Medical School · Year 3 · Psychiatry · includes a quiz and discussion video

Seminar 10: Eating Disorders

Year 3: Psychiatry Clerkship

Learning Objectives

By the end of this seminar, students will be able to:

1. Diagnose anorexia nervosa and bulimia nervosa
2. Recognize binge eating disorder
3. Identify medical complications of eating disorders
4. Apply levels of care criteria
5. Describe evidence-based treatments
6. Monitor and manage refeeding syndrome

Seminar Outline

I. Overview of Eating Disorders

Eating disorders encompass a group of psychiatric conditions characterized by persistent disturbances in eating behavior and related thoughts and emotions that significantly impair physical health, psychosocial functioning, or both. The DSM-5 classification includes anorexia nervosa, characterized by restriction leading to significantly low body weight; bulimia nervosa, defined by recurrent binge eating followed by compensatory behaviors; binge eating disorder, involving binge eating without subsequent compensation; and avoidant/restrictive food intake disorder (ARFID), representing eating disturbance without body image concerns. Other specified feeding and eating disorders capture clinically significant presentations that do not meet full criteria for the primary diagnoses, including atypical presentations, subthreshold conditions, and specific syndromes such as purging disorder and night eating syndrome. Understanding this classification helps clinicians recognize the spectrum of eating pathology and apply appropriate diagnostic categories.

Epidemiological data reveal that eating disorders affect a significant proportion of the population, with lifetime prevalence rates of approximately 0.5-1% for anorexia nervosa, 1-2% for bulimia nervosa, and 2-3% for binge eating disorder. Gender differences are pronounced, with female-to-male ratios of approximately 10:1 for anorexia nervosa and bulimia nervosa, though binge eating disorder shows more equal distribution between genders. Age of onset typically falls during adolescence and early adulthood, coinciding with developmental challenges around identity formation, body image, and autonomy, though eating disorders can emerge at any age and are increasingly recognized across the lifespan. Anorexia nervosa carries the highest mortality rate of any psychiatric disorder, with standardized mortality ratios five to six times higher than expected, making early recognition and treatment essential.

Risk factors for eating disorders span biological, psychological, and sociocultural domains, reflecting the multifactorial etiology of these conditions. Genetic factors contribute substantially, with heritability estimates of 50-80% for anorexia nervosa and significant familial clustering of eating disorder traits. Psychological risk factors include perfectionism, low self-esteem, negative emotionality, and body dissatisfaction, which may precede the development of clinical eating disorders. Sociocultural factors, particularly the thin ideal promoted in Western media and social environments that emphasize appearance, create a context in which body dissatisfaction and dietary restriction become normative. Specific occupational and recreational contexts, including dance, modeling, wrestling, and other activities with weight requirements or aesthetic evaluation, confer elevated risk through social pressure and functional reinforcement of eating pathology.

The biopsychosocial model of eating disorder etiology integrates multiple factors across development, recognizing that no single cause is sufficient to produce an eating disorder. Biological vulnerabilities may include genetic predisposition, neurobiological differences in reward and satiety systems, and temperamental factors such as harm avoidance and persistence. Psychological factors encompass cognitive patterns including dichotomous thinking and perfectionism, emotional regulation difficulties, and developmental experiences including attachment patterns and trauma. Social factors include family dynamics, peer influences, cultural messages about ideal body shape, and specific triggering events such as dieting, life transitions, or trauma. The interaction of these factors over time leads to the emergence and maintenance of eating disorder symptoms, with different factor combinations potentially leading to similar clinical presentations.

<image>Panel A: Comprehensive classification diagram showing DSM-5 eating disorder categories (anorexia nervosa, bulimia nervosa, binge eating disorder, ARFID, other specified) with key distinguishing features and diagnostic relationships indicated by connecting lines. Panel B: Epidemiological data visualization displaying lifetime prevalence rates, gender ratios, and age of onset distributions for each major eating disorder, with mortality data highlighted for anorexia nervosa. Panel C: Risk factor model showing biological (genetics, neurobiology), psychological (perfectionism, body dissatisfaction), and sociocultural (media, occupation) factors converging on eating disorder development. Panel D: Biopsychosocial etiological model illustrated as interconnected gears representing biological vulnerabilities, psychological factors, and social influences turning together across developmental timeline.</image>

II. Anorexia Nervosa

Anorexia nervosa is defined by three core diagnostic criteria that capture the essential features of this severe eating disorder. Criterion A requires restriction of energy intake relative to requirements, leading to a significantly low body weight in the context of age, sex, developmental trajectory, and physical health, with significantly low weight defined as weight that is less than minimally normal or, for children and adolescents, less than minimally expected. Criterion B specifies intense fear of gaining weight or of becoming fat, or persistent behavior that interferes with weight gain, even though at a significantly low weight, recognizing that patients may deny fear but demonstrate behavioral avoidance of weight gain. Criterion C addresses disturbance in the way 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, capturing the cognitive distortions central to anorexia nervosa.

