CURRENT Diagnosis and Treatment Pediatrics, (Current Pediatric Diagnosis & Treatment) 22nd Edition

6. Eating Disorders

Eric J. Sigel, MD

Adolescents as well as younger children engage in disordered eating behavior at an alarming rate, and many develop partial or full-blown eating disorders (EDs). The spectrum of eating disorders includes anorexia nervosa (AN), bulimia nervosa (BN), binge-eating disorder (BED), avoidant/restrictive food intake disorder (ARFID). These disorders are best defined in a biopsychosocial context. New diagnostic categories and criteria for EDs will be available upon release of DSM-V in 2013.


There is strong evidence for a genetic basis for eating disorders. The incidence of AN is 7% in first-degree relatives of anorexic patients compared with 1%–2% in the general population. The concordance rate in monozygotic twins is 55% compared with 7% in dizygotic twins. Twin studies estimate the heritability of AN as 33%–84% and BN as 28%–83%. First-degree female relatives of males with AN have a 20-fold relative risk of AN. Most studies also find a higher incidence of eating disorders among first-degree relatives of bulimic patients. The family of neurotrophin proteins has been shown to be involved in the regulation of eating behavior and energy metabolism and has been intensively studied to assess their potential role in the genetic susceptibility to EDs. In a study of European families with EDs, Mercader and associates found a strong association between rs7180942, a neurotrophin protein encoded by the NTRK3 gene and the presence of EDs, with an undertransmission of the heterozygous genotype and an overtransmission of the homozygous genotype associated with increased phenotypic expression of EDs.

There is evidence of altered serotonergic and dopaminergic function and alterations in neuropeptides and gut peptides in AN and BN. It remains unclear whether abnormalities of neurotransmitters contribute to the development of EDs or are a consequence of the physiologic changes associated with the disorders. Patients with BN or BED appear to have a blunted serotonin response to eating and satiety. With a decreased satiety response, patients continue to eat, leading to a binge. Treatment with selective serotonin reuptake inhibitors (SSRIs) tends to equilibrate satiety regulation. An alteration in dopamine has also been recognized, although its significance is not clear. Adiponectin is elevated in AN, although it is unclear whether this is merely secondary to the malnourished state. Cholecystokinin is decreased in BN, perhaps contributing to the lack of postingestion satiety that perpetuates a binge. Ghrelin, a gut peptide, is elevated in patients with AN, and it does not decrease normally after a meal in these patients. Obestatin, a gut peptide that inhibits appetite, is elevated in AN as well.

Leptin physiology is deranged in patients with AN. Abnormalities of leptin may mediate energy changes that affect the hypothalamic-pituitary axis and play a role in perpetuating AN. Leptin levels increase excessively as individuals with AN regain weight. The abnormally high levels of leptin may contribute to the difficulty AN patients have when trying to regain weight, as higher leptin levels signal the body to decrease energy intake. Leptin also plays a significant role in some of the sequelae of AN, with low levels signaling the hypothalamus to inhibit reproductive hormone production.

Some experts have hypothesized that the intrauterine hormonal milieu may explain the differences in prevalence of ED between females and males. Procopio and Marriott have studied the risk of developing AN in the same sex and opposite sex twin pairs when one twin has AN. There was approximately an eightfold risk of developing AN in males with a female twin with AN compared to the risk of developing AN in males who had a male twin with AN. Though the study could not separate environmental influences, evidence from animal models suggests that increased exposure to estrogen and/or decreased exposure to androgens influence brain development and may play a role in determining which individuals are at risk for AN. One study determined that season of birth actually influenced the rate of developing AN, with an excess in those born from March to June (OR 1.15, p = .01) and a deficit in those born September to October (OR 0.8, p < .001), suggesting an additional environmental effect.

Traditional psychological theory has suggested many environmental factors that might promote the development of eating disorders. Enmeshment of mother with daughter to the point that the teenager cannot develop her own identity (a key developmental marker of adolescence) may be a predisposing factor. The teenager may cope by asserting control over food, as she senses her lack of control in the developmental realm. A second theory involves father-daughter distancing. As puberty progresses and a girl’s sexuality blossoms, a father may experience difficulty in dealing with his daughter as a sexual being and may respond by withdrawing emotionally and physically. The teenage girl may intuitively recognize this and subconsciously decrease her food intake in order to become prepubertal again. A third theory is related to puberty itself. Some teenagers may fear or dislike their changing bodies. By restricting food intake they lose weight, stop menstruating, and effectively reverse pubertal development.

Society has promoted the message that being thin or muscular is necessary for attractiveness and success. The ease of access to diet products—foods and diet pills—as well as Internet instructions (proanorexia sites) makes it simple for adolescents to embark on a quest for thinness or muscularity.

Genetic predisposition, environmental factors, and psychological factors likely combine to create a milieu that promotes development of eating disorders.

Bailer UF, Kaye WH: A review of neuropeptide and neuroendocrine dysregulation in anorexia and bulimia nervosa. Curr Drug Target CNS Neurol Disord 2003;2:53 [PMID: 12769812].

Bulik CM, Slof-Op’t Landt MC, van Furth EF, Sullivan PF: The genetics of anorexia nervosa. Annu Rev Nutr 2007a;27:263–275.

Campbell IC, Mill J, Uher R, Schmidt U: Eating disorders, gene-environment interaction, and epigentics. Neurosci Biobehav Rev 2011;35:784–793 [PMID: 20888360].

Disanto G et al: Season of birth and anorexia nervosa. Brit J Psych 2011;198(5):404–407 [PMID: 21415047].

Germain N et al: Ghrelin/obestatin ratio in two populations with low bodyweight: constitutional thinness and anorexia nervosa. Psychoneuroendocrinology 2009;34(3):413–419 [PMID: 18995969].

Mercader JM et al: Association of NTRK3 and its interaction with NGF suggest an altered cross-regulation of the neurotrophin signaling pathway in eating disorders. Hum Mol Genet 2008;17(9):1234–1244.

Procopio M, Marriott P: Intrauterine hormonal environment and risk of developing anorexia nervosa. Arch Gen Psych 2007; 64(12):1402 [PMID: 18056548].

Strober M et al: Males with anorexia nervosa: a controlled study of eating disorders in first-degree relatives. Int J Eat Disord 2001;29:263 [PMID: 11262504].

Warren MP: Endocrine manifestations of eating disorders. J Clinical Endocrin Metabolism 2011;96(2):333 [PMID: 21159848].


