Definition and epidemiology
Eating disorders (ICD-10 F50) are a group of conditions marked by abnormal eating or weight-control behaviors driven by disturbed cognitions about body shape, weight, or food. The major subtypes are:
- Anorexia nervosa (AN) — restriction of energy intake leading to significantly low body weight, with intense fear of weight gain and body image distortion.
- Bulimia nervosa (BN) — recurrent binge eating followed by compensatory behaviors (self-induced vomiting, laxative misuse, excessive exercise), usually at normal or near-normal weight.
- Binge-eating disorder (BED) — recurrent binge eating without regular compensatory behaviors, often associated with obesity.
- Avoidant/restrictive food intake disorder (ARFID) — food avoidance not driven by body image concerns, more common in children.
Lifetime prevalence is approximately 1-2% for anorexia, 1-3% for bulimia, and 2-3% for binge-eating disorder, which is the most common eating disorder overall. Female-to-male ratio is roughly 10:1 for AN and BN, though BED has a more even distribution. Peak onset is mid-to-late adolescence, though BED often presents later. Eating disorders are more prevalent in industrialized, weight-conscious cultures but occur across all socioeconomic and ethnic groups.
- Anorexia nervosa has the highest mortality rate of any psychiatric disorder
- Purging causes hypokalemic, hypochloremic metabolic alkalosis
- Refeeding syndrome risk: watch phosphate, potassium, magnesium during renourishment
- Fluoxetine is the only FDA-approved drug for bulimia nervosa
- Lisdexamfetamine is FDA-approved for binge-eating disorder
- Family-based therapy is first-line for adolescent anorexia nervosa
- Russell sign = calluses on knuckles from self-induced vomiting
- Amenorrhea is no longer a required DSM-5 criterion for anorexia but remains a classic clue
Etiology and risk factors
Eating disorders are multifactorial, involving genetic, psychological, and sociocultural contributions.
- Genetic — first-degree relatives of affected individuals have markedly higher risk; twin studies show heritability of 50-80%.
- Personality traits — perfectionism, obsessionality, and anxiety disorders are common premorbid traits in AN; impulsivity and mood instability are more associated with BN and BED.
- Sociocultural — internalization of thin-body ideals, media/social media exposure, participation in weight-sensitive activities (ballet, gymnastics, wrestling, modeling).
- Psychological — history of trauma, sexual abuse, low self-esteem, and difficulty with emotional regulation.
- Family dynamics — overly controlling or critical family environments, family history of dieting or weight preoccupation.
- Biological — dysregulation of serotonergic and dopaminergic systems affecting satiety and reward.
Comorbid psychiatric conditions are common: major depression, anxiety disorders, obsessive-compulsive disorder, and substance use disorders.
Pathophysiology
In anorexia nervosa, chronic caloric restriction produces a hypometabolic state. The body downregulates thyroid function (euthyroid sick syndrome), suppresses the hypothalamic-pituitary-gonadal axis (causing amenorrhea), and shifts to a catabolic state with loss of fat and lean mass. Severe starvation leads to bradycardia, hypotension, and cardiac atrophy; electrolyte derangements and refeeding syndrome risk are major concerns during recovery.
In bulimia nervosa, binge-purge cycles cause fluctuating electrolyte disturbances, most notably hypokalemic, hypochloremic metabolic alkalosis from vomiting. Chronic vomiting also causes dental enamel erosion and parotid gland hypertrophy (sialadenosis).
Binge-eating disorder pathophysiology centers on dysregulated reward and satiety signaling (dopaminergic and serotonergic pathways) and impaired impulse control, often with resulting insulin resistance and obesity-related metabolic consequences.
Across disorders, cognitive distortions about body shape and weight serve as the core maintaining mechanism, reinforced by the physiologic and psychological rewards of restriction, bingeing, or purging.