The DSM-5 distinguishes two subtypes of anorexia nervosa based on the presence or absence of binge-eating and purging behaviors during the current episode. The restricting type describes presentations during which weight loss is accomplished primarily through dieting, fasting, and/or excessive exercise, without regular engagement in binge eating or purging behaviors during the past three months. The binge-eating/purging type applies when the individual has engaged in recurrent episodes of binge eating or purging behavior (self-induced vomiting or misuse of laxatives, diuretics, or enemas) during the past three months. Subtype classification has prognostic and treatment implications, as the binge-eating/purging type is associated with higher rates of impulsivity, comorbid substance use, and medical complications related to purging behaviors. Patients may cross over between subtypes during the course of illness, and subtype should be specified based on current rather than historical presentation.

Severity specification for anorexia nervosa is based on body mass index (BMI), with higher severity levels associated with increased medical risk and treatment intensity requirements. Mild severity corresponds to BMI greater than or equal to 17 kg/m squared; moderate severity to BMI between 16 and 16.99; severe to BMI between 15 and 15.99; and extreme severity to BMI less than 15. These severity levels guide clinical decision-making regarding level of care, intensity of medical monitoring, and urgency of intervention. BMI-based severity has limitations, however, as individuals at higher weights may still experience severe medical complications, and rapid weight loss regardless of current BMI represents significant risk. Clinicians must consider the totality of the clinical picture rather than relying solely on BMI when assessing severity and treatment needs.

The clinical presentation of anorexia nervosa extends beyond the diagnostic criteria to include characteristic physical, cognitive, and behavioral features. Physical findings include emaciation, lanugo hair (fine downy hair on the body), dry skin, hair loss, bradycardia, hypotension, and hypothermia reflecting the body's adaptation to starvation. Cognitive features include intense preoccupation with food, calories, and weight; body image distortion causing patients to perceive themselves as fat despite being severely underweight; and progressive cognitive narrowing with difficulty concentrating on non-food-related topics. Behavioral manifestations include ritualistic eating behaviors such as cutting food into tiny pieces, excessive exercise that may continue despite injury or medical risk, food hoarding, calorie counting, and social withdrawal as the illness progresses and eating becomes increasingly difficult in social contexts.

<image>Panel A: Three-criteria diagnostic diagram for anorexia nervosa showing Criterion A (restriction leading to low weight), Criterion B (intense fear or behavioral interference), and Criterion C (body image disturbance) with clinical examples for each. Panel B: Subtype comparison showing restricting type (fasting, excessive exercise) versus binge-eating/purging type (vomiting, laxatives, diuretics) with notation about crossover and prognostic differences. Panel C: BMI-based severity scale displayed as a vertical thermometer from mild (BMI 17+) through moderate (16-16.99), severe (15-15.99), to extreme (<15) with associated risk indicators at each level. Panel D: Full-body illustration showing characteristic physical signs of anorexia nervosa including lanugo, dry skin, hair loss, bradycardia, hypotension, and hypothermia with anatomical annotations.</image>

III. Medical Complications of Anorexia

Cardiovascular complications of anorexia nervosa represent some of the most dangerous medical consequences and are a leading cause of death in this population. Bradycardia occurs commonly, with resting heart rates frequently below 60 beats per minute and sometimes dropping below 40, reflecting the body's metabolic adaptation to starvation and reduced cardiac workload. Hypotension with orthostatic changes develops as intravascular volume decreases and cardiovascular reflexes become impaired, placing patients at risk for syncope and falls. QTc prolongation on electrocardiogram represents a particularly concerning finding, as it predisposes to potentially fatal ventricular arrhythmias including torsades de pointes, with risk further elevated by electrolyte abnormalities. Cardiomyopathy and decreased cardiac muscle mass can develop in severe or prolonged cases, with rare cases of heart failure, and mitral valve prolapse is found at elevated rates due to changes in heart size relative to valve structures.

Gastrointestinal complications affect nearly all patients with anorexia nervosa and contribute significantly to symptom maintenance through discomfort that reinforces food avoidance. Constipation is nearly universal, resulting from slowed gastrointestinal motility, reduced food intake, dehydration, and weakened abdominal musculature. Delayed gastric emptying causes early satiety, bloating, and abdominal discomfort after eating, creating physical sensations that patients interpret as evidence they should not eat and that complicate refeeding efforts. Superior mesenteric artery syndrome is a rare but serious complication in which the duodenum becomes compressed between the aorta and the superior mesenteric artery as the fat pad protecting this space is lost with severe weight loss, causing obstruction and vomiting. Elevated liver function tests indicating hepatic steatosis may be seen during both starvation and refeeding phases, reflecting metabolic stress on the liver.

Endocrine and metabolic complications are extensive, affecting virtually every hormonal axis as the body adapts to starvation. Amenorrhea, while no longer required for diagnosis, occurs in the majority of females with anorexia nervosa due to hypothalamic suppression of the gonadotropin axis, representing the body's appropriate response to a state incompatible with reproduction. Osteoporosis develops rapidly and may be irreversible, resulting from estrogen deficiency, hypercortisolism, nutritional deficiencies, and direct bone effects of low body weight, with fracture risk remaining elevated even after weight restoration. Hypothermia reflects reduced metabolic rate and impaired thermoregulation, with patients often complaining of feeling cold and needing excessive clothing. Euthyroid sick syndrome presents as low T3 with normal or low-normal TSH, representing an adaptive response to conserve energy rather than primary thyroid dysfunction. Hypoglycemia may occur as glycogen stores are depleted, potentially causing seizures or cardiac arrhythmias in severe cases.