AN is the third most common chronic illness of adolescent girls in the United States. The incidence has been increasing steadily in the United States since the 1930s. Although ascertaining exact incidence is difficult, most studies show that 1%–2% of teenagers develop AN and 2%–4% develop BN. Adolescents outnumber adults 5 to 1, although the number of adults with eating disorders is rising. Incidence is also increasing among younger children. Prepubertal patients often have associated psychiatric diagnoses. Males comprise about 10% of patients with EDs, though this prevalence appears to be increasing as well, associated with the increased media emphasis on muscular, chiseled appearance as the male ideal.

Literature on preadolescents with EDs suggests that patients younger than 13 years are more likely to be male compared to teenagers and more likely to have EDNOS. Younger patients are less likely to engage in behaviors characteristic of BN. They present with more rapid weight loss and lower percentile body weight than adolescents.

Teenagers’ self-reported prevalence of ED behavior is much higher than the official incidence of AN or BN. In the most recent Youth Risk Behavior Survey of US teenagers (2011), 61% of females and 32% of males had attempted to lose weight during the preceding 30 days. Twelve percent had fasted for more than 24 hours to lose weight, and 5% had used medications to lose weight (5.9% of girls and 4.2% of boys). Self-induced vomiting or laxative use was reported by 6% of females and 2.5% of males. Forty-six percent of females and 30% of males reported at least one binge episode during their lifetime. Although the number of youth with full-spectrum eating disorders is low, it is alarming that so many youth experiment with unhealthy weight control habits. These behaviors may be precursors to the development of eating disorders, and clinicians should explore these practices with all adolescent patients.

Eaton DK et al: Centers for Disease Control and Prevention (CDC): Youth Risk Behavior Surveillance: United States 2011. MMWR Surveill Summ June 8 2012;61(SS-4) [PMID: 22673000].

Halmi KA: Anorexia nervosa: an increasing problem in children and adolescents. Dialogues Clin Neurosci 2009;11(1):100–103 [PMID: 19432392].

Peebles R et al: How do children with eating disorders differ from adolescents with eating disorders at initial evaluation? J Adolesc Health 2006;39:800 [PMID: 17116508].


Children involved in gymnastics, figure skating, and ballet—activities that emphasize thin bodies—are at higher risk for AN than are children in sports that do not emphasize body image. Adolescents who believe that being thin represents the ideal frame for a female, those who are dissatisfied with their bodies, and those with a history of dieting are at increased risk for eating disorders. Sudden changes in dietary habits, such as becoming vegetarian, may be a first sign of anorexia, especially if the change is abrupt and without good reason.

The typical bulimic patient tends to be impulsive and to engage in risk-taking behavior such as alcohol use, drug use, and sexual experimentation. Bulimic patients are often an appropriate weight for height or slightly overweight. They have average academic performance. Youth with diabetes have an increased risk of BN. In males, wrestling predisposes to BN, and homosexual orientation is associated with binge eating.

Shaw H et al: Body image and eating disturbances across ethnic groups: more similarities than differences. Psychol Addict Behav 2004;18:8 [PMID: 15008651].

Striegel-Moore RH, Bulik CM: Risk factors for eating disorders. Am Psychol 2007;62:181 [PMID: 17469897].


Table 6–1 lists the diagnostic criteria for AN, according to the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-V). The new DSM-V contains significant changes to the diagnosis of AN, including the elimination of amenorrhea as a criterion as well as specific weight criteria, which used to be 85% of expected weight based on 50th percentile body mass index (BMI). These changes will significantly increase the number of youth receiving AN as a diagnosis.

There are two forms of AN. In the restricting type, patients do not regularly engage in binge eating or purging. In the binge-purge type, AN is combined with binge eating or purging behavior, or both. Distinguishing between the two is important as they carry different implications for prognosis and treatment. Although patients may not demonstrate all features of AN, they may still exhibit the deleterious symptoms associated with AN.

image Clinical Findings

A. Symptoms and Signs

Clinicians should recognize the early symptoms and signs of AN because early intervention may prevent the full-blown syndrome from developing. Patients may show some of the behaviors and psychology of AN, such as reduction in dietary fat and intense concern with body image, even before weight loss or amenorrhea occurs.

Table 6–1. Diagnostic criteria for anorexia nervosa.

1. Restriction of energy intake relative to requirements, leading to a significantly low body weight in the context of age, sex, development trajectory, and physical health. Significantly low weight is defined as a weight that is less than minimally normal or, for children and adolescents, less than that minimally expected.

2. Intense fear of gaining weight or of becoming fat, or persistent behavior that interferes with weight gain, even though at a significantly low weight.

3. Disturbance in the way in which one’s body weight or shape is experienced, undue influence of body weight or shape on self-evaluation, or persistent lack of recognition of the seriousness of the current low body weight.

Specify whether:

Restricting type: During the last 3 months, the individual has not engaged in recurrent episodes of binge eating or purging behavior (ie, self-induced vomiting or the misuse of laxatives, diuretics, or enemas). This subtype describes presentations in which weight loss is accomplished primarily through dieting, fasting, and/or excessive exercise. Binge-eating/purging type: During the last 3 months, the individual has engaged in recurrent episodes of binge eating or purging behavior (ie, self-induced vomiting or the misuse of laxatives, diuretics, or enemas).

Reprinted, with permission, from American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 5th ed, Arlington, VA: American Psychiatric Association; 2013.

Making the diagnosis of AN can be challenging because adolescents may try to conceal their illness. Assessing the patient’s body image is essential to determining the diagnosis. Table 6–2 lists screening questions that help tease out a teenager’s perceptions of body image. Other diagnostic screening tools (eg, Eating Disorders Inventory) assess a range of eating and dieting behaviors. Parental observations are critical in determining whether a patient has expressed dissatisfaction over body habitus and which weight loss techniques the child has used. If the teenager is unwilling to share his or her concerns about body image, the clinician may find clues to the diagnosis by carefully considering other presenting symptoms or signs. Weight loss from a baseline of normal body weight is an obvious red flag for the presence of an eating disorder. Additionally, AN should be considered in any girl with secondary amenorrhea who has lost weight.

Table 6–2. Screening questions to help diagnose anorexia and bulimia nervosa.

How do you feel about your body?

Are there parts of your body you might change?

When you look at yourself in the mirror, do you see yourself as overweight, underweight, or satisfactory?

If overweight, how much do you want to weigh?

If your weight is satisfactory, has there been a time when you were worried about being overweight?

If overweight (underweight), what would you change?

Have you ever been on a diet?

What have you done to help yourself lose weight?

Do you count calories or fat grams?

Do you keep your intake to a certain number of calories?

Have you ever used nutritional supplements, diet pills, or laxatives to help you lose weight?

Have you ever made yourself vomit to get rid of food or lose weight?

