Feeding and eating disorders sit at the dangerous intersection of psychiatry and internal medicine, carrying some of the highest mortality rates in all of mental health and demanding fluency in both domains. DSM-5-TR groups Anorexia nervosa, Bulimia nervosa, Binge-eating disorder, Avoidant/restrictive food intake disorder (ARFID), pica, and rumination disorder under a single chapter, reflecting their shared disturbance in eating or feeding behavior despite very different clinical pictures. The clinician's job is to recognize the disorder beneath the patient's presentation, stabilize medical risk, and route toward the treatment with the best evidence — which differs sharply by diagnosis. Family-based treatment leads in adolescent anorexia, cognitive behavioral therapy in bulimia and binge-eating disorder, and refeeding with weight restoration in any patient who is severely malnourished. The bottom line: weigh the body, listen for the cognitions, and never let a normal weight rule out a dangerous illness.

Eating disorders are common, female-predominant, and chronically under-recognized in primary care. Population data are converging on lifetime prevalences in the low single digits for each major disorder, with binge-eating disorder now the most prevalent.

Lifetime prevalence

• Anorexia nervosa affects approximately 0.8% to 1.4% of women and 0.1% to 0.3% of men over the lifetime in pooled international samples.^1-2
• Bulimia nervosa affects approximately 0.9% to 1.5% of women and 0.1% to 0.5% of men.^1-2
• Binge-eating disorder affects approximately 2.8% of women and 1.0% to 1.5% of men, making it the most prevalent eating disorder.^1-3
• ARFID prevalence is estimated at 0.3% to 3.0% in pediatric and community samples, with narrower male-female disparity than the classic eating disorders.^4-5

Age of onset

• Anorexia nervosa typically onsets between ages 14 and 18, with a smaller secondary peak in young adulthood.^2,6
• Bulimia nervosa typically onsets between ages 16 and 20.^2,6
• Binge-eating disorder onsets later, with median age in the early-to-mid 20s and a substantial subset presenting in midlife.^2-3
• ARFID often begins in childhood and may persist into adolescence and adulthood.⁴

Sex and demographic distribution

• Female-to-male ratios are roughly 10:1 for anorexia and bulimia, 2-3:1 for binge-eating disorder, and closer to 1:1 to 2:1 for ARFID.^2-3,5
• Eating disorders occur across racial, ethnic, and socioeconomic groups; longstanding assumptions of a white, affluent demographic have been refuted by community-based studies.⁷
• Sexual and gender minority youth — particularly transgender individuals — show elevated rates of disordered eating relative to cisgender peers.^7-8

Comorbidity

• Major depressive disorder, anxiety disorders, and obsessive-compulsive disorder co-occur in over half of patients with anorexia nervosa.^2,6
• Bulimia nervosa shows particularly high rates of substance use disorders, borderline personality disorder, and impulse-control problems.^2,9
• Binge-eating disorder is strongly associated with obesity, metabolic syndrome, and mood disorders.^3,10
• Suicide is the second leading cause of death in anorexia nervosa, with standardized mortality ratios for suicide exceeding 18 in some long-term cohorts.¹¹

Key risk factors

• Female sex, adolescence, prior dieting behavior, and elite athletic or aesthetic-sport participation increase risk.^6,12
• Childhood trauma — particularly sexual abuse — is associated with bulimic and binge-eating phenotypes more than restrictive ones.¹²
• Type 1 diabetes mellitus carries a markedly elevated risk for eating disorders involving insulin omission (so-called diabulimia).¹³

Eating disorders arise from interacting genetic, neurobiological, developmental, and sociocultural inputs, and no single model captures all phenotypes. Recent work has reframed anorexia nervosa in particular as a metabo-psychiatric illness rather than a purely psychological one.¹⁴

Genetics

• Twin studies estimate heritability of anorexia nervosa at approximately 50% to 60%, with similar ranges for bulimia nervosa and binge-eating disorder.^14-15
• The 2019 genome-wide association study of anorexia nervosa identified eight significant loci and demonstrated genetic correlations with both psychiatric traits (OCD, anxiety, depression) and metabolic traits (BMI, insulin sensitivity, HDL cholesterol).¹⁴
• This metabo-psychiatric signature is one reason patients with anorexia nervosa lose weight more readily than controls and regain it less easily — the genetic architecture appears to drive a low-weight set point.¹⁴

