Obsessive-compulsive features like thoughts of food, hoarding food, picking/pulling apart small portions of food or collecting recipes are common. Anxiety symptoms and concerns of eating in public are also frequent.

Bulimia Nervosa
The essential features are binge eating and inappropriate compensatory behaviors like fasting, vomiting, laxative use or exercising to prevent weight gain. Binge eating is typically triggered by dysphoric mood states, interpersonal stressors, intense hunger following dietary restraints or negative feelings related to body weight, shape and food. Individuals are typically ashamed of their eating problems and binge eating usually occurs in secrecy. Unlike AN, BN patients are typically within normal weight range and restrict their total caloric consumption between binges.

REPRESENTATIVE INSTRUMENTS

In addition to the clinical interview, Eating Attitudes Test, Eating Disorders Inventory, Body Shape Questionnaire etc can be used for assessment of eating disorders.24,25
PSYCHIATRIC COMORBIDITY OF
EATING DISORDERS

Common comorbid conditions26-30 include major depressive disorder or dysthymia (50% to 75%), bipolar disorder (4% to 13%), obsessive-compulsive disorder (25% with AN), sexual abuse (20% to 50%), substance abuse (12 to 18% with AN especially binge/purge subtype) and (30% to 37% with BN).
MEDICAL COMORBIDITY OF
EATING DISORDERS

Complications are related to weight loss and purging (vomiting and laxative abuse).18,31-33 (Table 4)
DIFFERENTIAL DIAGNOSIS

Anorexia Nervosa

  • Any medical illness like malignancy, brain tumors, gastrointestinal disease or AIDS that is associated with weight loss can simulate AN.
  • Depressive disorder: These patients generally do not have an intense fear of obesity or body image disturbance. Depressed patients usually have a decreased appetite as compared to AN patients who claim to have a normal appetite and to feel hungry.
  • Somatization disorder: These patients do not generally express a morbid fear of obesity. Severe weight loss and amenorrhea of more than three months is unusual in somatization disorder.
  • Schizophrenia: These patients may have delusions about food being poisoned but rarely are they concerned with caloric content. They also do not express a fear of gaining weight.
  • Bulimia nervosa: These patients usually maintain their weight within a normal range.

Bulimia Nervosa

  • Anorexia nervosa (Binge eating/purging type): These patients fail to maintain their weight within a normal range.
  • General medical conditions like epileptic-equivalent seizures or brain tumors can simulate BN.
  • Kluver-Bucy syndrome is a rare condition characterized by hyperphagia, hypersexuality, compulsive licking and biting etc.
  • Klein-Levin syndrome is more common in men and consists of hyperphagia and periodic hypersomnia.
  • Borderline personality disorder patients sometimes binge eat.
TREATMENT

A comprehensive treatment plan including a combination of nutritional rehabilitation, psychotherapy and medications is recommended.18,31-33 Weight, cardiac and metabolic status of the patient determines the acuity of the illness and the need for hospitalization. Treatment guidelines are well documented by the American Psychiatric Association in the Practice Guideline for treatment of Eating disorders.32

Anorexia nervosa:

Aims of treatment are to restore patients nutritional status and establish healthy eating patterns, treat medical complications, correct core dysfunctional thoughts related to the eating disorder, enlist family support and provide family counseling.

Indicators that merit hospitalization

  1. Weight less than 75% of individually estimated healthy weight. Serious electrolyte or metabolic abnormalities, hematemesis, vital sign changes like orthostatic hypotension, heart rate below 40 bpm or over 110 bpm or inability to sustain body core temperature. Rapid, persistent decline in oral intake or weight despite maximally intensive outpatient interventions. Prior knowledge of weight at which instability is likely to occur.
  2. Comorbid psychiatric illness (suicidal, depressed, unable to take care of themselves etc.)

Nutritional rehabilitation

  • Expected rates of controlled weight gain should be 2 to 3 lb/week for inpatient and 0.5 to 1 lb/week for outpatient programs. Intake levels should start at 30 to 40kcal/kg per day in divided meals.
  • Daily morning weights, vital signs, fluid intake and urine output and frequent physicals to detect circulatory overload, refeeding edema and bloating should be performed.
  • Monitor serum electrolyte levels (low potassium/phosphorus) and get an electrocardiogram if needed.
  • Use of stool softeners and not laxatives for treatment of constipation.
  • Use of vitamins and mineral supplements.
  • Use of positive reinforcers (praise) & negative reinforcers (restrictions of exercise & purging).
  • Close supervision and restricted access to bathrooms for at least 2 hours after meals.

