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3/20/2018 Eating disorders: Overview of epidemiology, clinical features, and diagnosis - UpToDate

Author: Sara F Forman, MD


Section Editor: Joel Yager, MD
Deputy Editor: David Solomon, MD

Contributor Disclosures

All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Feb 2018. | This topic last updated: Oct 25, 2017.

INTRODUCTION — Eating disorders are characterized by a persistent disturbance of eating that impairs health
or psychosocial functioning [1]. The disorders include anorexia nervosa, avoidant/restrictive food intake
disorder, binge eating disorder, bulimia nervosa, pica, and rumination disorder. Diagnoses are based upon the
American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-
5), which divides eating disorders into mutually exclusive categories that are based upon observed symptoms
[1]. Some diagnoses include a dimensional component that allows clinicians to specify the severity of illness [2-
4].

Many aspects of the United States culture display an obsession with weight loss. Women's magazines often
include stories about weight management, dieting, or how to tighten specific muscle groups. Models and actors
often display a level of thinness that is difficult to attain, computer programs are used to alter photographs to
make models look thinner, and some athletes relentlessly pursue a leaner body to enhance performance. This
preoccupation to lose weight and tying self-esteem to a thin body type often extends to maturing adolescents.

This topic reviews the epidemiology, pathogenesis, and diagnosis of eating disorders, as well as their course of
illness. Treatment of eating disorders, medical complications of eating disorders and their management,
evaluation for medical complications and criteria for hospitalization, and the refeeding syndrome in anorexia
nervosa are discussed separately.

● (See "Eating disorders: Overview of prevention and treatment".)

● (See "Anorexia nervosa in adults and adolescents: Medical complications and their management".)

● (See "Bulimia nervosa and binge eating disorder in adults: Medical complications and their management".)

● (See "Anorexia nervosa in adults: Evaluation for medical complications and criteria for hospitalization to
manage these complications".)

● (See "Anorexia nervosa in adults and adolescents: The refeeding syndrome".)

SCREENING — A number of screening instruments have been developed to identify patients with eating
disorders. Some are long and not ideally suited for screening in a primary care setting, but shorter instruments
have been developed that may help identify patients who need further evaluation [5,6].

We suggest the SCOFF, which consists of five clinician administered questions [5,7]:

● Do you make yourself Sick because you feel uncomfortably full?

● Do you worry you have lost Control over how much you eat?

● Have you recently lost more than One stone (14 pounds or 6.35 kg) in a three-month period?

● Do you believe yourself to be Fat when others say you are too thin?

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3/20/2018 Eating disorders: Overview of epidemiology, clinical features, and diagnosis - UpToDate

● Would you say that Food dominates your life?

A second short tool, the clinician administered Eating Disorder Screen for Primary Care, can also be used as a
screening tool for eating disorders [6]:

● Are you satisfied with your eating patterns? (No is abnormal)

● Do you ever eat in secret? (Yes is abnormal)

● Does your weight affect the way you feel about yourself? (Yes is abnormal)

● Have any members of your family suffered with an eating disorder? (Yes is abnormal)

● Do you currently suffer with or have you ever suffered in the past with an eating disorder? (Yes is
abnormal)

The original study describing the SCOFF reported that a "yes" to two or more questions was associated with a
sensitivity and specificity of 100 and 87.5 percent for the diagnosis of an eating disorder [5]. A subsequent
report that proposed and evaluated the ESP found that two abnormal responses to the ESP had a sensitivity
and specificity of 100 and 71 percent, and that the sensitivity and specificity of SCOFF was lower (78 and 88
percent, respectively) [6]. Further validation of both of these instruments is needed in broader populations.

The Eating Attitudes Test (EAT) is one of the most widely used self-report eating disorder instruments. The 26-
item version has an accuracy rate of at least 90 percent when screening patients for the presence of an eating
disorder, using a cutoff score of 20 (table 1) [8].

The Primary Care Evaluation of Mental Disorders Patient Health Questionnaire is a brief instrument that both
screens for and provides a categorical diagnosis for bulimia nervosa, as well as depressive, anxiety, alcohol,
and somatoform disorders [9]. It was specifically designed for use in primary care, is fully self-administered by
the patient, has good diagnostic validity overall (sensitivity 75 percent, specificity 90 percent), excellent
diagnostic validity for eating disorders (sensitivity 89 percent, specificity 96 percent), and the median physician
time to review the results is one to two minutes (table 2).