Neurobiology

• Serotonergic dysregulation, particularly altered 5-HT1A and 5-HT2A receptor function, has been demonstrated in patients with anorexia and bulimia using PET imaging.¹⁶
• Dopaminergic abnormalities in reward circuitry — involving the ventral striatum and orbitofrontal cortex — contribute to the altered reward valuation of food in anorexia nervosa and the binge-driving food-cue reactivity seen in bulimia and binge-eating disorder.^16-17
• Insular cortex hyperactivity and altered interoceptive processing distinguish patients with anorexia, who consistently misread internal hunger and satiety signals.¹⁷
• Structural imaging shows gray matter volume reduction during acute starvation that largely reverses with weight restoration, though some persistent differences in cortical thickness have been reported.¹⁷

Environmental and developmental factors

• Cultural thin-ideal internalization, social media exposure, and weight-related teasing are robust risk factors, particularly for bulimic and binge-eating phenotypes.^6,12
• Perfectionism and obsessive-compulsive personality traits are overrepresented in anorexia nervosa and often predate the illness.^6,18
• Family environment alone does not cause eating disorders; the historical model of the "anorexogenic family" has been discredited and replaced by family-as-resource frameworks like family-based treatment.¹⁹

Integrative current model

• Most contemporary models propose that genetic and neurobiological vulnerability sets a low threshold for dietary restriction, binge-purge cycles, or food avoidance, which is then triggered by dieting, stress, or developmental transitions and maintained by reinforcing neurocircuit and metabolic changes.^14,17
• Starvation itself produces obsessionality, food preoccupation, and mood symptoms — documented since the Minnesota Starvation Experiment — making the malnourished state a self-perpetuating driver of illness.²⁰

DSM-5-TR organizes feeding and eating disorders into six principal diagnoses, with specifiers that capture subtype, severity, and remission status. Two simultaneous diagnoses from this chapter are not permitted; the most severe presentation takes precedence.²¹

Anorexia nervosa

• Persistent restriction of energy intake leading to significantly low body weight relative to age, sex, developmental trajectory, and physical health.²¹
• Intense fear of gaining weight or becoming fat, or persistent behavior that interferes with weight gain, even at a significantly low weight.²¹
• Disturbance in the way body weight or shape is experienced, undue influence of weight or shape on self-evaluation, or persistent lack of recognition of the seriousness of the current low body weight.²¹
• Subtypes (over the past three months): restricting type (no recurrent binge-purge behavior) and binge-eating/purging type.²¹
• Severity is based on current BMI in adults: mild (≥17), moderate (16-16.99), severe (15-15.99), extreme (<15).²¹
• DSM-5-TR no longer requires amenorrhea — a change from DSM-IV that broadened diagnostic reach.²¹

Bulimia nervosa

• Recurrent episodes of binge eating, defined by both eating in a discrete period an amount of food larger than most people would eat, and a sense of loss of control during the episode.²¹
• Recurrent inappropriate compensatory behaviors to prevent weight gain — vomiting, laxatives, diuretics, fasting, or excessive exercise.²¹
• Binges and compensation occur on average at least once per week for three months.²¹
• Self-evaluation is unduly influenced by body shape and weight, and the disturbance does not occur exclusively during episodes of anorexia nervosa.²¹
• Severity is based on weekly frequency of compensatory behaviors: mild (1-3), moderate (4-7), severe (8-13), extreme (≥14).²¹

Binge-eating disorder

• Recurrent binge eating episodes meeting the same dual definition as in bulimia.²¹
• Episodes are associated with at least three of: eating rapidly, eating until uncomfortably full, eating when not physically hungry, eating alone due to embarrassment, and feeling disgusted, depressed, or guilty afterward.²¹
• Marked distress regarding binge eating.²¹
• Occurs on average at least once per week for three months.²¹
• No recurrent inappropriate compensatory behavior, and not exclusively during the course of bulimia nervosa or anorexia nervosa.²¹
• Severity is based on weekly binge frequency: mild (1-3), moderate (4-7), severe (8-13), extreme (≥14).²¹

Avoidant/restrictive food intake disorder (ARFID)

