040899 eating disorders
age of 40 years10 and are increasingly seen in youngchildren.11 Eating disorders are more prevalent inindustrialized societies than in nonindustrialized so-cieties and occur in all socioeconomic classes and
major ethnic groups in the United States.12-14 Thedisorders appear to be caused by a combination of
ANNE E. BECKER, M.D., PH.D.,
STEVEN K. GRINSPOON, M.D., ANNE KLIBANSKI, M.D.,
tal,19 and sociocultural20,21 factors. About half of those
AND DAVID B. HERZOG, M.D.
who have anorexia nervosa or bulimia nervosa havea full recovery, approximately 30 percent have a par-tial recovery, and 20 percent have no substantial im-
ATING disorders affect an estimated 5 mil-
provement in symptoms.
lion Americans every year. These illnesses —
anorexia nervosa, bulimia nervosa, binge-eat-
ing disorder, and their variants — are characterized
The assessment and management of eating disor-
by a serious disturbance in eating, such as restriction
ders address medical, nutritional, and psychological
of intake or bingeing, as well as distress or excessive
features of these illnesses and are ideally accomplished
concern about body shape or body weight. In addi-
by a multidisciplinary team working closely together.
tion to their effects on psychological well-being, they
have a potentially devastating effect on health throughthe physiologic sequelae of altered nutritional status
The medical assessment of an eating disorder fo-
or purging. The mortality rate associated with ano-
cuses on the complications of altered nutritional sta-
rexia nervosa alone, at 0.56 percent per year, is more
tus and purging, if present, and includes a careful
than 12 times as high as the mortality rate among
history of weight changes, dietary patterns, and the
young women in the general population.
frequency and severity of any purging behavior and
Although effective treatments are available for these
of excessive exercise. Purging behavior may include
disorders, substantial delays between the onset of
emesis induced with ipecac or by other means or
symptoms and treatment are common. Frequently, a
abuse of laxatives, enemas, diuretics, anorexic drugs,
person with an eating disorder does not disclose
caffeine, or other stimulants. The differential diag-
symptoms or may even conceal them because of a
nosis of weight loss includes inflammatory bowel dis-
lack of awareness of their effect on health, ignorance
ease and diabetes mellitus — illnesses that may co-
of available treatment, shame at the prospect of dis-
exist with and complicate the management of eating
cussing the symptoms, or unwillingness to consider
disorders — as well as cancer and thyroid disease.
relinquishing them. Moreover, eating disorders may
The patient's weight and height should be meas-
go unrecognized in clinical settings in up to 50 per-
ured and the appropriateness of weight for height,
cent of cases.
age, and sex determined according to the percentage
2-4 When these disorders are detected,
even dangerously ill patients can be averse to accept-
of his or her expected body weight or the body-mass
ing appropriate treatment.
index (the weight in kilograms divided by the squareof the height in meters) (Fig. 1). This information
EPIDEMIOLOGY, CAUSE, AND OUTCOME
can guide decision making with respect to medical,
Eating disorders typically occur in adolescent girls
nutritional, pharmacologic, and psychotherapeutic
or young women, although 5 to 15 percent of cases
of anorexia nervosa and bulimia nervosa
On physical examination, hypotension, bradycar-
percent of cases of binge-eating disorder occur in
dia, and hypothermia are often seen in association
boys and men.
with extremely low weight. Other findings associat-
6 An estimated 3 percent of young
women have these disorders, and probably twice
ed with anorexia nervosa include dry skin, hyper-
that number have clinically important variants.
carotenemia, lanugo, acrocyanosis, and atrophy of
though eating disorders usually develop in adoles-
the breasts. Swelling of the parotid and submandib-
cence or young adulthood, they can occur after the
ular glands, abnormal dentition, perimolysis (loss ofdentin on the lingual and occlusal surfaces of theteeth), and abrasions on the dorsum of the hand(caused by scraping against the incisors during at-tempts at vomiting) may be seen in association with
From the Departments of Psychiatry (A.E.B., D.B.H.), Pediatrics
chronic self-induced vomiting. The QT interval is
(D.B.H.), and Medicine (S.K.G., A.K.), Massachusetts General Hospitaland Harvard Medical School; and the Harvard Eating Disorders Center,
sometimes prolonged in patients with anorexia ner-
Harvard Medical School (A.E.B., D.B.H.) — all in Boston. Address reprint
vosa, even in the absence of abnormal serum elec-
requests to Dr. Herzog at the Harvard Eating Disorders Center, 356 Boyl-
trolyte levels. Left ventricular mass is often reduced
ston St., Boston, MA 02116, or at [email protected]
1999, Massachusetts Medical Society.