Physical symptoms and signs are usually secondary to weight loss and proportional to the degree of malnutrition. The body effectively goes into hibernation, becoming functionally hypothyroid (euthyroid sick) to save energy. Body temperature decreases, and patients report being cold. Bradycardia develops, especially in the supine position. Dizziness, light-headedness, and syncope may occur as a result of orthostasis and hypotension secondary to impaired cardiac function. Left ventricular mass is decreased (as is the mass of all striated muscle), stroke volume is compromised, and peripheral resistance is increased, contributing to left ventricular systolic dysfunction. Patients can develop prolonged QTc syndrome and increased QT dispersion (irregular QT intervals), putting them at risk for cardiac arrhythmias. Peripheral circulation is reduced. Hands and feet may be blue and cool. Hair thins, nails become brittle, and skin becomes dry. Lanugo develops as a primitive response to starvation. The gastrointestinal (GI) tract may be affected; inability to take in normal quantities of food, early satiety, and gastroesophageal reflux can develop as the body adapts to reduced intake. The normal gastrocolic reflex may be lost due to lack of stimulation by food, causing bloating and constipation. Delayed gastric emptying may be present in restricting type and purging type AN. Nutritional rehabilitation improves gastric emptying and dyspeptic symptoms in AN restricting type, but not in those who vomit. Neurologically, patients may experience decreased cognition, inability to concentrate, increased irritability, and depression, which may be related to structural brain changes and decreased cerebral blood flow.

Nutritional assessment is vital. Often, patients eliminate fat from their diets and may eat as few as 100–200 kcal/d. A gown-only weight after urination is the most accurate way to assess weight. Patients tend to wear bulky clothes and may hide weights in their pockets or drink excessive fluid (water-loading) to trick the practitioner. Assessing BMI is the standard approach to interpreting the degree of malnutrition. BMI below the 25th percentile indicates risk for malnutrition, and below 5th percentile indicates significant malnutrition. Median body weight (MBW) should be calculated as it serves both as the denominator in determining what percent weight an individual is, as well as to provide a general goal weight during recovery. MBW for height is calculated by using the 50th percentile of BMI for age.

A combination of malnutrition and stress causes hypothalamic hypogonadism. The hypothalamic-pituitary-gonadal axis shuts down as the body struggles to survive, directing finite energy resources to vital functions. This may be mediated by the effect of low serum leptin levels on the hypothalamic-pituitary axis. Pubertal development and skeletal growth may be interrupted, and adolescents may experience decreased libido.

Amenorrhea will continue to be an important clinical sign that the body is malnourished. Amenorrhea occurs for two reasons. The hypothalamic-pituitary-ovarian axis shuts down under stress, causing hypothalamic amenorrhea. In addition, adipose tissue is needed to convert estrogen to its activated form. When weight loss is significant, there is not enough substrate to activate estrogen. Resumption of menses occurs only when both body weight and body fat increase. Approximately, 73% of postmenarchal girls resume menstruating if they reach 90% of MBW. An adolescent female needs about 17% body fat to restart menses and 22% body fat to initiate menses if she has primary amenorrhea. Some evidence suggests that target weight gain for return of menses is approximately 1 kg higher than the weight at which menses ceased.

B. Laboratory Findings

All organ systems may suffer some degree of damage in the anorexic patient, related both to severity and duration of illness (Table 6–3). Initial screening should include complete blood count with differential; serum levels of electrolytes, blood urea nitrogen, creatinine, phosphorus, calcium, magnesium, and thyroid-stimulating hormone; liver function tests; and urinalysis. Increase in lipids, likely due to abnormal liver function, is seen in 18% of those with AN, with subsequent return to normal once weight is restored. An electrocardiogram (ECG) should be performed, because significant electrocardiographic abnormalities may be present, most importantly prolonged QTc syndrome. Bone densitometry should be done if illness persists for 6 months, as patients begin to accumulate risk for osteoporosis.

Table 6–3. Laboratory findings: anorexia nervosa.

Increased blood urea nitrogen and creatinine secondary to renal insufficiency

Decreased white blood cells, platelets, and less commonly red blood cells and hematocrit secondary to bone marrow suppression or fat atrophy of the bone marrow

Increased AST and ALT secondary to malnutrition

Increased cholesterol, thought to be related to altered fatty acid metabolism

Decreased alkaline phosphatase secondary to zinc deficiency

Low- to low-normal thyroid-stimulating hormone and thyroxine

Decreased follicle-stimulating hormone, luteinizing hormone, estradiol, and testosterone secondary to shutdown of hypothalamic pituitary-gonadal axis

Abnormal electrolytes related to hydration status

Decreased phosphorus

Decreased insulin-like growth factor

Increased cortisol

Decreased urine specific gravity in cases of intentional water intoxication

ALT, alanine aminotransferase; AST, aspartate aminotransferase.

image Differential Diagnosis

If the diagnosis is unclear (ie, the patient has lost a significant amount of weight but does not have typical body image distortion or fat phobia), the clinician must consider the differential diagnosis for weight loss in adolescents. This includes inflammatory bowel disease, diabetes, hyperthyroidism, malignancy, depression, and chronic infectious disease such as human immunodeficiency virus (HIV). Less common diagnoses include adrenal insufficiency and malabsorption syndromes such as celiac disease. The history and physical examination should direct specific laboratory and radiologic evaluation.

image Complications (Table 6–4)

A. Short-Term Complications

1. Early satiety— Patients may have difficulty tolerating even modest quantities of food when intake increases; this usually resolves after the patients adjust to larger meals. Gastric emptying is poor. Pancreatic and biliary secretion is diminished.

2. Superior mesenteric artery syndrome— As patients become malnourished, the fat pad between the superior mesenteric artery and the duodenum shrinks and compression of the transverse duodenum may cause obstruction and vomiting, especially with solid foods. The upper GI series shows to-and-fro movement of barium in the descending and transverse duodenum proximal to the obstruction. Treatment involves a liquid diet or nasoduodenal feedings until restoration of the fat pad has occurred, coincident with weight gain.

Table 6–4. Complications of anorexia and bulimia nervosa, by mechanism.


3. Constipation— Patients may be very constipated. Two mechanisms contribute—loss of the gastrocolic reflex and loss of colonic muscle tone. Typically stool softeners are not effective because the colon has decreased peristaltic amplitude. Agents that induce peristalsis, such as bisacodyl, as well as osmotic agents, such as polyethylene glycol-electrolyte solution (MiraLax), are helpful. Constipation can persist for up to 6–8 weeks after refeeding. Occasionally enemas are required.

4. Refeeding syndrome— This syndrome is described in the Treatment section.

5. Pericardial effusion— The degree of malnutrition correlates with increasing prevalence of pericardial effusion. One study demonstrated that 22% of those with AN had silent pericardial effusions, with 88% of effusions resolving after weight restoration.

