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 and adolescents: The refeeding syndrome".)
SCREENING — For patients with a normal or high body mass index, and no signs or symptoms of eating disorders, the evidence is insufficient to recommend for or against screening for eating disorders [5]. It is not known whether screening for eating disorders improves health outcomes [6], and the evidence is thus lacking to determine whether the benefits of screening outweigh the harms [5].
However, we suggest screening for eating disorders in primary care patients who are at increased risk of eating disorders, including [5,7,8]:
●Patients with a history of:
•Adversity during childhood
•Trauma
●Young adults
●Females
●Transgender individuals
●Athletes
●Patients who present with:
•Signs or symptoms of eating disorders (eg, rapid weight loss, preoccupation with eating and appearance, bradycardia, or amenorrhea)
•Anxiety disorders
•Depressive disorders
•Rigidity
•Perfectionism
Screening is important because eating disorders are often undetected and untreated [7].
Clinicians can screen for eating disorders by asking the patient or family whether they have any concerns about the patient’s weight, body shape, body image, or eating behaviors. In addition, relatively short and easy to interpret instruments that are suitable for screening in a primary care setting have been developed, which may help identify patients who need further evaluation [6,9,10].
If screening is implemented, we suggest the SCOFF questionnaire, which is the most commonly used instrument and is recommended by the United States Preventive Services Task Force [5,6]. The SCOFF consists of five clinician-administered questions [9,11]:
●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?
●Would you say that Food dominates your life?
Answering “yes” to two or more questions is generally regarded as a positive screen [6], and should prompt further assessment to establish or rule out a diagnosis.
The psychometric properties of the SCOFF are adequate. In a meta-analysis of 10 studies (n >3600), the sensitivity was 84 percent and specificity 80 percent [6]. However, a limitation of the SCOFF is that it was designed to screen only for anorexia nervosa and bulimia nervosa, and may fail to detect other eating disorders (eg, binge eating disorder) [7,8].
A reasonable alternative to the SCOFF is the clinician-administered Eating Disorder Screen for Primary Care (ESP) [8,10]:
●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)
A positive screen consists of two or more “abnormal” responses. In two studies (n = 627) of the ESP, the sensitivity ranged from 97 to 100 percent, and specificity from 40 to 71 percent [5,6].
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) [12].
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 [13]. 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 [14]. A study of Finnish twins found a higher lifetime prevalence of 2.2 percent [15]. These estimates are likely to be low due to the tendency of some individuals to conceal their illness [16]. In addition, diagnoses were based upon DSM-IV criteria, which are more restrictive than DSM-5 criteria [17]. In the Finnish study, diagnoses that were based upon criteria similar to DSM-5 found a lifetime prevalence of 4.2 percent [15].
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) [14]. In clinical settings, the ratio of females to males ranges from 10:1 [18] to 20:1 [19].
The median age of onset for anorexia nervosa in the general population is 18 years [14].
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) [20].
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 [21]. 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 [22]. 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 [23]. 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 [23]. 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 [24]. 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) [25]. 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) [23].
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
●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 [26]. 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 [27]. 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. (See "Anorexia nervosa in adults and adolescents: Medical complications and their management".)
All patients with anorexia nervosa should be evaluated for medical complications [28,29]. 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 [1,26].
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 [30].
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 [31-34].
●A retrospective study of youth (n >2200) age 8 to 18 years who presented to gastroenterology clinics found that avoidant/restrictive food intake disorder was present in 1 percent [35].
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 [32-34].
Onset of the disorder generally occurs in infancy or early childhood and may persist into adulthood [31].
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 [33]. In addition, bone mineral density is often diminished.
Comorbidity is common in avoidant/restrictive food intake disorder [33,36]. 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 [32].
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 [37]. 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 [26].
Binge eating disorder is more common in women than men [37]. In a nationally representative survey in the United States, the lifetime prevalence in females and males was 3.5 versus 2.0 percent [14]. 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 [37].
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 [14]. 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 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 [38].
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 [37]. 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 [37]. In the United States, impaired psychosocial functioning was found in 63 percent; severe impairment was reported by 19 percent [14].
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) [20].
When to suspect the disorder — Binge eating disorder can be difficult to detect because patients often feel ashamed [39]. 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
●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 [40]. Approximately 50 percent of individuals in the community with binge eating disorder are overweight or obese, similar to the community at large [14,41]. The remaining individuals with binge eating disorder are of normal weight, and they are less likely to present for treatment [42,43]. The effect of binge eating cessation on subsequent weight loss and/or medical comorbidities of obesity are not clearly established [44].
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 [14]:
●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 [45]:
●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) [46].
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) [47].
Observational studies indicate that the course of illness among patients with binge eating disorder is often chronic [14]:
●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) [48].
●A study of 68 inpatients with binge eating disorder found that after 12 years, 36 percent still met criteria for an eating disorder diagnosis [49].
Body dissatisfaction (undue influence of body weight or shape), impulsivity, and a history of sexual abuse are associated with a poor outcome [49,50].
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 [51].
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 [37]. 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 [16]. In addition, diagnoses were based upon DSM-IV criteria, which were more restrictive than DSM-5 criteria [1,26].
Bulimia nervosa is more common in women than men [37]. 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) [14]. In clinical settings, the ratio of females to males with a first time diagnosis is even higher (13 to 1) [18].
The median age of onset of bulimia nervosa is 18 years [37].
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 [37]. In the United States, impaired psychosocial functioning was found in 78 percent; severe impairment was reported by 44 percent [14].
Analyses of different birth (age) cohorts suggest that the risk of bulimia nervosa has increased over time [14,37].
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) [20].
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 [24]. 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).
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) [52]. 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 [53]. 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 4) [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 [28,29,54,55]. 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 [28,29]. 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.
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 5) 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 6) 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-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” [1,26]. 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 [17].
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 [56].
●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) [57].
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 [58-60]. As an example, concordance for either anorexia nervosa or bulimia nervosa is greater in monozygotic twins compared with dizygotic twins [61].
●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 [61].
●Sexual abuse [62].
●History of dieting [63].
●Preoccupation with a thin body and social pressure about weight [64].
●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 eating disorder, amenorrhea, and osteoporosis [65]. (See "Functional hypothalamic amenorrhea: Pathophysiology and clinical manifestations".)
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Eating disorders".)
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
●Screening – The SCOFF is a five-item, clinician administered measure that screens for some eating disorders. (See 'Screening' above.)
●Anorexia nervosa – 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 7). (See 'Anorexia nervosa' above.)
●Avoidant/restrictive food intake disorder – 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.)
●Binge eating disorder – 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.)
●Bulimia nervosa – 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 4). Complications include dehydration, hypokalemia, menstrual irregularities, Mallory-Weiss syndrome, and erosion of dental enamel. (See 'Bulimia nervosa' above.)
ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Sara F Forman, MD, who contributed to an earlier version of this topic review.