Additional information about assessing patients with a possible diagnosis of anorexia nervosa or bulimia
nervosa is discussed separately. (See "Anorexia nervosa in adults: Clinical features, course of illness,
assessment, and diagnosis", section on 'Assessment' and "Bulimia nervosa in adults: Clinical features, course
of illness, assessment, and diagnosis", section on 'Assessment'.)

ANOREXIA NERVOSA

Epidemiology

Adults — The estimated lifetime prevalence of anorexia nervosa in the United States adult general
population is 0.6 percent [10]. A study of Finnish twins found a higher lifetime prevalence of 2.2 percent [11].
These estimates are likely to be low due to the tendency of some individuals to conceal their illness [12]. In
addition, diagnoses were based upon DSM-IV criteria, which are more restrictive than DSM-5 criteria [13]. In
the Finnish study, diagnoses that were based upon criteria similar to DSM-5 found a lifetime prevalence of 4.2
percent [11].

Anorexia nervosa is more common in women than men. In one nationally representative survey, the estimated
lifetime prevalence was three times greater in females than males (0.9 versus 0.3 percent) [10]. In clinical
settings, the ratio of females to males ranges from 10:1 [14] to 20:1 [15].

The median age of onset for anorexia nervosa in the general population is 18 years [10].
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3/20/2018 Eating disorders: Overview of epidemiology, clinical features, and diagnosis - UpToDate

Adolescents — A nationally representative survey of adolescents (aged 13 to 18 years) in the United States
found that the lifetime prevalence of anorexia nervosa was 0.3 percent; the prevalence for females and males
was identical (0.3 percent) [16].

Pathogenesis and neurobiology — The pathogenesis of anorexia nervosa is not known. However,
aggregation of anorexia nervosa in families suggests that genetic factors (and/or environmental factors) may be
involved [17]. Other evidence supporting a genetic basis comes from a meta-analysis of genome wide
association studies that included nearly 3500 individuals with a lifetime diagnosis of anorexia nervosa and
nearly 11,000 controls [18]. The study identified a significant locus on chromosome 12 (rs4622308) that was
associated with anorexia nervosa. In addition, the study found positive genetic correlations between anorexia
nervosa and neuroticism, schizophrenia, and educational attainment, suggesting that the same genes are
involved across these phenotypes.

Multiple lines of evidence demonstrate altered brain function and structure in anorexia nervosa [19]. However, it
is not clear whether the observed changes are etiologic and lead to anorexia nervosa, or whether the
differences represent consequences of the disorder. Some of the functional and structural changes reverse
following weight restoration, and others persist.

Functional magnetic resonance imaging studies suggest that abnormal functioning of different brain areas may
contribute to onset of maintenance of anorexia nervosa [19]. As an example:

● Abnormal functioning of corticolimbic circuits involved in appetite may contribute to anorexia nervosa. A
study examined responses to tasting sucrose in patients who recovered from anorexia nervosa (n = 14)
and in healthy controls (n = 14); blood flow in the right anterior insula was diminished in the patients,
compared with controls [20]. This suggests that restricted eating and weight loss may occur in anorexia
nervosa because hunger signals are not accurately recognized (the anterior insula is thought to integrate
sensory aspects of feeding).

● A second study examined inpatients with anorexia nervosa (n = 21) and healthy controls (n = 21) while
they chose foods to eat, and found that activity in the dorsal striatum was greater among patients (who
were less likely to choose high-fat foods) [21]. In addition, connectivity in fronto-striatal circuits differed
between the groups. The dorsal striatum is involved in habitual behavior, and the study suggests that
maladaptive food choices in anorexia nervosa are well established behaviors that are subserved by fronto-
striatal networks.

In addition, neuroimaging studies have shown structural brain changes in patients with anorexia nervosa. (See
"Anorexia nervosa in adults and adolescents: Medical complications and their management", section on
'Neurologic'.)

Neurotransmitter systems are also disrupted in anorexia nervosa. Deficits have been found in dopaminergic
function (dopamine is thought to be involved with eating behavior, motivation, and reward) and serotonergic
function (serotonin may be involved with mood, impulse control, and obsessional behavior) [19].