B. Long-Term Complications

1. Osteoporosis—Approximately 50% of females with AN have reduced bone mass at one or more sites. The lumbar spine has the most rapid turnover and is the area likely to be affected first. Teenagers are particularly at risk as they accrue 40% of their bone mineral during adolescence. Low body weight is most predictive of bone loss. The causes of osteopenia and osteoporosis are multiple. Estrogen and testosterone are essential to potentiate bone development. Bone minerals begin to resorb without estrogen. Elevated cortisol levels and decreased insulin-like growth factor-1 also contribute to bone resorption. Amenorrhea is highly correlated with osteoporosis. Studies show that as few as 6 months of amenorrhea is associated with osteopenia or osteoporosis. Males may also develop osteoporosis due to decreased testosterone and elevated cortisol.

Until recently, the only proven treatment for bone loss in girls with AN has been regaining sufficient weight and body fat to restart the menstrual cycle. Studies did not support use of hormone replacement therapy delivered orally to improve bone recovery; however, a recent randomized controlled trial demonstrated that physiologic doses of estrogen, delivered transdermally, over 18 months did improve bone density. Clinicians may consider transdermal estrogen treatment if patients are recalcitrant to intervention and do not restore weight in a timely manner. Bisphosphonates, used to treat postmenopausal osteoporosis, are currently being studied in adolescents. Two small randomized controlled trials have shown small positive effects on bone density with alendronate and risedronate, although clinical effectiveness has not yet been determined. Newer treatments with possible effectiveness, including recombinant insulin-like growth factor-1 injection and dehydroepiandrosterone, are under investigation.

2. Brain changes—As malnutrition becomes pronounced, brain tissue—both white and gray matter—is lost, with a compensatory increase in cerebrospinal fluid in the sulci and ventricles. Follow-up studies of weight-recovered anorexic patients show a persistent loss of gray matter, although white matter returns to normal. Functionally, there does not seem to be a direct relationship between cognition and brain tissue loss, although studies have shown a decrease in cognitive ability and decreased cerebral blood flow in very malnourished patients. Making patients and family aware that brain tissue can be lost may improve their perception of the seriousness of this disorder. There is a burgeoning literature on functional brain imaging. Neurochemical changes, including changes related to serotonin and dopamine systems, occur as a result of starvation and lead to altered metabolism in frontal, cingulate, temporal, and parietal regions (for a detailed review, see Kaye et al, 2009).

3. Effects on future children—This area has just recently been studied. Findings suggest that there may be feeding issues for infants who are born to mothers who have a history of either AN or BN. Infants born to mothers with a history of AN have more feeding difficulties at 0 and 6 months and tend to be lower weight (30th percentile on average). Infants born to mothers with current or past BN are more likely to be overweight and have faster growth rates than controls. Pediatricians should ascertain an eating disorder history from mothers of patients who are having feeding issues.

American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 5th ed. Arlington, VA: American Psychiatric Association; 2013.

Asiero D, Frishman WH: Cardiovascular complications of eating disorders. Cardiol Rev 2006;14:227 [PMID: 16924163].

Golden NH et al: Treatment goal weight in adolescents with anorexia nervosa: use of BMI percentiles. Int J Eat Disord 2008;41(4):301–306.

Kastner S, Salbach-Andrae H, Renneberg B, Pfeiffer E, Lehmkuhl U, Schmitz L: Echocardiographic findings in adolescents with anorexia nervosa at beginning of treatment and after weight recovery. Eur Child Adolesc Psychiatry Jan 2012 21(1):15–21 [PMID: 22086424].

Kaye WH, Fudge JL, Paulus M: New insights into symptoms and neurocircuit function of anorexia nervosa. Nat Rev Neurosci 2009;10(8):573–584 [PMID: 19603056].

Micali N, Simonoff E, Treasure J: Infant feeding and weight in the first year of life in babies of women with eating disorders. J Pediatr 2009;154(1):55–60.e1 [PMID: 18783793].

Misra M et al: Physiologic estrogen replacement increases bone density in adolescent girls with anorexia nervosa. J Bone Miner Res Oct 2011;26(10):2430–2438 [PMID: 21698665].

C. Mortality

Patients with eating disorders are at a higher risk of death than the general population and those with AN have the highest risk of dying among those with eating disorders. Meta-analysis estimates the standardized mortality ratio associated with AN to be 5.9. Death in anorexic patients is due to suicide, abnormal electrolytes, and cardiac arrhythmias.

image Treatment

A. General Approach

Factors that determine treatment interventions are severity of illness, duration of illness, specific manifestations of disease, previous treatment approaches and outcomes, program availability, financial resources, and insurance coverage. Treatment options include outpatient management, day treatment hospitalization, inpatient medical or psychiatric hospitalization, and residential treatment. The key to determining level of intervention is the degree of malnutrition, the rapidity of weight loss, the degree of medical compromise, and the presence of life-threatening electrolyte abnormalities. No absolute criteria determine level of intervention. The practitioner must examine the degree of medical compromise and consider immediate risks and the potential for an individual to reverse the situation on his or her own. Day treatment programs are a good intervention for patients who do not yet need inpatient care but who are not improving with outpatient management. Treatment is costly. Many patients do not have insurance benefits that adequately cover the cost of treatment, leaving parents and practitioners with profound dilemmas as to how to best provide treatment in the face of financial constraints. Legally, however, eating disorders are now recognized as a parity mental health diagnosis similar to the other biologically based mental health illnesses in many states, which has increased the ease of obtaining insurance coverage.

A multidisciplinary approach is most effective and should include medical monitoring, nutrition therapy, and individual and family psychotherapy by experienced practitioners. Family therapy is an important means of helping families understand the development of the disease and addressing issues that may be barriers to recovery. Both types of psychotherapy are encouraged in most treatment programs, and recovery without psychotherapy is unusual. The average length of psychotherapy is roughly 6–9 months, although some individuals continue therapy for extended periods. Adjunctive modalities include art and horticulture therapy, therapeutic recreation, and massage therapy.

Manualized family therapy, developed in Britain by Maudsley and adapted by Lock and LeGrange, has shifted the therapeutic approach to adolescents with AN. Traditional therapy allowed the adolescent to control his or her eating and the parents to remain uninvolved with the food portion of recovery. The manualized approach gives power and control back to parents. Treatment is prescribed for 20 weekly sessions. The first 10 weeks are devoted to empowering parents, putting them in control of their child’s nutrition and exercise. Parents are educated about the dangers of malnutrition and are instructed to supervise each meal. The next phase, sessions 11–16, returns control over eating to the adolescent once he or she accepts the demands of the parents. The last phase of treatment, sessions 17–20, occurs when the patient is maintaining a healthy weight and shifts the focus away from the eating disorder, examining instead the impact that the eating disorder has had on establishing a healthy adolescent identity. This approach is reported to result in good or intermediate outcomes in 90% of treated adolescents.