in anorexia nervosa, although systolic function typi-
140 145 150 155 160 165 170 175 180 185 191 196 201 206 211 216
Weight Ranges for Adults According to the Body-Mass Index.
Anorexia nervosa is characterized by a body-mass index of 17.5 or lower. Adapted from the National EatingDisorders Screening Program Body Weight Assessment Tool, with permission from the Harvard Eating Disor-ders Center, Boston.
cally is preserved. Mitral-valve prolapse may develop,
a normal or moderately decreased level of thyroid-
but it is usually only slight, and substantial mitral re-
stimulating hormone28; these tests are indicated only
gurgitation is uncommon.24 Intestinal dilatation from
if true thyroid disease is likely. Hypercortisolemia
chronic severe constipation and diminished intestin-
and elevated urinary levels of free cortisol may be
al motility as a result of chronic laxative abuse or
present both in patients of low weight who have an-
withdrawal may be associated with either anorexia
orexia nervosa29 and in patients of normal weight
nervosa or bulimia nervosa (Table 1).
who have bulimia nervosa.30
Routine laboratory tests include measurements of
Despite the many signs of eating disorders, labora-
serum electrolyte and serum glucose levels and a
tory values and findings on physical examination may
complete blood count. Although the pattern of elec-
be normal, particularly in patients of normal weight
trolyte abnormalities may provide evidence of vom-
who have bulimia nervosa. Amenorrhea is a cardinal
iting or abuse of laxatives or diuretics, the results of
manifestation of anorexia nervosa, but oligomenor-
these tests are often normal.25 Hypokalemia with an
rhea or amenorrhea may also occur in patients of
increase in the serum bicarbonate level may indicate
normal weight who have bulimia nervosa.31 In ano-
frequent vomiting or use of diuretics, whereas non–
rexia nervosa, amenorrhea is most often the result of
anion-gap acidosis is common in cases of laxative
a decrease in the pulsatility of gonadotropin-releas-
abuse. Hypokalemia is not typically seen in associa-
ing hormone, resulting in hypogonadotropic hypo-
tion with restrictive eating alone. Hyponatremia,
gonadism and low or undetectable levels of serum es-
however, is common in anorexia nervosa and may re-
tradiol. Puberty, including the onset of menarche,
flect excess water intake or inappropriate regulation
may be delayed in adolescents with anorexia nervosa,
of antidiuretic hormone.26 Hypoglycemia is com-
leading to the arrest of linear growth. In men, low
mon among patients of low weight but is usually
weight is also associated with clinical hypogonadism
asymptomatic. Leukopenia, neutropenia, anemia, and
and decreased levels of serum testosterone.32 A thresh-
thrombocytopenia have been well described in ano-
old level of weight or body fat is thought to be nec-
rexia nervosa.27 Thyroid-function tests often reflect
essary for normal pulsatility of gonadotropin-releas-
the euthyroid sick syndrome, characterized by de-
ing hormone,33 but the underlying mechanism of
creased levels of triiodothyronine and thyroxine but
this association is unknown. Attention has focused
on leptin, a product of the ob
gene in adipocytes,34
SIGNS, SYMPTOMS, AND MEDICAL
as a hormone that may regulate reproductive func-
COMPLICATIONS OF ANOREXIA NERVOSA
tion and signal the hypothalamus when fat mass is
AND BULIMIA NERVOSA.
decreased. Leptin levels are decreased in patientswith anorexia nervosa, and this abnormality is closely
correlated with fat mass.35 Although resumption of
menses typically accompanies weight gain, in some
cases amenorrhea persists even after the attainment
Enlargement of the parotid glandSubmandibular adenopathy
of normal body weight and may be attributable to a
low percentage of body fat, inadequate intake of di-
Postural and nonpostural hypotension
etary fats, excessive exercise, or depression or may be
an adverse effect of a psychotropic medication.