Clinical features — The clinical features of anorexia nervosa are discussed separately. (See "Anorexia
nervosa in adults: Clinical features, course of illness, assessment, and diagnosis".)

Diagnosis — According to DSM-5, the diagnosis of anorexia nervosa requires each of the following (table 3)
[1]:

● Restriction of energy intake that leads to a low body weight, given the patient’s age, sex, developmental
trajectory, and physical health

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3/20/2018 Eating disorders: Overview of epidemiology, clinical features, and diagnosis - UpToDate

● Intense fear of gaining weight or becoming fat, or persistent behavior that prevents weight gain, despite
being underweight

● Distorted perception of body weight and shape, undue influence of weight and shape on self-worth, or
denial of the medical seriousness of one’s low body weight

Amenorrhea commonly occurs in anorexia nervosa and was a diagnostic criterion in DSM-IV-TR [22]. However,
DSM-5 eliminated amenorrhea as a criterion because patients who menstruate but otherwise meet criteria for
anorexia nervosa have similar outcomes to patients who do not menstruate [23]. Additional information about
the diagnosis is discussed separately. (See "Anorexia nervosa in adults: Clinical features, course of illness,
assessment, and diagnosis", section on 'Diagnosis'.)

Medical complications and evaluation — Many medical complications can occur during starvation or
persistent purging [24-27]. Complications of anorexia nervosa include myocardial atrophy, mitral valve prolapse,
pericardial effusion, bradycardia, functional hypothalamic amenorrhea, antenatal and postpartum problems,
osteoporosis, gastroparesis, and constipation (table 4). In addition, growth disturbance can occur in
adolescents. Medical complications of anorexia nervosa and their management are discussed separately. (See
"Anorexia nervosa in adults and adolescents: Medical complications and their management".)

All patients with anorexia nervosa should be evaluated for medical complications [24,27]. The evaluation should
include a history, physical examination, and focused laboratory testing. The evaluation for medical
complications and criteria for hospitalization to manage these complications are discussed separately. (See
"Anorexia nervosa in adults: Evaluation for medical complications and criteria for hospitalization to manage
these complications".)

AVOIDANT/RESTRICTIVE FOOD INTAKE DISORDER — The DSM-5 diagnosis of avoidant/restrictive food


intake disorder replaces and extends the DSM-IV-TR diagnosis of feeding disorder of infancy or early childhood
[1,22].

Epidemiology — The prevalence of avoidant/restrictive food intake disorder in community settings is not
known. A prospective study of children age 8 to 13 years (n >1400) using a screening instrument found that at
least one feature of the disorder was present in 3 percent, but it’s not clear whether any of the individuals met
criteria for the disorder [28].

In clinical settings, the prevalence of avoidant/restrictive food intake disorder varies depending upon the
specific setting. Retrospective studies in the United States and Canada have found that among pediatric
patients evaluated and treated in eating disorder programs (total n >2300), avoidant/restrictive food intake
disorder was present in approximately 5 to 15 percent [29-32]. A retrospective study of youth (n >2231) age 8 to
18 years who presented to gastroenterology clinics found that avoidant/restrictive food intake disorder was
present in 1 percent [33].

In eating disorder programs, the proportion of patients with avoidant/restrictive food intake disorder who are
male ranges from approximately 20 to 30 percent, and patients with avoidant/restrictive food intake disorder are
more likely to be male than patients with anorexia nervosa or bulimia nervosa [30-32].

Onset of the disorder generally occurs in infancy or early childhood and may persist into adulthood [29].

Clinical features — Patients with avoidant/restrictive food intake disorder are often underweight. One study of
patients (n = 34) with avoidant/restrictive food intake disorder found that the average body mass index
(calculator 1) was 16 kg/m2 [31]. In addition, bone mineral density is often diminished.

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Comorbidity is common in avoidant/restrictive food intake disorder [31]. As an example, a study of patients (n =
98) with the disorder found that a comorbid anxiety disorder (eg generalized anxiety disorder) was present in
approximately 60 percent, and a general medical disorder or symptom was present in about 50 percent [30].

Little is known about the course of illness in avoidant/restrictive food intake disorder.