Careful instruction in nutrition helps the teenager and family dispel misconceptions about nutrition, identify realistic nutritional goals, and normalize eating. Initially, nutrition education may be the most important intervention as the teenager slowly works through his or her fears of fat-containing foods and weight gain. The teenager begins to trust the nutrition therapist and restore body weight, eventually eating in a well-balanced, healthy manner.

B. Inpatient Treatment

Table 6–5 lists the criteria for hospital admission generally used in the medical community. It is usually quite difficult for a patient who is losing weight rapidly (> 2 lb/wk) to reverse the weight loss because the body is in a catabolic state.

Goals of hospitalization include arresting weight loss and stabilizing hemodynamics. Nutrition is the most vital inpatient medicine. Clinicians can safely begin with a meal plan containing approximately 250 kcal more than the patient has been routinely eating, which can usually be accomplished orally. Recent studies suggest that meal plans can begin with as high as 1750 kcal regardless of baseline intake. Meal plans should be well balanced with appropriate proportions of carbohydrate, protein, and fat. Oral meals are usually tolerated, although it is important to be supervised by medical staff. If the patient resists, nasogastric or intravenous alimentation can be used. Aside from caloric needs, the clinician needs to consider the patient’s hydration and include the appropriate amount of fluid with the meal plan. Dehydration should be corrected slowly. The oral route is usually adequate. Aggressive intravenous fluid administration should be avoided because left ventricular mass is compromised and a rapid increase in volume may not be tolerated. Regulating fluid intake is important, because water intoxication can contribute to abnormal electrolytes and falsified weights.

Table 6–5. Criteria for inpatient treatment of anorexia nervosa.

Body weight < 75% of ideal body weight

Supine heart rate < 45 beats/min

Symptomatic hypotension or syncope

Hypokalemia: K+ < 2.5 mEq/L

Rapid weight loss that cannot be interrupted as outpatient

Failure of outpatient management

Acute food refusal

During the initial introduction of food, the clinician should monitor the patient for refeeding syndrome, a phenomenon that occurs if caloric intake is increased too rapidly. Signs of refeeding syndrome are decreased serum phosphorus (as the body resumes synthesis of adenosine triphosphate), decreased serum potassium (as increased insulin causes K+ to shift from extracellular fluid into K+-depleted cells), and, rarely, edema related to fluid shifts or congestive heart failure.

Although specific guidelines do not exist, many practitioners begin phosphorus supplementation if patients are severely malnourished (< 70% MBW) or their intake has been consistently less than 500 kcal/d.

Caloric intake can be increased 250 kcal/d as long as refeeding syndrome does not occur. Weight goals vary depending on programmatic approach. Typically, intake is adjusted to reach a goal of 0.1–0.25 kg/d weight gain.

Overnight monitoring for bradycardia is helpful in assessing degree of metabolic compromise. Usually the more rapid and severe the weight loss, the worse the bradycardia. Improving bradycardia correlates with weight recovery. Orthostatic hypotension is most severe around hospital day 4, improving steadily and correcting by the third week of nutritional rehabilitation. An ECG should be obtained because the patient is at risk for prolonged QTc syndrome and junctional arrhythmias related to the severity of bradycardia.

It usually takes 2–3 weeks to reach the initial goals of hospitalization—steady weight gain, toleration of oral diet without signs of refeeding syndrome, corrected bradycardia (heart rate > 45 beats/min for three consecutive nights), and correction of orthostasis. Specific weight criteria are used by many programs when considering discharge. This depends partly on admission weight. Ideally a patient gains at least 5% of his or her MBW. Some programs set discharge at 80%, 85%, or 90% MBW. Patient outcomes are improved with discharge at a higher body weight. Some evidence exists that patients do better if discharged at 95% MBW. In many practitioners’ experience, relapse rates are high if patients are discharged at less than 75% MBW. Frequently, insurance companies do not pay for hospital stays beyond strict medical stabilization (normal vital signs and normal electrolytes).

C. Pharmacotherapy

Practitioners frequently use psychotropic medications for treatment of AN, despite the lack of evidence supporting efficacy. Several open label trials suggest that atypical antipsychotics (risperidone, olanzapine, quetiapine) may be helpful. One review found that olanzapine (2.5–15 mg/d) was associated with improved body weight, decreased delusional thinking, improvement in body image, and decreased agitation and premeal anxiety. However, a recent randomized controlled trial did not show any difference in outcomes between risperidone and placebo.

SSRIs repeatedly have been shown to not be helpful in the initial therapy of AN. However, once the patient has achieved approximately 85% MBW, SSRIs (fluoxetine, citalopram, or sertraline) may help prevent relapse.

Zinc deficiency is common in AN, and several studies support its use as a supplement during the initial phases of treatment. Because zinc deficiency adversely affects neurotransmitters, administering zinc helps restore neurotransmitter action to baseline. Additionally zinc may restore appetite and improve depressive mood. Zinc should be administered for approximately 2 months from the beginning of therapy, with at least 14 mg of elemental zinc daily.

Because of global nutritional deficits, a multivitamin with iron is also recommended daily. Symptomatic treatment for constipation and reflux should be used appropriately until symptoms resolve.

D. Outpatient Treatment

Not all patients with AN require inpatient treatment, especially if parents and clinicians recognize the warning signs early. These patients can receive treatment as outpatients, employing the same multidisciplinary team approach. Manualized family-based treatment is ideal for the outpatient setting if a trained therapist is available. Appropriate nutrition counseling is vital in guiding a patient and family through the initial stages of recovery. As the nutrition therapist is working at increasing the patient’s caloric intake, a practitioner needs to monitor the patient’s weight and vital signs. Often, activity level needs to be decreased to help reverse the catabolic state. A reasonable weight gain goal may be 0.2–0.5 kg/wk. If weight loss persists, careful monitoring of vital signs, including supine heart rate, is important in determining whether an increased level of care is needed. Concomitantly, the patient should be referred to a psychotherapist and, if indicated, assessed by a psychiatrist.

Arcelus J et al: Mortality rates in patients with anorexia nervosa and other eating disorders. A meta-analysis of 36 studies. Arch Gen Psychiatry 2011;68(7):724–731 [PMID: 21727255].

Birmingham CL, Gritzner S: How does zinc supplementation benefit anorexia nervosa? Eat Weight Disord 2006;11:e109 [PMID: 17272939].

Claudino AM et al: Antidepressants for anorexia nervosa. Cochrane Database Syst Rev 2006;(1):CD004365 [PMID: 16437485].