Clinical features
Anorexia nervosa
- Significantly low body weight (BMI often <17.5 kg/m2, though DSM-5 removed a strict cutoff)
- Intense fear of weight gain, distorted body image
- Restricting subtype vs binge-eating/purging subtype
- Amenorrhea (no longer a required criterion but common finding)
- Physical signs: lanugo hair, bradycardia, hypotension, cold intolerance, hair thinning
Bulimia nervosa
- Recurrent binge eating (at least once weekly for 3 months)
- Recurrent compensatory behavior (vomiting, laxatives, diuretics, fasting, excessive exercise)
- Weight typically normal or near-normal
- Russell sign (calluses on knuckles from self-induced vomiting)
- Dental erosion, parotid gland swelling
Binge-eating disorder
- Recurrent binge eating without compensatory behavior
- Eating rapidly, until uncomfortably full, alone due to embarrassment
- Marked distress about bingeing
- Often overweight or obese
ARFID
- Avoidance based on sensory characteristics, lack of interest, or fear of aversive consequences (choking, vomiting)
- No body image disturbance
- Can cause significant nutritional deficiency or growth faltering in children
Diagnosis
Diagnosis is clinical, based on DSM-5/ICD-10 criteria and history; no single lab test confirms an eating disorder, but labs assess severity and complications.
- History and screening — tools such as SCOFF questionnaire are useful for screening in primary care.
- Physical exam — vital signs (bradycardia, hypotension, orthostasis), weight/BMI trend, signs of purging (Russell sign, dental erosion, parotid swelling).
- Laboratory workup — complete blood count, electrolytes (hypokalemia, metabolic alkalosis in purging), glucose, renal and liver function, magnesium and phosphate (critical before refeeding), thyroid function, and gonadotropins/estradiol if amenorrheic.
- ECG — assess for bradycardia, QT prolongation, arrhythmia risk, especially before refeeding.
- Bone density (DEXA) — in longstanding AN to assess for osteopenia/osteoporosis from hypoestrogenism and malnutrition.
DSM-5 criteria remain the diagnostic standard; psychiatric/psychological evaluation establishes severity and comorbidities.
Differential diagnosis
- Major depressive disorder — can cause appetite and weight changes but lacks body image distortion
- Hyperthyroidism — weight loss with increased appetite, tachycardia rather than bradycardia
- Inflammatory bowel disease / malabsorption — weight loss with GI symptoms, no body image concern
- Malignancy — unintentional weight loss, typically older patients, systemic symptoms
- Obsessive-compulsive disorder — food rituals may overlap but primary focus is not weight/shape
- Body dysmorphic disorder — distorted body image but not specifically focused on weight/shape in the context of eating
- Substance use disorder — can cause appetite suppression or weight loss
- Addison disease — weight loss, hypotension, electrolyte disturbance without psychological eating pathology
Management
Treatment is multidisciplinary, combining medical stabilization, nutritional rehabilitation, and psychotherapy. Pharmacotherapy plays a supportive, not primary, role in most eating disorders except BED.
Medical stabilization
- Inpatient admission indicated for severe bradycardia, arrhythmia, hypotension, electrolyte derangement, BMI critically low, or suicidality.
- Careful, gradual refeeding to avoid refeeding syndrome (hypophosphatemia, hypokalemia, hypomagnesemia, fluid overload, cardiac failure) — monitor electrolytes and phosphate closely during early refeeding.
Psychotherapy (first-line for all subtypes)
- Family-based therapy (FBT/Maudsley approach) — first-line for adolescents with AN; parents take an active role in renourishment.
- Cognitive behavioral therapy for eating disorders (CBT-ED) — first-line for adults with BN and BED, also used in AN.
- Interpersonal psychotherapy (IPT) — effective alternative for BN and BED.
Pharmacotherapy
- Fluoxetine — only FDA-approved medication for bulimia nervosa; reduces binge-purge frequency.
- Lisdexamfetamine — FDA-approved for moderate-to-severe binge-eating disorder.
- SSRIs generally — used for comorbid depression/anxiety in AN but limited evidence for weight restoration; antipsychotics (e.g., olanzapine) sometimes used off-label to assist weight gain and reduce anxiety around eating in AN.
- Medication alone is not recommended as sole treatment for AN; psychotherapy and nutritional rehabilitation remain central.
Guideline note: NICE and APA guidelines both emphasize psychotherapy as first-line across subtypes; they differ slightly on preferred modality sequencing in adults with AN (CBT-ED vs specialist supportive clinical management), reflecting limited high-quality comparative evidence.