• A disturbance in eating or feeding manifested by persistent failure to meet appropriate nutritional or energy needs, associated with one or more of: significant weight loss or growth failure, significant nutritional deficiency, dependence on enteral feeding or oral supplements, or marked interference with psychosocial functioning.²¹
• Not better explained by lack of available food or a culturally sanctioned practice.²¹
• Does not occur exclusively during anorexia or bulimia and is not associated with disturbance in body image.²¹
• Not attributable to a concurrent medical condition or better explained by another mental disorder.²¹
• Three commonly described clinical presentations are sensory-based avoidance, lack of interest in eating, and fear of aversive consequences (such as choking or vomiting), though these are not formal subtypes.^4,21

Pica and rumination disorder

• Pica: persistent eating of nonnutritive, nonfood substances for at least one month, inappropriate to developmental level and not part of a culturally supported practice.²¹
• Rumination disorder: repeated regurgitation of food for at least one month, with re-chewing, re-swallowing, or spitting out, not attributable to a gastrointestinal or other medical condition.²¹

Other and unspecified

• Other specified feeding or eating disorder (OSFED) captures clinically significant presentations that do not meet full criteria, including atypical anorexia (all features of anorexia but weight remains in or above the normal range), purging disorder, and night eating syndrome.²¹
• Unspecified feeding or eating disorder is used when the clinician chooses not to specify or has insufficient information.²¹

The phenotypes diverge sharply at the bedside even though all share an eating-related core disturbance. Recognizing the prototypical and atypical presentations is the difference between catching the disorder at first contact and missing it for years.

Anorexia nervosa, prototypical presentation

• Adolescent or young adult woman with low BMI, often presenting via a parent's concern, a sports physical, or a primary care visit for amenorrhea or fatigue.⁶
• Restrictive eating with rigid food rules, ritualized eating behaviors, and compensatory exercise.⁶
• Cognitive features include relentless drive for thinness, body-image distortion, denial of medical severity, and pervasive food preoccupation.^6,20
• Physical signs: bradycardia, hypotension, hypothermia, lanugo, dry skin, alopecia, parotid hypertrophy if purging, and Russell sign (knuckle calluses) in self-induced vomiting.²³

Bulimia nervosa, prototypical presentation

• Normal-weight or slightly overweight woman in late adolescence or young adulthood, presenting with shame-laden disclosure of binge-purge cycles.⁶
• Binges often involve thousands of calories of palatable foods consumed in secret.⁶
• Compensatory behaviors include self-induced vomiting (most common), laxative misuse, diuretic misuse, fasting, and exercise.⁶
• Physical signs: parotid hypertrophy, dental enamel erosion (perimolysis), Russell sign, calluses on dorsum of hand, esophagitis, and electrolyte abnormalities.²³

Binge-eating disorder, prototypical presentation

• Adult of either sex, often with overweight or obesity, presenting via weight-loss seeking or routine primary care.³
• Binges occur without compensation, are associated with shame, and frequently coexist with depression.^3,10
• Subjective loss of control is the cognitive hallmark; the discrete-period quantity criterion can mask high-frequency grazers who functionally binge.³

ARFID, prototypical presentations

• Sensory subtype: a child or adolescent with extreme selectivity (color, texture, brand), often with overlapping autism spectrum features.^4-5
• Low-appetite subtype: failure to thrive or weight loss without psychological preoccupation with shape or weight.⁴
• Fear-based subtype: abrupt food refusal following choking, vomiting, or allergic reaction.⁴

Red flags requiring urgent action

• Severe bradycardia (HR <40), orthostatic hypotension, hypothermia, or arrhythmia.²⁴
• Potassium <3.0 mEq/L, sodium <125 mEq/L, phosphate <2.5 mg/dL, or magnesium below normal.²⁴
• BMI <15 in adults, <70% of expected body weight in children and adolescents, or acute weight loss >1 kg/week sustained.²⁴
• Syncope, seizure, hematemesis, or suicidal ideation with plan.²⁴

Eating disorders mimic — and are mimicked by — a long list of medical and psychiatric conditions. Anchoring on cognitions (fear of weight gain, body-image disturbance, loss-of-control eating) and on compensatory behaviors is the most reliable way to discriminate.