Dunican KC, DelDotto D: The role of olanzapine in the treatment of anorexia nervosa. Ann Pharmacother 2007;41:111 [PMID: 17190846].

Hagman J et al: A double-blind, placebo-controlled study of risperidone for the treatment of anorexia nervosa. J Am Acad Child Adolesc Psychiatry 2011;50(9):915–924 [PMID: 21871373].

LeGrange D et al: Manualized family-based treatment for anorexia nervosa: a case series. J Am Acad Child Adolesc Psychiatry 2005;44:41 [PMID: 15608542].

Swenne I: Weight requirements for return of menstruations in teenage girls with eating disorders, weight loss, and secondary amenorrhea. Acta Paediatr 2004;93:1449 [PMID: 08035253].

Table 6–6. Diagnostic criteria for bulimia nervosa.

1. Recurrent episodes of binge eating. An episode of binge eating is characterized by both of the following:

a. Eating, in a discrete period of time (eg, within any 2-h period), an amount of food that is definitely larger than most people would eat during a similar period of time and under similar circumstances.

b. A sense of lack of control over eating during the episode (eg, a feeling that one cannot stop eating or control what or how much one is eating).

2. Recurrent inappropriate compensatory behaviors in order to prevent weight gain, such as self-induced vomiting; misuse of laxatives, diuretics, or other medications, fasting; or excessive exercise.

3. The binge eating and inappropriate compensatory behaviors both occur, on average, at least once a week for 3 mo.

4. Self-evaluation is unduly influenced by body shape and weight.

5. The disturbance does not occur exclusively during episodes of anorexia nervosa.

Specify if:

In partial remission: After full criteria for bulimia nervosa were previously met, some, but not all, of the criteria have been met for a sustained period of time.

In full remission: After full criteria for bulimia nervosa were previously met, none of the criteria have been met for a sustained period of time.

Specify current severity:

The minimum level of severity is based on the frequency of inappropriate compensatory behaviors (see as follows). The level of severity may increase to reflect other symptoms and the degree of functional disability.

Mild: An average of 1–3 episodes of inappropriate compensatory behaviors per week.

Moderate: An average of 4–7 episodes of inappropriate compensatory behaviors per week.

Severe: An average of 8–13 episodes of inappropriate compensatory behaviors per week.

Extreme: An average of ≥ 14 episodes of inappropriate compensatory behaviors per week.

Reprinted, with permission, from American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 5th ed. Arlington, VA: American Psychiatric Association; 2013.


Table 6–6 lists the diagnostic criteria for BN. Binge eating is either eating excessive amounts of food during a normal mealtime or having a meal that lasts longer than usual. Bulimic individuals feel out of control while eating, unable or unwilling to recognize satiety signals. Any type of food may be eaten in a binge, although typically it includes carbohydrates or junk food. Extreme guilt is often associated with the episode. At some point, either prior to or during a binge, bulimic individuals often decide to purge as a means of preventing weight gain. The most common ways to purge are self-induced vomiting, exercise, and laxative use. Some individuals will vomit multiple times during a purge episode, after using large amounts of water to cleanse their system. This can induce significant electrolyte abnormalities such as hyponatremia and hypokalemia, which may put the patient at acute risk for arrhythmia or seizure. Other methods of purging include diuretics, diet pills, cathartics, and nutritional supplements that promote weight loss, such as Metabolife or Sensa.

Diagnosing BN can be difficult unless the teenager is forthcoming or parents or caregivers can supply direct observations. Bulimic patients are usually average or slightly above average in body weight and have no physical abnormalities. Screening all teenagers for body image concerns is crucial. If the teenager expresses concern about being overweight, the clinician needs to screen the patient about dieting methods. Asking whether patients have binged, feel out of control while eating, or whether they cannot stop eating can clarify the diagnosis. Parents may report that significant amounts of food are missing or disappearing more quickly than normal. If the physician is suspicious, direct questioning about all the ways to purge should follow. Indicating first that the behavior is not unusual can make questioning less threatening and more likely to elicit a truthful response. For example, the clinician might say, “Some teenagers who try to lose weight make themselves vomit after eating. Have you ever considered or done that yourself?” (See Table 6–2 for additional screening questions.)

image Clinical Findings

A. Symptoms and Signs

Symptoms are related to the mechanism of purging. GI problems are most prominent. Abdominal pain is common. Gastroesophageal reflux occurs as the lower esophageal sphincter becomes compromised due to repetitive vomiting. Frequent vomiting may also cause esophagitis or gastritis, as the mucosa is irritated by acid exposure. Early satiety, involuntary vomiting, and complaints that food is “coming up” on its own are frequent. Hematemesis and esophageal rupture have been reported. Patients may report diarrhea or constipation, especially if laxatives have been used. Sialadenitis (parotid pain and enlargement) may be caused by frequent vomiting. Erosion of dental enamel results from increased oral acid exposure during vomiting. Because comorbid depression is common in BN, patients may report difficulty sleeping, decreased energy, decreased motivation, and headaches. Light-headedness or syncope may develop secondary to dehydration.

It is important to note that most purging methods are ineffective. When patients binge, they may consume thousands of calories. Digestion begins rapidly. Although the patient may be able to vomit some of the food, much is actually digested and absorbed. Laxatives work in the large intestine, leading to fluid and electrolyte loss, but consumed calories are still absorbed from the small intestine. Use of diuretics may result in decreased fluid weight and electrolyte imbalance.

On physical examination, bulimic patients may be dehydrated and have orthostatic hypotension. Sialadenitis, tooth enamel loss, dental caries, and abdominal tenderness are the most common findings. Abrasion of the proximal interphalangeal joints may occur secondary to scraping the fingers against teeth while inducing vomiting. Rarely, a heart murmur is heard which may be due to mitral valve prolapse. Irreversible cardiomyopathy can develop secondary to ipecac use. Tachycardia and hypertension may occur secondary to caffeine and diet pill use.

B. Laboratory Findings

Electrolyte disturbances are common in bulimic patients. The method of purging results in specific abnormalities. Vomiting causes metabolic alkalosis, hypokalemia, and hypochloremia. If laxatives are used, a metabolic acidosis develops with hypokalemia and hypochloremia. Diuretic use may lead to hypokalemia, hyponatremia, hypocalcemia, and metabolic alkalosis. Amylase may be increased secondary to chronic parotid stimulation.

image Complications

A. Short-Term Complications

Complications in normal-weight bulimic patients are related to the mechanisms of purging, and many of these complications are listed under Symptoms and Signs. If the bulimic patient is significantly malnourished, complications may be the same as those encountered in the anorexic patient. Other complications of bulimia include esophageal rupture, acute or chronic esophagitis, and, rarely, Barrett esophagitis. Chronic vomiting can lead to metabolic alkalosis, and laxative abuse may cause metabolic acidosis. Patients may develop aspiration pneumonia from vomiting. Diet pill use can cause insomnia, hypertension, tachycardia, palpitations, seizures, and sudden death.