Diagnosis — The DSM-5 diagnosis of avoidant/restrictive food intake disorder requires each of the following
[1]:

● Avoiding or restricting food intake, which may be based upon lack of interest in food, the sensory
characteristics of food, or a conditioned negative response associated with food intake following an
aversive experience (eg, choking). The eating behavior leads to a persistent failure to meet nutritional
and/or energy needs, manifested by at least one of the following:

• Clinically significant weight loss, or in children, poor growth or failure to achieve expected weight gain

• Nutritional deficiency

• Supplementary enteral feeding or oral nutritional supplements are required to provide adequate intake

• Impaired psychosocial functioning

● The eating or feeding disturbance is not due to lack of available food or associated with a culturally
sanctioned practice.

● The disturbance does not occur solely in the course of anorexia nervosa or bulimia nervosa, and body
weight and shape are not distorted.

● The disturbance is not due to a general medical condition (eg, gastrointestinal disease, food allergies, or
occult malignancy) or another mental disorder. When avoidant/restrictive food intake disorder occurs in the
context of another illness, the eating disturbance is both out of proportion to what is expected for the other
illness and warrants additional clinical attention.

BINGE EATING DISORDER

Epidemiology

Adults — Pooled results from nationally representative surveys of adults in 14 countries (Europe, Latin
America, New Zealand, and the United States) estimate that the lifetime prevalence of binge eating disorder is
1.9 percent, and the 12-month prevalence is 0.8 percent [34]. In the United States survey, the lifetime and 12-
month prevalence rates are 2.6 and 1.2 percent. The average prevalence of binge eating disorder in clinical
samples (weight-control programs) is 30 percent [22].

Binge eating disorder is more common in women than men [34]. In a nationally representative survey in the
United States, the lifetime prevalence in females and males was 3.5 versus 2.0 percent [10]. However,
prevalence rates were not associated with race, marital status, or employment status.

The median age of onset of binge eating disorder is approximately 23 years [34].

Patients with binge eating disorder commonly suffer comorbid psychopathology. A survey in the United States
found that 79 percent of individuals with binge eating disorder had a lifetime history of at least one other
psychiatric disorder, and 49 percent had a lifetime history of three or more comorbid disorders [10]. The most
common comorbid illnesses were specific phobia (37 percent of individuals), social phobia (32 percent),
unipolar major depression (32 percent), posttraumatic stress disorder (26 percent), and alcohol abuse or

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3/20/2018 Eating disorders: Overview of epidemiology, clinical features, and diagnosis - UpToDate

dependence (21 percent). These rates are higher than what is found in the general population. As an example,
the lifetime prevalence rate of specific phobia in the general population is 12 percent [35].

Compared to individuals without a lifetime history of an eating disorder, individuals with a history of binge eating
disorder are at increased risk to develop comorbid general medical disorders, including chronic pain, diabetes
mellitus, and hypertension [34]. In addition, individuals with a history of binge eating disorder have a higher
body mass index and are more likely to be obese.

In surveys from 14 countries that identified individuals with binge eating disorder during the past 12 months,
impaired (mild, moderate, or severe) psychosocial functioning was reported by 47 percent; severe impairment
occurred in 13 percent [34]. In the United States, impaired psychosocial functioning was found in 63 percent;
severe impairment was reported by 19 percent [10].

Adolescents — A nationally representative survey of adolescents (aged 13 to 18 years) in the United States
found that the lifetime prevalence of binge eating disorder was 1.6 percent; the prevalence was greater in
females than males was (2.3 versus 0.8 percent) [16].

When to suspect the disorder — Binge eating disorder can be difficult to detect because patients often feel
ashamed [36]. The presence of the disorder is suggested by clues such as:

● Greater than expected weight dissatisfaction

● Large weight fluctuations

● Depressive symptoms

Diagnosis — The DSM-5 diagnosis of binge eating disorder requires each of the following [1]:

● Episodes of binge eating, defined as consuming an amount of food in a discrete period of time (eg, two
hours) that is definitely larger than what most people would eat in a similar amount of time under similar
circumstances. During episodes, patients feel they lack control over eating (eg, patients feel they cannot
stop eating or control the amount or what they are eating).

● Binge eating episodes are marked by at least three of the following:

• Eating more rapidly than normal

• Eating until feeling uncomfortably full

• Eating large amounts of food when not feeling physically hungry

• Eating alone because of embarrassment by the amount of food consumed

• Feeling disgusted with oneself, depressed, or guilty after overeating

● Episodes occur, on average, at least once a week for three months.