Additional complications span hematologic, neurologic, dermatologic, and renal systems, reflecting the body-wide impact of severe malnutrition. Pancytopenia with anemia, leukopenia, and thrombocytopenia results from bone marrow hypoplasia and fat replacement, though infectious complications from leukopenia are surprisingly rare. Neurologic findings include brain atrophy visible on imaging, cognitive deficits in concentration and memory that may persist after weight restoration, and peripheral neuropathy in some cases. Dermatologic manifestations include lanugo, dry skin, yellow-orange discoloration from carotenemia, hair loss, and poor wound healing. Electrolyte abnormalities including hypokalemia, hypophosphatemia, and hypomagnesemia may occur due to inadequate intake, purging behaviors, or shifts during refeeding, with potentially life-threatening cardiac and neurologic consequences.

<image>Panel A: Cardiovascular system diagram showing bradycardia, hypotension, QTc prolongation, and cardiomyopathy with ECG tracing demonstrating prolonged QTc interval and risk indicators for sudden cardiac death. Panel B: Gastrointestinal tract illustration depicting constipation, delayed gastric emptying, and superior mesenteric artery syndrome with anatomical detail showing duodenal compression between aorta and SMA. Panel C: Endocrine axis diagram showing hypothalamic-pituitary suppression affecting gonadal, thyroid, and adrenal function with downstream consequences including amenorrhea, euthyroid sick syndrome, and osteoporosis. Panel D: Body systems overview showing hematologic (pancytopenia), neurologic (brain atrophy), dermatologic (lanugo, dry skin), and electrolyte complications with severity indicators.</image>

IV. Bulimia Nervosa

Bulimia nervosa is characterized by five diagnostic criteria that define the syndrome of recurrent binge eating with compensatory behaviors driven by overvaluation of weight and shape. Criterion A requires recurrent episodes of binge eating, defined by both eating in a discrete period of time an amount of food that is definitely larger than what most individuals would eat in a similar period under similar circumstances, and a sense of lack of control over eating during the episode. Criterion B specifies recurrent inappropriate compensatory behaviors to prevent weight gain, which may include self-induced vomiting, misuse of laxatives, diuretics, or other medications, fasting, or excessive exercise. Criterion C requires that the binge eating and compensatory behaviors both occur, on average, at least once per week for three months. Criterion D establishes that self-evaluation is unduly influenced by body shape and weight. Criterion E specifies that the disturbance does not occur exclusively during episodes of anorexia nervosa, distinguishing bulimia nervosa from the binge-eating/purging subtype of anorexia nervosa.

Severity specification for bulimia nervosa is based on the frequency of inappropriate compensatory behaviors, providing guidance for treatment intensity and prognosis assessment. Mild severity corresponds to an average of one to three episodes of compensatory behaviors per week; moderate to four to seven episodes; severe to eight to thirteen episodes; and extreme to fourteen or more episodes per week. The frequency-based severity specification acknowledges that the number of compensatory episodes provides a reasonable proxy for overall illness severity, though clinicians should consider other factors including duration of illness, medical complications, functional impairment, and comorbid conditions when formulating treatment plans. Severity may fluctuate over time, and patients may experience periods of remission followed by relapse.

The clinical presentation of bulimia nervosa differs notably from anorexia nervosa in that patients are typically at normal weight or may be overweight, with the disorder often hidden due to the secretive nature of binge-purge behaviors. Purging behaviors may involve self-induced vomiting, which becomes easier with practice as patients learn to trigger their gag reflex more efficiently, or misuse of laxatives, diuretics, or other agents believed to prevent weight gain. Non-purging compensatory behaviors include fasting for extended periods following binges and excessive exercise that may be compulsive and performed despite injury or illness. The binge episodes themselves are typically experienced as shameful and secretive, occurring when the patient is alone, with large quantities of food consumed rapidly until physical discomfort or interruption ends the episode. The cycle of restriction, binge, and purge becomes self-perpetuating, as restriction increases vulnerability to binges and the distress of binging triggers compensatory behaviors.

Medical complications of bulimia nervosa result primarily from the purging behaviors rather than from malnutrition, distinguishing them from the complications of anorexia nervosa. Dental erosion from repeated exposure to stomach acid during vomiting affects the lingual surfaces of teeth and may cause permanent damage, sensitivity, and discoloration. Parotid gland hypertrophy produces the characteristic "chipmunk cheeks" appearance as the salivary glands enlarge in response to repeated stimulation during purging. Russell's sign refers to calluses on the knuckles or dorsum of the hand from using fingers to induce vomiting, though this sign may be absent in patients who have learned to vomit without mechanical stimulation. Hypokalemia from vomiting or laxative abuse poses significant cardiac risk, including arrhythmias and potentially fatal cardiac events. Esophageal complications include Mallory-Weiss tears from repeated retching and, rarely, esophageal rupture, while chronic laxative abuse can cause dependence and rebound constipation.