Patients who stop taking laxatives can have severe constipation. Treating constipation can be difficult psychologically, because the practitioner may need to prescribe agents similar to the drugs of abuse used during the eating disorder.

B. Mortality

The mortality rate in bulimic patients is similar to that in anorexic patients. Death usually results from suicide or electrolyte derangements.

image Treatment

Treatment of BN depends on the frequency of bingeing and purging and the severity of biochemical and psychiatric derangement. If K+ is less than 3.0 mEq/L, inpatient medical admission is warranted. Typically extracellular K+ is spared at the expense of intracellular K+, so a patient may become hypokalemic several days after the serum K+ concentration appears to be corrected. Usually cessation of purging is sufficient to correct K+ concentration and is the recommended intervention for K+ above 3.0 mEq/L. If K+ is 2.5–2.9 mEq/L, oral supplementation is suggested. If K+ is less than 2.5 mEq/L, intravenous therapy is recommended. Supplements can be stopped once K+ levels are more than 3.5 mEq/L. Total body K+ can be assumed to be normal when serum K+ corrects and remains normal 2 days after supplements are stopped. Continued hospitalization depends on the patient’s psychological status.

Some bulimic patients who abuse laxatives may become chronically dehydrated. The renin-angiotensin-aldosterone axis is activated, and the antidiuretic hormone level may be elevated to compensate. These systems do not shut down automatically when laxatives are stopped, and fluid retention of up to 10 kg/wk may result. This puts patients at risk for congestive heart failure and can scare them as their weight increases dramatically. Diuresis often occurs after 7–10 days. Parents and patients should be advised of this possible complication of initial therapy to help maintain their confidence in the care plan.

Hospitalization of bulimic patients is also recommended if there has been failure of outpatient management. The binge-purge cycle is addictive and can be difficult for patients to interrupt on their own. Hospitalization can offer a forced break from the cycle, allowing patients to normalize their eating, interrupt the addictive behavior, and regain the ability to recognize satiety signals.

Outpatient management can be pursued if patients are medically stable. Cognitive-behavioral therapy is crucial to help bulimic patients understand their disease and to offer suggestions for decreasing bingeing and purging. Nutrition therapy offers patients ways to regulate eating patterns so that they can avoid the need to binge. Medical monitoring should be done to check electrolytes periodically, depending on the purging method used.

SSRIs are generally helpful in treating the binge-purge cycle. Fluoxetine has been studied most extensively; a dose of 60 mg/d is most efficacious in teenagers. Other SSRIs appear to be effective as well and may be used in patients experiencing side effects of fluoxetine. Treatment for gastroesophageal reflux and gastritis should be used when appropriate. The pain and swelling of enlarged parotid glands can be helped by sucking on tart candy and by the application of heat.

American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 5th ed. Arlington, VA: American Psychiatric Association; 2013.

Bacaltchuk J et al: Antidepressant versus placebo for the treatment of bulimia nervosa: a systematic review. Aust N Z J Psychiatry 2000;34:310 [PMID: 10789536].

Benini LT et al: Gastric emptying in patients with restricting and binge/purging subtypes of anorexia nervosa. Am J Gastroenterol 2004;99:1448 [PMID: 15307858].

Mehler PS: Medical complications of bulimia nervosa and their treatments. Int J Eat Disord (0276-3478) 2011, Mar;44(2):95 [PMID: 21312201].

Panagiotopoulos C et al: Electrocardiographic findings in adolescents with eating disorders. Pediatrics 2000;105:1100 [PMID: 10790469].

Steinhausen HC, Weber S: The outcome of bulimia nervosa: Findings from one-quarter century of research. Am J Psychiatry 2009;166:1331–1341 [PMID: 19884225].

Sysko R, Sha N, Wang W: Early response to antidepressant treatment in bulimia nervosa. Psychol Med 2010;40(6):999 [PMID: 20441691].


Binge-eating disorder (BED) is now an official diagnosis described in the DSM-V. Studies show that most adults who have BED (a prevalence of 2%–4%) develop symptoms during adolescence. Table 6–7 lists the diagnostic criteria.

image Clinical Findings

A. Symptoms and Signs

BED most often occurs in overweight or obese individuals. Eighteen percent of such patients report binging at least once in the past year. Patients with BED have an increased incidence of depression and substance abuse. The possibility of BED should be raised for any significantly overweight patient. Specific questionnaires are available for evaluating patients suspected of BED.

B. Laboratory Findings

The clinician should assess causes and complications of obesity, and laboratory evaluation should include thyroid function tests and measurement of cholesterol and triglyceride levels.

Table 6–7. Diagnostic criteria for binge-eating disorder.

1. Recurrent episodes of binge eating. An episode of binge eating is characterized by both of the following:

a. Eating, in a discrete period of time (eg, within any 2-hour period), an amount of food that is definitely larger than what most people would eat in a similar period of time under similar circumstances.

b. A sense of lack of control over eating during the episode (eg, a feeling that one cannot stop eating or control what or how much one is eating).

2. The binge-eating episodes are associated with three (or more) of the following:

a. Eating much more rapidly than normal.

b. Eating until feeling uncomfortably full.

c. Eating large amounts of food when not feeling physically hungry.

d. Eating alone because of feeling embarrassed by how much one is eating.

e. Feeling disgusted with oneself, depressed, or very guilty afterward.

3. Marked distress regarding binge eating is present.

4. The binge eating occurs, on average, at least once a week for 3 months.

5. The binge eating is not associated with the recurrent use of inappropriate compensatory behavior as in bulimia nervosa and does not occur exclusively during the course of bulimia nervosa and anorexia nervosa.

Specify if:

In partial remission: After full criteria for binge-eating disorder were previously met, binge eating occurs at an average frequency of less than one episode per week for a sustained period of time. In full remission: After full criteria for binge-eating disorder were previously met, none of the criteria have been met for a sustained period of time.

Reprinted, with permission, from American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 5th ed. Arlington, VA: American Psychiatric Association; 2013.

image Treatment

A combination of cognitive-behavioral therapy and antidepressant medication has been helpful in treating BED in adults. Use of SSRIs for BED in adolescents has not been studied, but in adults fluoxetine and citalopram help decrease binge episodes, improve depressive symptoms, and possibly decrease appetite. This evidence suggests that SSRIs in adolescents with BED may be helpful as well. BED has been recognized only recently, and outcomes have not been studied. Little is known regarding long-term prognosis.