● No regular use of inappropriate compensatory behaviors (eg, purging, fasting, or excessive exercise) as
are seen in bulimia nervosa.

● Binge eating does not occur solely during the course of bulimia nervosa or anorexia nervosa.

The current level of severity is based upon the number of binge eating episodes per week:

● Mild – 1 to 3

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● Moderate – 4 to 7

● Severe – 8 to 13

● Extreme – 14 or more

Although the prevalence increases with increasing weight, the etiologic relationships between obesity and binge
eating disorder are not clear [37]. Approximately 50 percent of individuals in the community with binge eating
disorder are overweight or obese, similar to the community at large [10,38]. The remaining individuals with
binge eating disorder are of normal weight, and they are less likely to present for treatment [39,40]. The effect
of binge eating cessation on subsequent weight loss and/or medical comorbidities of obesity are not clearly
established [41].

Comorbidity

Psychiatric — Comorbid psychopathology often occurs in binge eating disorder. A nationally representative
survey in the United States found that among individuals with a lifetime history of binge eating disorder, the
prevalence of comorbid disorders was as follows [10]:

● Specific phobia – 37 percent of patients with binge eating disorder

● Social anxiety disorder (social phobia) – 32 percent

● Unipolar major depression – 32 percent

● Posttraumatic stress disorder – 26 percent

● Attention deficit hyperactivity disorder – 20 percent

● Alcohol use disorder – 21 percent

The prevalence of these disorders in patients with binge eating disorder exceeded the rate in the general
population.

Comorbid personality disorders are also common in binge eating disorder. In a meta-analysis of nine studies,
the frequency of personality disorders in 838 patients with binge eating disorder (nearly all were assessed with
structured clinical interviews) was as follows [42]:

● Any personality disorder – 29 percent of patients

● Avoidant personality disorder – 12 percent

● Borderline personality disorder – 10 percent

● Obsessive-compulsive personality disorder – 10 percent

Diabetes — A hospital and national registry study identified patients with binge eating disorder (n = 113) and
controls matched for age and sex (n = 655), and found that the lifetime prevalence of type II diabetes was
greater in patients than controls (34 versus 4 percent) [43].

Course of illness — Development of binge eating disorder occurs in a variety of ways. A study of 284 patients
with binge eating disorder found that becoming overweight usually occurred first, compared with dieting or
binge eating first (63 versus 21 and 16 percent of patients) [44].

Observational studies indicate that the course of illness among patients with binge eating disorder is often
chronic [10]:
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● One study found that the mean lifetime duration of binge eating disorder (n = 131) was 14 years, which
was longer than that for bulimia nervosa (n = 17; 6 years) or anorexia nervosa (n = 18; 6 years) [45].

● A study of 68 inpatients with binge eating disorder found that after 12 years, 36 percent still met criteria for
an eating disorder diagnosis [46].

Body dissatisfaction (undue influence of body weight or shape), impulsivity, and a history of sexual abuse are
associated with a poor outcome [46,47].

The diagnostic stability of adolescent binge eating disorder is low. A prospective study of adolescents (n >1500)
found that binge eating disorder at age 14 was associated with bulimia nervosa at age 17, and that binge eating
disorder at age 17 was associated with bulimia nervosa at age 20 [48].

BULIMIA NERVOSA

Epidemiology

Adults — Pooled results from nationally representative surveys of adults in 14 countries (Europe, Latin
America, New Zealand, and the United States) estimate that the lifetime prevalence of bulimia nervosa is 1.0
percent, and the 12-month prevalence is 0.4 percent [34]. Nearly identical figures are seen in the United States
general population. These estimates are low due to the tendency of some individuals to conceal their illness
[12]. In addition, diagnoses were based upon DSM-IV criteria, which were more restrictive than DSM-5 criteria
[1,22].

Bulimia nervosa is more common in women than men [34]. A nationally representative survey in the United
States estimated that the lifetime prevalence was three times greater in females than males (1.5 versus 0.5
percent) [10]. In clinical settings, the ratio of females to males with a first time diagnosis is even higher (13 to 1)
[14].

The median age of onset of bulimia nervosa is 18 years [34].

In surveys from 14 countries that identified individuals with bulimia nervosa during the past 12 months, impaired
(mild, moderate, or severe) psychosocial functioning was reported by 55 percent; severe impairment occurred
in 22 percent [34]. In the United States, impaired psychosocial functioning was found in 78 percent; severe
impairment was reported by 44 percent [10].