<image>Panel A: Five-criteria diagnostic diagram for bulimia nervosa showing binge eating (large amount plus loss of control), compensatory behaviors, frequency (weekly for 3 months), weight/shape influence on self-evaluation, and exclusion criterion regarding anorexia nervosa. Panel B: Severity scale based on compensatory behavior frequency from mild (1-3/week) through moderate (4-7), severe (8-13), to extreme (14+/week) with associated treatment intensity recommendations. Panel C: Binge-purge cycle diagram showing restriction leading to hunger, then binge eating, then guilt and distress, then compensatory behavior, then temporary relief, returning to restriction. Panel D: Medical complications illustration showing dental erosion, parotid hypertrophy ("chipmunk cheeks"), Russell's sign on hands, and metabolic consequences including hypokalemia and metabolic alkalosis with ECG changes.</image>

V. Binge Eating Disorder

Binge eating disorder is defined by recurrent binge eating episodes in the absence of the regular compensatory behaviors that characterize bulimia nervosa, making it the most prevalent eating disorder in the United States. Criterion A requires recurrent episodes of binge eating, using the same definition as in bulimia nervosa: eating in a discrete period an amount definitely larger than most people would eat in similar circumstances, accompanied by a sense of lack of control over eating during the episode. Criterion B specifies that binge eating episodes are associated with three or more of five features: eating much more rapidly than normal; eating until feeling uncomfortably full; eating large amounts of food when not feeling physically hungry; eating alone because of feeling embarrassed by how much one is eating; and feeling disgusted with oneself, depressed, or very guilty afterward. Criterion C requires marked distress regarding binge eating. Criterion D specifies that binge eating occurs, on average, at least once per week for three months. Criterion E states that the binge eating is not associated with the recurrent use of inappropriate compensatory behaviors and does not occur exclusively during the course of bulimia nervosa or anorexia nervosa.

The clinical features of binge eating disorder reflect the distress and impairment associated with recurrent loss-of-control eating without compensatory behaviors. Patients are commonly overweight or obese, though binge eating disorder can occur at any weight and should not be conflated with obesity, which is a medical condition rather than a psychiatric diagnosis. Unlike bulimia nervosa, there is no purging behavior to undo the caloric effects of binges, leading to weight gain over time for many patients. The emotional distress associated with binge episodes is significant, with patients reporting shame, guilt, depression, and self-disgust during and after binge eating. Comorbid psychiatric conditions are common, particularly major depressive disorder and anxiety disorders, with the relationship between mood symptoms and binge eating often bidirectional.

Severity specification for binge eating disorder parallels that for bulimia nervosa, based on the frequency of binge eating episodes. Mild severity corresponds to one to three binge eating episodes per week; moderate to four to seven episodes; severe to eight to thirteen episodes; and extreme to fourteen or more episodes per week. The frequency criterion provides a standardized approach to severity assessment, though clinical severity should also consider factors such as duration of illness, degree of weight-related medical complications, functional impairment, and subjective distress. Weight is not included in the severity specification because binge eating disorder can occur across the weight spectrum and because weight is determined by many factors beyond binge eating behavior.

Differential diagnosis of binge eating disorder requires distinguishing it from other eating disorders and from non-pathological overeating patterns. Bulimia nervosa is differentiated by the regular presence of compensatory behaviors, which by definition are absent in binge eating disorder. Normal overeating, such as at holiday meals or special occasions, lacks the loss of control and marked distress that characterize binge eating episodes. Obesity is a medical condition that may or may not be associated with binge eating disorder; many individuals with obesity do not engage in binge eating, and many with binge eating disorder maintain normal weight through other mechanisms. Night eating syndrome, characterized by recurrent episodes of eating after awakening from sleep or excessive food consumption after the evening meal with awareness and recall, represents a distinct syndrome with different treatment implications.

<image>Panel A: Five-criteria diagnostic diagram for binge eating disorder showing binge eating definition, associated features (eating rapidly, uncomfortably full, eating alone, feeling guilty), marked distress, frequency, and absence of compensatory behaviors. Panel B: Clinical presentation comparison showing binge eating disorder patients at various weights (normal, overweight, obese) with notation that weight alone does not determine diagnosis. Panel C: Severity scale based on binge eating episode frequency from mild (1-3/week) through moderate (4-7), severe (8-13), to extreme (14+/week). Panel D: Differential diagnosis flowchart distinguishing binge eating disorder from bulimia nervosa (no compensatory behaviors), normal overeating (loss of control and distress), and night eating syndrome (timing and awareness).</image>

VI. Other Eating Disorders

Avoidant/restrictive food intake disorder represents a feeding and eating disturbance characterized by failure to meet nutritional or energy needs, manifesting in significant weight loss, nutritional deficiency, dependence on enteral feeding or oral nutritional supplements, or marked interference with psychosocial functioning. Unlike anorexia nervosa, ARFID does not involve disturbance in the way body weight or shape is experienced or undue influence of weight on self-evaluation. Three common presentations of ARFID have been described: apparent lack of interest in eating or food, avoidance based on the sensory characteristics of food (texture, smell, taste, appearance), and concern about aversive consequences of eating such as choking, vomiting, or gastrointestinal distress. ARFID is more commonly recognized in children and adolescents and shows elevated rates in individuals with autism spectrum disorder, though it can occur across the lifespan and in the absence of developmental conditions.