Psychosocial Treatments

They are required both during hospitalization as well as after discharge. Commonly used models include dynamic expressive-supportive therapy and cognitive behavioral techniques (planned meals and self-monitoring, exposure and response prevention).

Group therapy, support groups, 12-step programs like Overeaters Anonymous may be useful as adjunctive treatment and for relapse prevention. Family therapy and marital therapy is helpful in case of dysfunctional family patterns and interpersonal distress.

Medications for Treatment of AN

They are most frequently used after weight has been restored but may begin earlier when indicated. They help maintain weight and normal eating behaviors as well as treat associated psychiatric symptoms.

  • Antidepressants: Serotonin-specific reuptake inhibitors like fluoxetine (Prozac) are commonly considered for patients with AN who have depressive, obsessive or compulsive symptoms that persist in spite of or in the absence of weight gain. Tricyclic antidepressants should be used with caution because of greater risks of cardiac complications like arrhythmias, hypotension, etc.
  • Low doses of antipsychotics can be used for marked agitation and psychotic thinking.
  • Antianxiety medications like benzodiazepenes may be used for extreme anticipatory anxiety concerning eating.
  • Estrogen replacement alone does not generally appear to reverse osteoporosis or osteopenia, and unless there is weight gain, it does not prevent further bone loss.
  • There is no evidence regarding efficacy of biphosphonates in treatment of associated osteoporosis.
  • Promotility agents such as metoclopramide are commonly used for bloating and abdominal pains due to gastroparesis and premature satiety but require monitoring for drug-related extrapyramidal side effects.

Medications for Treatment of BN

  • Antidepressants. They are used primarily to reduce the frequency of disturbed eating behaviors and treat comorbid depression, anxiety, obsessions and certain impulse-disorder symptoms. The only medication approved by the Food and Drug Administration for BN is the serotonin-reuptake inhibitor fluoxetine (Prozac). Several studies have demonstrated efficacy of serotonin-reuptake inhibitors eg, fluoxetine (Prozac), sertraline (Zoloft), paroxetine (Paxil) and citalopram (Celexa); tricyclic antidepressants eg, imipramine (Tofranil), nortryptyline (Pamelor) and desipramine (Norpramin); and monoamine oxidase inhibitors (MAOI). Doses of tricyclic antidepressants and MAOI antidepressants parallel those used to treat depression, but higher doses of fluoxetine (up to 60 or 80 mg/day) may be needed to treat BN. Bupropion (Wellbutrin) has been associated with seizures in purging bulimic patients and its use is not recommended.
  • Lithium continues to be used occasionally as an adjunct for comorbid disorders.
COURSE AND PROGNOSIS

As a general guideline, it appears that one third of individuals fully recover, one third retain sub-threshold symptoms and one third remain chronically eating disordered.

Psychiatric comorbidity is associated with the latter third. Additional prognostic factors are as follows:

Anorexia Nervosa
Long-term follow-up shows recovery rates ranging from 44 to 76% with prolonged recovery time (57 to 59 months). Mortality (up to 20%) is primarily from cardiac arrest or suicide. Good prognostic factors are admission of hunger, lessening of denial and improved self-esteem. Poorer prognostic factors are initial lower minimum weight, presence of vomiting/laxative abuse, failure to respond to previous treatment, disturbed family relationships and parental conflicts.

Bulimia Nervosa
Little long-term follow-up data exists. Short-term success is 50 to 70%, with relapse rates between 30 and 50% after 6 months. Patients have an overall better prognosis as compared to AN patients. Poor prognostic factors are hospitalization, higher frequency of vomiting, poor social and occupational functioning, poor motivation for recovery, severity of purging and presence of medical complications, high levels of impulsivity, longer duration of illness, delayed treatment and premorbid history of obesity and substance abuse.
NATIONAL GUIDELINES
The clinical practice guideline for the diagnosis and treatment of eating disorders is available at the American Psychiatric Association (APA) website. An abridged, up-to-date version is available at www.guidelines.gov/
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