Analyses of different birth (age) cohorts suggest that the risk of bulimia nervosa has increased over time
[10,34].

Adolescents — A nationally representative survey of adolescents (aged 13 to 18 years) in the United States
found that the lifetime prevalence of bulimia nervosa was 0.9 percent; the prevalence was greater in females
than males was (1.3 versus 0.5 percent) [16].

Neurobiology — Multiple studies demonstrate altered brain function and structure in bulimia nervosa.
However, it is not clear whether any of the observed changes are etiologic and lead to bulimia nervosa, or
whether the changes represent consequences of the disorder.

Abnormal functioning of corticolimbic circuits involved in appetite may contribute to bulimia nervosa. A
functional magnetic resonance imaging study examined responses to tasting sucrose in patients who recovered
from bulimia nervosa (n = 14) and in healthy controls (n = 14); blood flow in the right anterior insula was
elevated in the patients, compared with controls [20]. This suggests that overeating may occur in bulimia
nervosa because hunger and satiety states are not accurately recognized (the anterior insula is thought to
integrate sensory aspects of feeding).

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In addition, magnetic resonance imaging studies have shown structural brain changes in bulimia nervosa,
including frontal and temporoparietal areas:

● One study examined gray and white matter volumes in patients with active bulimia nervosa (n = 20) and in
healthy controls (n = 24); the medial orbitofrontal cortex and antero-ventral insula was larger in patients
than controls, after controlling for covariates (eg, age, anxiety, depression, and medications) [49]. In
addition, temporal and parietal areas were reduced in patients.

● A second study compared age matched patients (n = 34) and healthy controls (n = 34), and found that the
cerebral surface of the frontal and temporoparietal areas was reduced in patients [50]. In addition,
reductions were greater in patients with more episodes of bingeing and purging, more preoccupation with
shape and weight, and a longer duration of illness. Reduction of cerebral surfaces was also associated
with poorer neuropsychological functioning.

Clinical features — The clinical features of bulimia nervosa are discussed separately. (See "Bulimia nervosa in
adults: Clinical features, course of illness, assessment, and diagnosis".)

Diagnosis — The DSM-5 criteria for bulimia nervosa include recurrent episodes of both binge eating and
inappropriate compensatory behavior to prevent weight gain, occurring on average at least once per week for
three months (table 5) [1]. (See "Bulimia nervosa in adults: Clinical features, course of illness, assessment, and
diagnosis", section on 'Diagnosis'.)

Medical complications and evaluation — Persistent purging can lead to many medical complications,
including dehydration, hypokalemia, menstrual irregularities, Mallory-Weiss syndrome, ipecac-induced
myopathy, and erosion of dental enamel [24-27]. Electrocardiogram changes can occur as well. The medical
complications of bulimia nervosa and their management are discussed separately. (See "Bulimia nervosa and
binge eating disorder in adults: Medical complications and their management".)

Patients with bulimia nervosa should be evaluated for medical complications that are secondary to persistent
purging [24,27]. The evaluation includes a history, physical examination, and laboratory testing. The evaluation
for medical complications is discussed separately, and the criteria for hospitalization to manage these
complications are discussed separately in the context of anorexia nervosa. (See "Bulimia nervosa and binge
eating disorder in adults: Medical complications and their management" and "Anorexia nervosa in adults:
Evaluation for medical complications and criteria for hospitalization to manage these complications", section on
'Inpatient hospitalization'.)

PICA

Epidemiology — The prevalence of pica is not known, but may be greater in patients with intellectual disability
[1]. Onset most often occurs during childhood, but can occur during adolescence or adulthood.

Diagnosis — The DSM-5 diagnosis of pica requires each of the following [1]:

● Repeated eating of nonfood substances (eg, chalk, clay, cloth, coal, dirt, gum, hair, metal, paint, paper,
pebbles, soap, string, or wool) that are not nutritional, for at least one month.

● The eating behavior is inappropriate to the patient’s developmental level, and is not culturally supported or
socially normal.

● If the eating behavior occurs in the context of another mental disorder (eg, autism, intellectual disability, or
schizophrenia) or general medical condition (including pregnancy), the severity of the eating behavior
warrants additional clinical attention.