Electrocardiographic abnormalities: low voltage, pro-
Bone loss is a serious clinical problem that may
longed QT interval, prominent U waves
accompany amenorrhea and undernutrition, and it
Atrial and ventricular arrhythmias
should be assessed by bone densitometry. In 50 per-
Left ventricular changes: decreased mass, decreased
cent of women with anorexia nervosa, bone-density
measurements are more than 2 SD below normal,29,36
Cardiomyopathy (due to ipecac poisoning)
and both cortical and trabecular compartments are
affected. Symptomatic compression fractures and ky-
Esophagitis, hematemesis (including the Mallory–
phosis have been reported. Bone loss can occur in
Delayed gastric emptying
young women after as short a period of illness as six
Decreased intestinal motility
months29,37 and may also occur in men.38 Since bone
loss can persist even after the recovery of weight,39
Rectal prolapseGastric dilatation and rupture
women with a history of anorexia nervosa may be at
Abnormal results on liver-function tests
increased long-term risk for fractures.40
Elevated serum amylase level
Severe bone loss in anorexia nervosa probably has
Endocrine and metabolic
a variety of causes, including estrogen deficiency, vi-
Hypokalemia (including hypokalemic nephropathy)Hyponatremia, (rarely) hypernatremia
tamin and micronutrient deficiencies, hypercortisol-
emia, and a direct inhibitory effect of undernutrition
on bone formation and osteoblast function.29,41 Fur-
thermore, anorexia nervosa often occurs during ad-
Euthyroid sick syndrome
olescence, when accrual of bone mass is at its peak.
Hypercortisolism, elevated free cortisol level in urine
Therefore, bone loss and inadequate bone formation
Low serum estradiol levelDecreased serum testosterone level
in adolescents with anorexia nervosa may result in
severe osteopenia. Periodic assessment of the lumbar-
Delay in pubertyArrested growth
spine bone density by dual-energy x-ray absorptiom-
etry is reasonable to determine the risk of compres-
sion fractures and the degree of ongoing bone loss.
The psychiatric assessment of patients with an eat-
ing disorder focuses on establishing a diagnosis, iden-
InfertilityInsufficient weight gain during pregnancy
tifying any concurrent psychiatric illness, evaluating
the risk of suicide, and exploring the psychosocial
context of the symptoms. Although patients with an
Dry skin and hair
eating disorder may appear to be unwilling to par-
ticipate in their treatment, clinicians can often elicit
LanugoYellow skin due to hypercarotenemia
information about symptoms by remaining aware of
the characteristic signs of these disorders (Table 2)
and by taking a straightforward, empathic, and non-
Reversible cortical atrophyVentricular enlargement
To establish a diagnosis of anorexia nervosa, bulimia
nervosa, or binge-eating disorder, all the criteria listed
in Table 3 must be met. There is considerable overlapamong the features of eating disorders; for example,both anorexia nervosa and bulimia nervosa are markedby excessive concern about body shape or bodyweight, which contributes to efforts to control weight
by restrictive eating or by inappropriate behavior to
ABNORMALITIES THAT MAY INDICATE
compensate for overeating. Binge eating characterizes
AN UNDISCLOSED EATING DISORDER.
both binge-eating disorder and bulimia nervosa, andas many as half of patients with anorexia nervosa also
binge and purge.42 The differential diagnosis of disor-
Arrested growthMarked change or frequent fluctuation in weight
dered eating includes depression and several organic
Inability to gain weight
brain syndromes (e.g., hypothalamic tumor).