Pica is characterized by persistent eating of nonnutritive, nonfood substances over a period of at least one month, with the behavior being inappropriate to the developmental level and not part of a culturally supported or socially normative practice. Common substances consumed include clay, dirt, ice, paper, soap, chalk, and many others, with patterns sometimes reflecting specific nutritional deficiencies such as iron deficiency associated with ice consumption (pagophagia). Medical risks include intestinal obstruction, perforation, toxicity from ingested substances, parasitic infections, and nutritional deficiencies. Pica occurs with increased frequency in pregnancy, intellectual disability, and autism spectrum disorder, and may be associated with obsessive-compulsive disorder or schizophrenia. Treatment addresses underlying nutritional deficiencies when present and uses behavioral approaches to reduce and eliminate the consumption of inappropriate substances.

Rumination disorder involves the repeated regurgitation of food over a period of at least one month, with regurgitated food possibly being re-chewed, re-swallowed, or spit out. The behavior is not attributable to an associated gastrointestinal or other medical condition, must occur in the context of normal eating behavior if the individual has an intellectual disability or autism spectrum disorder, and if occurring in the context of another mental disorder or medical condition, must be sufficiently severe to warrant independent clinical attention. Rumination typically occurs within the first 30 minutes after eating and involves voluntary but often automatic regurgitation of recently ingested food. Complications include malnutrition, weight loss, dental erosion, and social impairment. Treatment typically involves behavioral approaches, particularly diaphragmatic breathing techniques that interfere with the motor pattern of regurgitation.

Other specified feeding or eating disorder captures clinically significant presentations that cause distress or impairment but do not meet full criteria for any disorder in the diagnostic class. Atypical anorexia nervosa describes individuals who meet all criteria for anorexia nervosa except that despite significant weight loss, the individual's weight remains within or above the normal range. Subthreshold bulimia nervosa and binge eating disorder apply when criteria for frequency or duration are not fully met. Purging disorder involves recurrent purging behavior in the absence of binge eating, suggesting a distinct presentation. Night eating syndrome is characterized by recurrent episodes of eating after awakening from sleep or excessive food consumption after the evening meal, with awareness and recall of the eating, causing significant distress or impairment.

<image>Panel A: ARFID clinical presentation showing three subtypes: lack of interest in eating (child pushing away food), sensory-based avoidance (child refusing foods based on texture/color), and fear of aversive consequences (patient anxious about choking) with developmental considerations noted. Panel B: Pica illustration showing commonly ingested substances (ice, clay, paper, dirt) with anatomical diagram depicting potential complications including intestinal obstruction, toxicity, and nutritional deficiencies. Panel C: Rumination disorder mechanism diagram showing normal swallowing, voluntary regurgitation pathway, and re-chewing/re-swallowing or spitting cycle with timeline indicating typical onset within 30 minutes of eating. Panel D: Other specified eating disorders grid showing atypical anorexia nervosa (significant weight loss but normal BMI), subthreshold conditions, purging disorder (no binges), and night eating syndrome with key distinguishing features.</image>

VII. Assessment and Medical Evaluation

Comprehensive assessment of eating disorders integrates psychiatric evaluation with careful attention to medical complications and functional impairment. The clinical history should systematically explore eating patterns including restriction, binge eating, and compensatory behaviors; weight history including highest and lowest weights, rate of weight loss, and relationship to symptoms; body image concerns and degree to which weight influences self-evaluation; menstrual history in females; and use of diet pills, supplements, or other substances for weight control. Physical examination should include measurement of weight and height for BMI calculation, vital signs with attention to bradycardia, hypotension, and orthostatic changes, and physical findings such as lanugo, parotid enlargement, Russell's sign, and dental abnormalities. Mental status examination assesses mood, anxiety, cognitive flexibility, and insight into illness severity.

Screening tools provide standardized methods for detecting eating disorders in clinical and community settings. The SCOFF questionnaire asks five questions: 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) in a 3-month period? Do you believe yourself to be Fat when others say you are thin? Would you say that Food dominates your life? Two or more positive responses suggest the presence of an eating disorder and warrant further evaluation. The Eating Disorder Examination Questionnaire (EDE-Q) provides a more comprehensive self-report measure of eating disorder psychopathology across four subscales. The Eating Attitudes Test (EAT-26) is widely used in research and clinical screening, identifying attitudes and behaviors associated with eating disorders.