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DSM-5 distinguishes pica from nonsuicidal self-injurious behaviors in which patients swallow potentially harmful
objects (eg, batteries, knives, or needles) [1]. Little is known about the course of illness in pica.

Pica may be a clinical manifestation of iron deficiency anemia. (See "Causes and diagnosis of iron deficiency
and iron deficiency anemia in adults", section on 'Pica and ice craving'.)

RUMINATION DISORDER

Epidemiology — The prevalence of rumination disorder is not clear [1].

Diagnosis — The DSM-5 diagnosis of rumination disorder requires each of the following [1]:

● Repeated regurgitation of food, which may be rechewed, reswallowed, or spit out; the eating disturbance
occurs for at least one month.

● Regurgitation of food is not due to a general medical condition, such as gastroesophageal reflux disease or
pyloric stenosis. (See "Clinical manifestations and diagnosis of gastroesophageal reflux in adults" and
"Approach to the infant or child with nausea and vomiting", section on 'Pyloric stenosis'.)

● Regurgitation does not occur solely during the course of avoidant/restrictive food intake disorder, anorexia
nervosa, binge eating disorder, or bulimia nervosa.

● If the eating behavior occurs in the context of another mental disorder (eg, intellectual disability) or general
medical condition (including pregnancy), the severity of the eating behavior warrants additional clinical
attention.

Little is known about the course of illness in rumination disorder.

OTHER SPECIFIED FEEDING OR EATING DISORDER

Diagnosis — Other specified feeding or eating disorder applies to patients with symptoms that cause
significant distress or impair psychosocial functioning but do not meet the full criteria for a specific feeding and
eating disorder [1]. Clinicians record the diagnosis “other specified feeding or eating disorder,” followed by the
reason that the presentation does not meet full criteria for an eating disorder. Examples of syndromes that can
be specified when using the diagnosis other specified feeding or eating disorder include:

● Atypical anorexia nervosa – All of the criteria for anorexia nervosa (table 6) are met, except that body mass
index is ≥18.5 kg/m2. One example is obese patients who demonstrate the signs and symptoms of
anorexia nervosa during rapid weight loss to a normal weight; the diagnosis is “other specified feeding or
eating disorder, atypical anorexia nervosa.”

● Bulimia nervosa of low frequency and/or limited duration – All of the criteria for bulimia nervosa (table 7)
are met, except that episodes of binge eating and inappropriate compensatory behavior occur, on average,
less than once per week and/or less than three months.

● Binge eating disorder of low frequency and/or limited duration – All of the criteria for binge eating disorder
are met, except that episodes of binge eating occur, on average, less than once per week and/or less than
three months.

● Purging disorder – Recurrent episodes of purging (self-induced vomiting, or misuse of laxatives, diuretics,
or enemas) to influence body weight or shape, in the absence of binge eating.

● Night eating syndrome – Recurrent episodes of night eating, defined as eating after awakening from sleep
or eating excessively after the evening meal. The night eating is not explained by changes in the sleep-

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wake cycle (eg, night shift work), medication effects, binge eating disorder, substance use disorders, or
general medical disorders.

Other specified feeding or eating disorder replaced the DSM-IV category “eating disorder not otherwise
specified” [1,22]. However, the two diagnoses overlap only partially. Some patients who were previously
diagnosed with DSM-IV-TR eating disorder not otherwise specified are classified in DSM-5 as either anorexia
nervosa or binge eating disorder [13].

Mortality — It is not clear if mortality is increased in patients with the DSM-5 diagnosis of other specified
feeding or eating disorder, because the studies of mortality examined patients with DSM-IV-TR eating disorder
not otherwise specified, which overlaps only partially with other specified feeding or eating disorder (see
'Diagnosis' above):

● A meta-analysis of four studies (n >1800 patients with DSM-IV-TR eating disorder not otherwise specified;
mean follow-up 11 years) found that all cause mortality was two times greater among patients than the
general population [51].

● A retrospective study of 802 patients with an eating disorder not otherwise specified, who were followed for
a mean of 17 years through the United States National Death Index, found that all cause mortality was
nearly twice as high compared with the general population (standardized mortality ratio 1.8, 95% CI 1.3-
2.5), and that the rate of suicide was nearly four times greater (standardized mortality ratio 3.9, 95% CI 1.1-
10.0) [52].