Evaluation for concomitant psychiatric illness and
Constipation or diarrheaSusceptibility to fractures
assessment of the risk of suicide should be routine,
because eating disorders are often accompanied by
Hypokalemia, hyperphosphatemia, metabolic acido-
sis or alkalosis, or high serum amylase levels
mood, anxiety, and personality disorders. In addi-tion, anorexia nervosa is frequently accompanied by
Change in eating habits
obsessive–compulsive disorder, and bulimia nervosa
Difficulty eating in social settings
and binge-eating disorder are often associated with
Reluctance to be weighed
substance abuse.42 Suicidal behavior often accompa-
nies anorexia nervosa and bulimia nervosa and is a
Absence from school or work
chief contributor to the high mortality rate among
Deceptive or secretive behavior
patients with anorexia nervosa.1,43 Finally, evaluation
Stealing (e.g., to obtain food)Substance abuse
of the psychosocial context and precipitants of the
illness may guide the approach to psychotherapy.
The goals of treatment for all eating disorders in-
clude stabilization of medical and nutritional status,identification and resolution of psychosocial precip-itants of the disorder, and reestablishment of health-
DIAGNOSTIC CRITERIA FOR EATING DISORDERS.*
ful patterns of eating. Although treatment in an out-patient setting is usually adequate, patients at medical
or psychiatric risk may initially or periodically re-
Body weight <85% of expected weight (or body-mass index «17.5)Intense fear of weight gain
quire hospital-based day treatment or inpatient care.
Inaccurate perception of own body size, weight, or shape
Indications for inpatient care include extremely low
Amenorrhea (in girls and women after menarche)
weight (generally defined as 75 percent or less of
expected body weight) or rapid weight loss; severe
Recurrent binge eating (at least two times per week for three months)†
electrolyte imbalances, cardiac disturbances, or other
Recurrent purging, excessive exercise, or fasting (at least two times per
week for three months)
acute medical disorders; severe or intractable purg-
Excessive concern about body weight or shape
ing; psychosis or a high risk of suicide; and symp-
Absence of anorexia nervosa
toms refractory to outpatient treatment.
Recurrent binge eating (at least two days per week for six months)†
Marked distress with at least three of the following:
Eating very rapidly
Medical treatment of eating disorders is directed
Eating until uncomfortably full
at correcting and preventing the complications of ab-
Eating when not hungryEating alone
normal weight and purging. Treatment routinely in-
Feeling disgusted or guilty after a binge
cludes educating the patient about the importance
No recurrent purging, excessive exercise, or fasting
of addressing symptoms, as well as monitoring weight,
Absence of anorexia nervosa
vital signs (heart rate, blood pressure, and temper-
Other (atypical) eating disorders
ature) and, if purging or excessive water intake is
Clinically important disordered eating, inappropriate weight control, or ex-
cessive concern about body weight or shape that does not meet all the
ongoing, serum electrolyte levels. Weight gain is a
criteria for anorexia nervosa, bulimia nervosa, or binge-eating disorder
primary goal of treatment of anorexia nervosa andrequires active management. Education about nutri-
*Adapted from the Diagnostic and Statistical Manual of Mental Disor-
4th ed.,6 with the permission of the publisher.
tion, adjustment of caloric and nutritional intake,
†A binge is characterized by the consumption of an unusually large
and limitations on exercise and other modifications
quantity of food during a discrete period of time, with lack of control over
of behavior are the preferred methods of effecting
weight gain and usually require collaboration with anutritionist. Enteral or parenteral nutrition is reservedfor patients with severe undernutrition that has beenrefractory to treatment by these methods.44,45
Weight gain by any method for patients with se-
vere anorexia nervosa warrants close medical super-
vision, since rapid refeeding and weight gain may
nutrition is prolonged, even if estrogen replacement
lead to gastric bloating, edema, and in rare cases,
is begun, the primary goal of treatment in patients
congestive heart failure.46 Weight loss is often a pri-
with anorexia nervosa should be to increase weight.
mary goal of treatment for obese patients with binge-
Vitamin supplementation should be provided, in-
eating disorder. For some patients, however — par-
cluding calcium at a dose of 1000 to 1500 mg per
ticularly those with a history of repeated weight loss
day and a multivitamin to ensure that vitamin D in-
and weight gain or with an early onset of binge eat-
take is adequate (400 IU per day). The role of bis-
ing — it may be advantageous to provide specific
phosphonates and other antiresorptive agents in the
treatment for binge eating before proceeding with
management of osteopenia in anorexia nervosa has
not been established.