Fairburn CG et al: The natural course of bulimia nervosa and binge eating disorder in young women. Arch Gen Psychiatry 2000;57:659 [PMID: 10891036].

Johnson WG et al: Measuring binge eating in adolescents: adolescent and parent versions of the questionnaire of eating and weight patterns. Int J Eat Disord 1999;26:301 [PMID: 10441246].

McElroy SL et al: Citalopram in the treatment of binge-eating disorder: a placebo-controlled trial. J Clin Psychiatry 2003;64:807 [PMID: 12934982].

Schneider M: Bulimia nervosa and binge eating disorder in adolescents. Adolesc Med State Art Rev 2003;14:119 [PMID: 12529196].


Historically, eating disorder not otherwise specified (EDNOS) was the most common eating disorder diagnosis, assigned to individuals who did not meet full criteria for AN or BN. The DSM-V has eliminated EDNOS as a diagnostic category and created a diagnosis of “other specified feeding or eating disorder.” The majority of youth who previously were diagnosed with EDNOS will be categorized as having AN or avoidant/restrictive food intake disorder (ARFID). However, youth can be categorized as having atypical AN if they display characteristics of AN, but are at a normal weight, or as having BN of low frequency if they binge-eat less than once per week.

Regardless of specific diagnostic criteria, it is imperative for clinicians to pay careful attention to patient concerns about body weight and dieting behaviors to facilitate recognition of eating disorder behavior. Symptoms and sequelae depend on specific behaviors. Some patients with eating disorders that do not meet criteria for categorization will go on to develop full-blown AN or BN, and early recognition and treatment may decrease further complications.


ARFID is a new diagnosis in the DSM-V that extends the DSM-IV diagnosis of feeding disorder of infancy or early childhood. Studies show that about 10%–15% of those currently diagnosed with EDNOS will be reclassified as ARFID. The hallmark feature is avoidance or restriction of oral food intake, in the absence of criteria for AN (body image disturbance, fear of weight gain/body fat). For teenagers, food avoidance may be associated with more generalized emotional difficulties that do not meet diagnostic criteria for anxiety or depression. Diagnostic criteria for ARFID (Table 6–8) include the following:

Table 6–8. Diagnostic criteria for avoidant/restrictive food intake disorder.

1. Eating or feeding disturbance (including, but not limited to, apparent lack of interest in eating or food; avoidance based on the sensory characteristics of food; concern about aversive consequences of eating) as manifested by persistent failure to meet appropriate nutritional and/or energy needs associated with one (or more) of the following:

a. Significant weight loss (or failure to achieve expected weight gain or faltering growth in children).

b. Significant nutritional deficiency.

c. Dependence on enteral feeding or oral nutritional supplements.

d. Marked interference with psychosocial functioning.

2. The disturbance is not better explained by lack of available food or an associated culturally sanctioned practice.

3. The eating disturbance does not occur exclusively during the course of anorexia nervosa or bulimia nervosa, and there is no evidence of a disturbance in the way of which one’s body weight or shape is experienced.

4. The eating disturbance is not attributable to a concurrent medical condition or not better explained by another mental disorder. When the eating disturbance occurs in the context of another condition or disorder, the severity of the eating disturbance exceeds that routinely associated with the condition or disorder and warrants additional clinical attention.

Specify if:

In remission: After full criteria for avoidant/restrictive food intake disorder were previously met, the criteria have not been met for a sustained period of time.

Note: Text will include description of three main subtypes: individuals who do not eat enough/show little interest in feeding; individuals who only accept a limited diet in relation to sensory features; and individuals whose food refusal is related to aversive experience.

Reprinted, with permission, from American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 5th ed. Arlington, VA: American Psychiatric Association; 2013.

1. Eating or feeding disturbance (including, but not limited, to apparent lack of interest in eating or food; avoidance based on the sensory characteristics of food; or concern about aversive consequences of eating) as manifested by persistent failure to meet appropriate nutritional and/or energy needs is associated with one or more of the following:

a. Significant weight loss (or failure to gain weight or faltering growth in children)

b. Significant nutritional deficiency

c. Dependence on enteral feeding

d. Marked interference with psychosocial functioning

2. There is no evidence that lack of available food or an associated culturally sanctioned practice is sufficient to account alone for the disorder.

3. The eating disturbance does not occur exclusively during the course of AN or BN, and there is no evidence of a disturbance in the way one’s body weight or shape is experienced.

4. If the eating disturbance occurs in the context of a medical condition or another mental disorder, it is sufficiently severe to warrant independent clinical attention.

American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 5th ed. Arlington, VA: American Psychiatric Association; 2013.


Outcome in eating disorders, especially AN, has been studied extensively. Unfortunately, most studies have focused on specific inpatient treatment programs, and few have evaluated less ill patients who do not need hospitalization. About 40%–50% of patients receiving treatment recover; 20%–30% have intermittent relapses; and 20% have chronic, unremitting illness. As time from initial onset lengthens, the recovery rate decreases and mortality associated with AN and BN increases.

The course of AN often includes significant weight fluctuations over time, and it may be a matter of years until recovery is certain. The course of BN often includes relapses of bingeing and purging, although bulimic patients initially recover faster than do anorexic patients. Up to 50% of anorexic patients may develop bulimia, as well as major psychological complications, including depression, anxiety, and substance abuse disorders. Bulimic patients also develop similar psychological illness but rarely develop anorexia. Long-term medical sequelae, aside from low body weight and amenorrhea, have not been systematically studied, although AN is known to have multiple medical consequences, including osteoporosis and structural brain changes.

It is unclear whether age at onset affects outcome, but shorter length of time between symptom onset and therapy tends to improve outcome. Various treatment modalities can prove effective. Favorable outcomes have been found with brief medical hospitalization and long psychiatric or residential hospitalization. Higher discharge weight, as well as more rapid weight gain during inpatient treatment (> 0.8 kg/wk), seems to improve the initial outcome. It is difficult to compare treatment regimens, because numbers are small and the type of patient and illness varies among studies. No existing studies compare outpatient to inpatient treatment or the effects of day treatment on recovery.

Chamay-Weber C et al: Partial eating disorders among adolescents: a review. J Adolesc Health 2005;37:417 [PMID: 16227132].

Eddy KT et al: Eating disorder not otherwise specified in adolescents. J Am Acad Child Adolesc Psychiatry 2008;47(2):156–164.

Lund BC et al: Rate of inpatient weight restoration predicts outcome in anorexia nervosa. Int J Eat Disord 2009;42(4):301–305 [PMID: 19107835].

Steinhausen HC: Outcome of eating disorders. Child Adolesc Psychiatr Clin N Am 2009;18(1):225–242 [PMID: 19014869].