UNSPECIFIED FEEDING OR EATING DISORDER — The diagnosis “unspecified feeding or eating disorder”
applies to patients with symptoms of a feeding and eating disorder that cause significant distress or impair
psychosocial functioning, but do not meet the full criteria for a specific eating disorder [1]. This diagnosis is
used when clinicians decide to not specify the reason that the presenting syndrome does not meet the full
criteria for an eating disorder, including situations in which there is insufficient information to make a more
specific diagnosis (eg, in the emergency department).

PATHOGENESIS — There is no consensus regarding the causes of eating disorders. A combination of genetic,
biologic, psychological, family, environmental, and social factors probably contribute to developing an eating
disorder. Factors associated with the development of eating disorders include:

● Genetics – Genetic factors are involved in the pathogenesis of eating disorders [53-55]. As an example,
concordance for either anorexia nervosa or bulimia nervosa is greater in monozygotic twins compared with
dizygotic twins [56].

● Family distress – Family characteristics associated with eating disorders may include high perceived
parental expectations for achievement and appearance, families who communicate poorly, have members
who are enmeshed with or estranged from each other, devalue the mother or the maternal role, have
marital tension, or have difficulties managing conflict [56].

● Sexual abuse [57].

● History of dieting [58].

● Preoccupation with a thin body and social pressure about weight [59].

● Athletic and artistic endeavors (eg, running, wrestling, or ballet) which emphasize leanness and sports in
which scoring is partly subjective (eg, skating or gymnastics). Young women with restrictive eating
disorders and amenorrhea have been referred to as having the "female athlete triad," which consists of an

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eating disorder, amenorrhea, and osteoporosis [60]. (See "Functional hypothalamic amenorrhea:
Pathophysiology and clinical manifestations".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, “The Basics” and
“Beyond the Basics.” The Basics patient education pieces are written in plain language, at the 5th to 6th grade
reading level, and they answer the four or five key questions a patient might have about a given condition.
These articles are best for patients who want a general overview and who prefer short, easy-to-read materials.
Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles
are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and
are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these
topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on
“patient info” and the keyword(s) of interest.)

● Basics topics (see "Patient education: Anorexia nervosa (The Basics)" and "Patient education: Bulimia
nervosa (The Basics)")

SUMMARY

● The SCOFF is a five-item, clinician administered measure that screens for some eating disorders. (See
'Screening' above.)

● The estimated lifetime prevalence of anorexia nervosa in women is 0.9 and in men 0.3 percent. The
diagnosis requires each of the criteria listed in the table (table 3). Complications include myocardial
atrophy, mitral valve prolapse, pericardial effusion, bradycardia, functional hypothalamic amenorrhea,
antenatal and postpartum problems, osteoporosis, gastroparesis, and constipation (table 4). (See 'Anorexia
nervosa' above.)

● The point prevalence of avoidant/restrictive food intake disorder in eating disorder programs is
approximately 5 to 15 percent. The diagnostic criteria are as follows: avoiding or restricting food intake,
which leads to a persistent failure to meet nutritional and/or energy needs; the eating disturbance is not
due to lack of available food or associated with a culturally sanctioned practice; the disturbance does not
occur solely in the course of anorexia nervosa or bulimia nervosa, and body weight and shape are not
distorted; and the disturbance is not due to a general medical condition or another mental disorder. (See
'Avoidant/restrictive food intake disorder' above.)

● The lifetime prevalence of binge eating disorder in adults is 1.9 percent, and the 12-month prevalence is
0.8 percent. Binge eating disorder is characterized by episodes of eating an amount of food in a discrete
period of time that is definitely larger than what most people would eat in a similar period of time under
similar circumstances. These episodes occur on average at least once a week for three months. Episodes
of binge eating are associated with a lack of control and with distress over the eating. (See 'Binge eating
disorder' above.)

● The lifetime prevalence of bulimia nervosa in women is 1.5 percent and in men is 0.5 percent. The
diagnostic criteria include binge eating (consuming a large amount of food in a discrete period of time) and
inappropriate compensatory behavior to prevent weight gain, both occurring on average at least once per
week for three months (table 5). Complications include dehydration, hypokalemia, menstrual irregularities,
Mallory-Weiss syndrome, and erosion of dental enamel. (See 'Bulimia nervosa' above.)

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