Medical laboratory evaluation provides essential information about physiological status and guides medical monitoring and intervention. Basic testing should include complete blood count to assess for anemia and other cytopenias; comprehensive metabolic panel for electrolyte abnormalities, glucose, renal function, and hepatic enzymes; and magnesium and phosphorus levels that are critical for refeeding monitoring. Thyroid function tests help distinguish euthyroid sick syndrome from primary thyroid disease. Amylase elevation suggests recent purging behavior. Electrocardiogram should be obtained in patients with electrolyte abnormalities, bradycardia, or significant malnutrition to assess for QTc prolongation and other rhythm disturbances. Additional testing including bone density measurement should be considered based on duration and severity of illness.

Criteria for medical hospitalization in eating disorders reflect the severity of medical compromise that may necessitate inpatient stabilization. Heart rate below 50 beats per minute or severe instability warrants immediate medical attention. Blood pressure with significant orthostatic changes indicates cardiovascular compromise requiring monitoring and intervention. Weight below 75% of expected or rapid weight loss regardless of current weight suggests severe malnutrition with high medical risk. Electrolyte abnormalities including severe hypokalemia or hypophosphatemia require medical management. Temperature below 96 degrees Fahrenheit indicates impaired thermoregulation. Acute suicidality requires psychiatric safety measures in addition to medical treatment. These criteria should be applied in clinical context, recognizing that individual patients may require hospitalization based on factors not fully captured by any single criterion.

<image>Panel A: Comprehensive assessment diagram showing integration of psychiatric history (eating patterns, weight history, body image), physical examination (vital signs, BMI, physical findings), and mental status examination (mood, insight, cognitive flexibility) in eating disorder evaluation. Panel B: Screening tools comparison showing SCOFF questions with scoring, EDE-Q subscales, and EAT-26 format with sensitivity and specificity data for detecting eating disorders. Panel C: Laboratory monitoring panel showing CBC, CMP, magnesium, phosphorus, thyroid function, amylase, and ECG with clinical indications and concerning findings highlighted. Panel D: Medical hospitalization criteria displayed as alarm indicators with specific thresholds for heart rate, blood pressure, weight, electrolytes, temperature, and suicidality.</image>

VIII. Treatment - Anorexia Nervosa

Levels of care for anorexia nervosa treatment range from outpatient management to medical hospitalization, with placement determined by medical stability, psychiatric safety, and capacity for self-care and treatment adherence. Outpatient treatment is appropriate for medically stable patients who demonstrate motivation for recovery, have adequate psychosocial support, and can maintain nutritional intake without supervision. Intensive outpatient or partial hospitalization programs provide structured treatment several days per week while allowing patients to live in the community, serving as a step-up from outpatient or step-down from higher levels. Residential treatment offers 24-hour supervised care in a non-medical setting for patients needing more structure than partial hospitalization but not requiring medical hospitalization. Medical hospitalization is indicated for medical instability, including cardiovascular compromise, severe electrolyte abnormalities, or extreme low weight, while psychiatric hospitalization addresses acute safety concerns including suicidality.

Nutritional rehabilitation represents the cornerstone of anorexia nervosa treatment, with the primary goal of restoring weight to a medically and psychologically healthy range. The approach involves gradual caloric increases, often starting at 1200-1500 kilocalories per day in severely malnourished patients to minimize refeeding risk, then advancing by approximately 200-300 kilocalories every one to two days as tolerated toward weight gain targets. Weight gain goals typically range from 1-2 pounds per week in outpatient settings to 2-3 pounds per week in inpatient or residential programs, with target weight established based on premorbid weight, growth charts for adolescents, and resumption of menses in females. Meal support involves supervision during and after meals to provide emotional support, prevent compensatory behaviors, and ensure adequate intake, with decreasing supervision as patients demonstrate ability to maintain intake independently.

Refeeding syndrome represents a potentially life-threatening complication of nutritional rehabilitation in severely malnourished patients, requiring prevention through careful monitoring and management. The pathophysiology involves the shift from catabolic to anabolic metabolism when nutrition is reintroduced, causing rapid cellular uptake of phosphorus, potassium, and magnesium as cells begin rebuilding. Hypophosphatemia is the hallmark finding, potentially causing cardiac failure, respiratory failure, rhabdomyolysis, and neurologic dysfunction. Prevention strategies include starting with conservative caloric levels (avoiding aggressive early refeeding), monitoring electrolytes daily during the initial refeeding period, and providing phosphorus supplementation prophylactically or at the first sign of decline. Thiamine supplementation before carbohydrate reintroduction prevents Wernicke encephalopathy in patients who may have thiamine deficiency.

Psychotherapy for anorexia nervosa complements nutritional rehabilitation by addressing the cognitive, emotional, and relational factors that maintain the disorder. Family-Based Treatment, also known as the Maudsley approach, is the first-line treatment for adolescents with anorexia nervosa, engaging parents as the primary agents of refeeding in Phase 1, gradually returning eating control to the adolescent in Phase 2, and addressing normal adolescent developmental issues in Phase 3. Cognitive-Behavioral Therapy for Eating Disorders (CBT-E) is considered first-line for adults, addressing the core psychopathology of over-evaluation of weight and shape, dietary restriction, and compensatory behaviors through behavioral experiments and cognitive restructuring. Specialist supportive clinical management provides a less structured alternative emphasizing clinical management, education, and supportive psychotherapy. Psychodynamic approaches may address underlying developmental and relational issues contributing to the disorder in longer-term treatment.