Because of the complications associated with an-
orexia nervosa and bulimia nervosa, an electrocar-
diogram is essential for determining whether hypo-
Eating disorders respond to a variety of psycho-
kalemia or palpitations are present and for assessing
therapeutic approaches, and a combination of indi-
the safety of any planned psychopharmacologic man-
vidual, group, and family treatment is often benefi-
agement. Prolongation of the QT interval contrain-
cial. Anorexia nervosa may respond best to family
dicates the use of tricyclic antidepressants for the
therapy among those with early-onset, nonchronic
treatment of an eating disorder and requires imme-
disease,52 but because of cognitive deficits associated
diate medical intervention and correction of any ab-
with undernutrition in this disorder, the efficacy of
normal electrolyte levels, since a prolonged QT in-
psychotherapy may be limited until weight gain oc-
terval may increase the risk of ventricular tachycardia
curs.53 For bulimia nervosa, the best-established ap-
and sudden death. Although gastric-motility agents
proach is cognitive–behavioral therapy — a struc-
have limited value in relieving the bloating associat-
tured, time-limited therapy that addresses the relations
ed with refeeding,48 alleviation of the severe consti-
among thoughts, affect, and behavior. Interpersonal
pation associated with long-term use of laxatives or
psychotherapy, also focused and time-limited, ad-
their withdrawal may require stool softeners and bulk-
dresses interpersonal sources of stress that are pre-
forming laxatives.46 Specific medical treatment is not
sumed antecedents to disordered eating, and this ap-
indicated when laboratory analysis reveals the pres-
proach has been found to be as effective as the
ence of the euthyroid sick syndrome; the results of
cognitive–behavioral approach in the treatment of
thyroid tests return to normal with weight gain.
bulimia nervosa.54,55 Both cognitive–behavioral ther-
Persons who have induced vomiting benefit from den-
apy and interpersonal therapy are also effective in
patients with binge-eating disorder.56
Primary therapy for amenorrhea in patients with
Psychodynamic psychotherapy is useful in the treat-
anorexia nervosa is directed toward improvement in
ment of all these disorders, and the concomitant use
overall nutritional status. The decision to treat amen-
of behavioral strategies early in treatment to control
orrhea with a combination of estrogen and proges-
symptoms is often indispensable.57 Whether or not
tin must be individualized for each patient. For ex-
family therapy is initiated, education of the patient's
ample, in patients who have symptoms of estrogen
parents or partner concerning the illness is often
deficiency, such as atrophy of the breasts or dry skin,
helpful in enlisting the family's support of the treat-
estrogen replacement may be warranted. However,
ment. Parents of adolescent patients should be in-
estrogen has no established effect on bone density in
formed that clinician–patient discussions are confi-
women with anorexia nervosa and cannot be recom-
dential unless there is concern about the patient's
mended for use in all cases.49 Periodic administration
of progestin (e.g., medroxyprogesterone acetate) is
Psychopharmacologic therapy is generally not ef-
not likely to be useful, because of decreased serum
fective in treating the primary symptoms of anorexia
estrogen levels and endometrial atrophy. Although
nervosa, but fluoxetine may stabilize recovery in pa-
fertility is usually impaired in patients who currently
tients with anorexia who have attained 85 percent
have or who have a history of amenorrhea, concep-
of their expected body weight.48 Zinc and cypro-
tion can occur. A variety of obstetrical complica-
heptadine have not been therapeutically useful, and
tions, including insufficient weight gain during preg-
antidepressant and neuroleptic agents, though com-
nancy and low birth weight in infants, have been
monly used in treating anorexia nervosa, have not
reported in patients with active anorexia nervosa or
been shown to improve symptoms in controlled tri-
bulimia nervosa. Bulimia nervosa may increase the
als.48 A variety of other pharmacologic agents have
risk of miscarriage, and anorexia nervosa may increase
some role in treating mood changes, anxiety, or psy-
the risk of premature birth and prenatal death.50 Post-
chotic symptoms associated with anorexia nervosa
ponement of conception until remission is therefore
but have limited efficacy in patients with inadequate
Because bone loss may continue if severe under-
In contrast with its limited value in treating ano-
rexia nervosa, psychopharmacologic therapy is mod-
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