Complications and prognosis
- Cardiac — bradyarrhythmias, QT prolongation, sudden cardiac death; most common cause of death in AN
- Electrolyte — hypokalemia, metabolic alkalosis (purging), refeeding syndrome (hypophosphatemia) during treatment
- Endocrine — amenorrhea, osteopenia/osteoporosis, growth impairment in adolescents
- GI — esophageal tears (Mallory-Weiss), rare esophageal rupture (Boerhaave syndrome), gastroparesis, constipation
- Dental/oral — enamel erosion, dental caries, parotid gland hypertrophy
- Psychiatric — high rates of depression, anxiety, OCD; suicide is a major cause of death in AN
Anorexia nervosa has the highest mortality rate of any psychiatric disorder, with standardized mortality ratios several-fold higher than age-matched peers, due to both medical complications and suicide. Long-term recovery rates for AN are roughly 50%, with the remainder having chronic or relapsing courses. Bulimia nervosa and BED generally have better prognoses with treatment, though relapse is common. Early intervention improves outcomes significantly, particularly in adolescent-onset AN treated with family-based therapy.
SCOFF screening questions: Sick (make yourself Sick), Control (loss of Control over eating), One stone (lost One stone/~14 lb in 3 months), Fat (believe you are Fat), Food (Food dominates your life). Two or more 'yes' answers suggests an eating disorder.
Practice questions
1. A 16-year-old girl is brought in by her parents due to a 20-lb weight loss over 4 months. She exercises for 2 hours daily, restricts intake to under 800 kcal/day, and states she is 'still too fat' despite a BMI of 15.5 kg/m2. Vital signs show HR 42/min and BP 85/55 mmHg. Which of the following is the most likely cause of death if untreated?
2. A 24-year-old woman with normal BMI reports recurrent episodes of eating large quantities of food in under 2 hours, followed by self-induced vomiting, occurring 3 times weekly for the past 4 months. Labs show K+ 3.0 mEq/L and a metabolic alkalosis. Which physical exam finding would most support this diagnosis?
3. A 19-year-old man with anorexia nervosa is admitted for medical stabilization after months of severe caloric restriction. Nutritional rehabilitation begins with cautious caloric reintroduction. Which electrolyte abnormality is most important to monitor closely in the first week to prevent a life-threatening complication?
Frequently asked questions
What causes eating disorders?
Eating disorders result from a combination of genetic predisposition, psychological traits like perfectionism and anxiety, and sociocultural pressure around body image. Twin studies show heritability of 50-80%. Trauma, family dynamics, and participation in weight-sensitive activities (dance, gymnastics, modeling) are additional risk factors. No single cause explains any individual case.
What are the first signs of an eating disorder?
Early signs include preoccupation with calories or weight, skipping meals, rigid food rules, excessive exercise, frequent bathroom trips after meals, and social withdrawal around food. Physical clues can include unexplained weight change, cold intolerance, or dental erosion. Family and friends often notice behavioral changes before significant weight loss occurs.
How is an eating disorder diagnosed?
Diagnosis is clinical, based on DSM-5 criteria assessed through detailed history, physical exam, and screening tools like the SCOFF questionnaire. Labs (electrolytes, ECG, thyroid function) help assess medical severity rather than confirm the diagnosis. A mental health professional typically confirms the specific subtype and comorbidities.
Can eating disorders be cured?
Many people fully recover, especially with early treatment, though eating disorders can also be chronic or relapsing. Roughly half of patients with anorexia nervosa achieve full long-term recovery, while bulimia nervosa and binge-eating disorder generally respond well to cognitive behavioral therapy. Ongoing follow-up reduces relapse risk even after initial recovery.
Anorexia vs bulimia — what is the difference?
Anorexia nervosa involves restriction leading to significantly low body weight, while bulimia nervosa involves binge eating followed by compensatory behaviors like vomiting, usually at normal or near-normal weight. Both share body image distortion and fear of weight gain. Some anorexia patients also binge and purge (binge-eating/purging subtype), creating overlap between the conditions.
Key drugs
Related conditions and differentials
Sources and further reading
StatPearls (NCBI Bookshelf)MedlinePlusWHO ICD-10: F50
Educational content for medical students, prepared by the WhiteCoat Pro editorial team with AI assistance; every page is reviewed by a second AI model for factual errors. It is not medical advice and does not replace the product label, local guidelines or a clinician.