<image>Panel A: Levels of care continuum from outpatient through intensive outpatient/partial hospitalization, residential, and inpatient (medical and psychiatric) with criteria for placement at each level and arrows indicating step-up and step-down transitions. Panel B: Nutritional rehabilitation protocol showing starting calories (1200-1500 kcal), advancement schedule, weight gain targets (1-3 lbs/week by setting), and meal support structure. Panel C: Refeeding syndrome pathophysiology diagram showing shift from catabolism to anabolism, electrolyte shifts (phosphorus, potassium, magnesium), and potential organ system consequences (cardiac, respiratory, neurologic) with prevention strategies. Panel D: Family-Based Treatment three-phase diagram showing Phase 1 (parents control eating), Phase 2 (gradual return of control to adolescent), and Phase 3 (normal adolescent development) with key interventions at each phase.</image>

IX. Treatment - Bulimia and BED

Treatment for bulimia nervosa utilizes evidence-based psychotherapy as the first-line intervention, with medication serving an important adjunctive role. Cognitive-Behavioral Therapy for Eating Disorders (CBT-E) is the most effective treatment, addressing the maintaining mechanisms of dietary restriction, over-evaluation of weight and shape, and mood intolerance that perpetuate the binge-purge cycle. Treatment typically spans 20 sessions and involves establishing regular eating patterns, reducing dietary restriction, addressing triggers for binge eating, and restructuring cognitive distortions about weight and shape. Interpersonal Therapy provides an effective alternative when CBT is unavailable or ineffective, focusing on interpersonal problems that maintain the eating disorder without directly addressing eating behaviors. Nutritional counseling to establish regular eating patterns complements psychotherapy, and most patients with bulimia nervosa can be treated effectively in outpatient settings.

Binge eating disorder treatment shares many features with bulimia nervosa treatment but must also address weight management for patients with comorbid obesity. Cognitive-Behavioral Therapy is first-line, with research demonstrating significant reductions in binge eating frequency and associated psychopathology. Interpersonal Therapy shows comparable efficacy to CBT and may be particularly useful when interpersonal difficulties are prominent maintaining factors. Behavioral weight loss interventions may be appropriate for patients with comorbid obesity, though the relationship between binge eating reduction and weight loss is complex and binge eating should be addressed first or concurrently. Self-help approaches using CBT-based materials can be effective for some patients with binge eating disorder, potentially serving as a first step before more intensive treatment.

Pharmacotherapy for bulimia nervosa and binge eating disorder provides valuable treatment options, particularly when combined with psychotherapy. Fluoxetine is FDA-approved for bulimia nervosa at doses of 60 mg daily, higher than typical antidepressant doses, demonstrating significant reductions in binge eating and purging independent of effects on mood. Lisdexamfetamine is FDA-approved for binge eating disorder, reducing binge eating frequency through mechanisms that likely include effects on impulsivity and reward processing. Topiramate shows efficacy for both conditions off-label, with benefits including weight loss, though cognitive side effects limit tolerability. Important cautions include avoiding bupropion due to elevated seizure risk in patients with eating disorders and purging behaviors, and recognizing that no medications improve weight gain in anorexia nervosa as a primary effect.

Family-Based Treatment approaches have been adapted beyond adolescent anorexia nervosa for use in bulimia nervosa and younger patients with binge eating disorder. FBT for bulimia nervosa follows a similar structure to FBT for anorexia nervosa, with parents initially taking control of the adolescent's eating to interrupt binge-purge cycles, then gradually returning autonomy as symptoms remit. The evidence base for FBT in bulimia nervosa is growing, though CBT remains the first-line treatment for adults. For all eating disorders, family involvement provides valuable support even when not using formal FBT, and family therapy may address family dynamics that contribute to symptom maintenance. Couples therapy may be indicated when eating disorder symptoms are embedded in relationship patterns.

<image>Panel A: CBT-E treatment components for bulimia nervosa showing regular eating establishment, reduction of dietary restriction, addressing triggers, and cognitive restructuring with typical 20-session timeline. Panel B: Binge eating disorder treatment algorithm showing CBT and IPT as first-line, with behavioral weight loss for comorbid obesity and self-help as potential first step. Panel C: Medication options showing fluoxetine 60mg for bulimia nervosa, lisdexamfetamine for BED, topiramate as off-label option, and bupropion contraindication with mechanism of action and side effect profiles. Panel D: Family-Based Treatment adaptation for bulimia nervosa showing three-phase structure with modifications from anorexia protocol and parent involvement in interrupting binge-purge cycles.</image>

X. Prognosis and Special Considerations

Prognosis in eating disorders varies considerably by diagnosis, with bulimia nervosa and binge eating disorder generally showing better response to treatment than anorexia nervosa. For anorexia nervosa, longitudinal studies suggest approximately 50% of patients recover fully, 30% show partial improvement with residual symptoms, and 20% develop a chronic course. The mortality rate of 5-10% makes anorexia nervosa one of the most lethal psychiatric disorders, with causes of death including cardiac complications, suicide, and other medical consequences. Bulimia nervosa shows higher rates of treatment response, with the majority of patients showing significant improvement with evidence-based treatment, though relapse rates remain substantial. Binge eating disorder demonstrates good response to treatment with significant reductions in binge eating frequency, though weight management may require additional intervention.

Comorbid psychiatric conditions are the rule rather than the exception in eating disorders and significantly impact treatment planning and prognosis. Major depressive disorder occurs in 50-75% of patients with eating disorders, with depressive symptoms often improving with nutritional rehabilitation but sometimes requiring concurrent treatment. Anxiety disorders including social anxiety, generalized anxiety, and obsessive-compulsive disorder commonly co-occur, particularly in anorexia nervosa where obsessive-compulsive features are prominent. Substance use disorders show elevated rates particularly in bulimia nervosa and the binge-eating/purging subtype of anorexia nervosa, where impulsivity is a shared risk factor. Personality disorders, particularly borderline and obsessive-compulsive personality disorders, may complicate treatment and require integrated approaches addressing both eating and personality pathology.

Special populations require adapted approaches that address unique considerations in eating disorder presentation and treatment. Males with eating disorders are frequently underdiagnosed due to clinical stereotypes associating eating disorders with females, and may present with emphasis on muscularity rather than thinness or through excessive exercise. Athletes face elevated risk due to sport-specific pressures around weight and body composition, with "relative energy deficiency in sport" (RED-S) now recognized as a spectrum of consequences from inadequate energy intake in athletic contexts. LGBTQ+ individuals show higher rates of eating disorders, potentially related to minority stress, body image concerns specific to these communities, and higher rates of trauma. Older adults may develop or relapse with eating disorders and are frequently overlooked in clinical settings focused on adolescents and young adults.

Prevention efforts span primary prevention targeting populations before eating disorder development, secondary prevention through early identification, and tertiary prevention focused on reducing complications in those already affected. Media literacy programs teach critical evaluation of idealized images and messages about body shape and weight, potentially reducing internalization of unrealistic standards. Body positivity and body acceptance movements promote appreciation of diverse body types and de-emphasize weight as a determinant of worth. Early intervention when symptoms first emerge offers the best opportunity for full recovery, making screening in high-risk populations and settings an important prevention strategy. Education of healthcare providers, coaches, teachers, and parents about eating disorder warning signs facilitates early identification and appropriate referral.

<image>Panel A: Prognosis comparison across eating disorders showing recovery rates (50% for AN, higher for BN and BED), chronicity rates, mortality data for anorexia nervosa, and factors associated with better versus worse outcomes. Panel B: Comorbidity prevalence chart showing rates of depression, anxiety disorders, OCD, substance use, and personality disorders across eating disorder diagnoses. Panel C: Special populations grid showing males (muscle dysmorphia focus), athletes (RED-S), LGBTQ+ (minority stress), older adults (missed diagnosis), and type 1 diabetes ("diabulimia") with unique considerations for each. Panel D: Prevention continuum from primary (media literacy, body positivity) through secondary (screening, early intervention) to tertiary (complication reduction) with target populations and strategies at each level.</image>

Summary

• Anorexia nervosa requires restriction leading to low BMI, fear of weight gain or behavioral interference with weight gain, and body image disturbance; subtypes include restricting and binge-eating/purging; severity is based on BMI (mild 17+, moderate 16-16.99, severe 15-15.99, extreme <15)
• Medical complications of anorexia nervosa include bradycardia, QTc prolongation, electrolyte abnormalities, osteoporosis, and multiple organ system effects requiring comprehensive medical monitoring
• Bulimia nervosa is characterized by binge eating plus compensatory behaviors occurring at least weekly for three months, with self-evaluation unduly influenced by weight and shape; patients are typically normal weight
• Bulimia nervosa complications result from purging: dental erosion, parotid hypertrophy, Russell's sign, hypokalemia with cardiac risk, and esophageal tears
• Binge eating disorder involves binge eating without compensatory behaviors, commonly associated with overweight or obesity but occurring across the weight spectrum
• Refeeding syndrome with hypophosphatemia is a life-threatening complication of nutritional rehabilitation, prevented through conservative initial calories and electrolyte monitoring/supplementation
• Family-Based Treatment (Maudsley) is first-line for adolescent anorexia nervosa, with parents taking control of eating in Phase 1, gradual return of control in Phase 2, and focus on adolescent development in Phase 3
• CBT-E is first-line for adult anorexia nervosa, bulimia nervosa, and binge eating disorder, addressing over-evaluation of weight/shape and maintaining mechanisms
• Fluoxetine 60 mg is FDA-approved for bulimia nervosa; lisdexamfetamine is FDA-approved for binge eating disorder; no medications improve weight gain in anorexia nervosa
• Anorexia nervosa has the highest mortality rate of any psychiatric disorder (5-10%), with causes including cardiac complications and suicide

Key Terms

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