Medical mimics of weight loss or restrictive eating:

• Hyperthyroidism: weight loss with increased appetite, tremor, tachycardia; TSH and free T4 differentiate.⁶
• Inflammatory bowel disease, celiac disease, malabsorption syndromes: weight loss with GI symptoms and abnormal labs.⁶
• Type 1 diabetes mellitus: weight loss with polyuria, polydipsia, hyperglycemia.¹³
• Malignancy, chronic infection (HIV, tuberculosis), Addison disease: weight loss with systemic features.⁶
• CNS lesions (hypothalamic tumor, brainstem lesion): weight loss without the cognitive features of anorexia.⁶

Psychiatric differentials

• Major depressive disorder with reduced appetite: weight loss is a byproduct of anhedonia, not driven by fear of weight gain or body-image distortion.⁶
• Obsessive-compulsive disorder with food contamination obsessions: avoidance is driven by contamination fear, not weight concern.⁶
• Avoidant/restrictive food intake disorder: restriction without body-image disturbance or weight-gain fear is the cardinal distinction from anorexia.^4,21
• Body dysmorphic disorder: preoccupation with a non-weight body feature; can coexist.²¹
• Psychotic disorders with food-related delusions: bizarre beliefs about food (e.g., poisoning) drive avoidance, with other psychotic features.⁶

Substance-related differentials

• Stimulant use disorder: weight loss with appetite suppression, sympathomimetic signs, and a positive history.⁶
• Cannabis withdrawal can suppress appetite, opioid use can drive binging through reward dysregulation.⁶

Pediatric-specific differentials

• Failure to thrive of medical origin: organic causes must be excluded before ARFID is diagnosed.⁴
• Selective eating in autism spectrum disorder: overlap with ARFID is significant; ARFID is diagnosed when impairment exceeds what autism alone would predict.^4,21

Assessment of suspected eating disorder integrates a focused psychiatric interview, a targeted physical exam, validated screening and severity measures, and selective laboratory and ECG workup. Skipping any one of these is how patients deteriorate undetected.

History — mandatory elements

• Weight history: highest, lowest, premorbid, and rate of recent change.⁶
• Eating behavior: typical 24-hour intake, food rules, forbidden foods, binge episodes (objective vs. subjective).⁶
• Compensatory behaviors: vomiting, laxatives, diuretics, diet pills, fasting, exercise — frequency and onset.⁶
• Body-image cognitions: fear of weight gain, body-checking, body-avoidance, shape and weight overvaluation.⁶
• Menstrual history in females, sexual function in males, exercise history including compulsive features.⁶
• Substance use, prior treatment, family history of eating disorders or other psychiatric illness.⁶

Physical examination

• Vital signs including orthostatic measurements; significant orthostasis is a hospitalization indicator.²⁴
• Weight, height, BMI, and growth percentiles in children and adolescents; obtain weight in a gown after voiding.²⁴
• Skin and mucous membranes: lanugo, hypercarotenemia, perimolysis, Russell sign.²³
• Cardiovascular: bradycardia, hypotension, murmurs (mitral valve prolapse in chronic anorexia).²⁴
• Mental status including suicidal ideation.⁶

Validated rating scales

• Eating Disorder Examination-Questionnaire (EDE-Q): 28-item self-report covering restraint, eating concern, shape concern, weight concern.²⁵
• SCOFF questionnaire: 5-item screening tool; ≥2 affirmative answers warrants further evaluation.²⁶
• Eating Disorder Inventory-3 (EDI-3): broader self-report covering eating-disorder-specific and general psychological scales.²⁵
• Eating Disorder Examination (EDE): semi-structured interview considered the gold-standard diagnostic measure.²⁵

Laboratory workup

• CBC: leukopenia, anemia, and thrombocytopenia in advanced malnutrition.²⁷
• Comprehensive metabolic panel: hypokalemia (purging), hyponatremia (water loading), elevated BUN (dehydration), hypoglycemia (severe restriction), low albumin (late finding).²⁷
• Magnesium, phosphate, calcium — phosphate is critical before and during refeeding.^27-28
• TSH and free T4, urinalysis, urine pregnancy test in females of reproductive age.²⁷
• ECG: prolonged QTc, bradycardia, low voltage, T-wave changes; obtain in any moderate-to-severe presentation.^24,27
• DXA scan after 6-12 months of amenorrhea to assess bone mineral density.²⁷

What not to order

• Routine brain imaging is not indicated unless atypical features (neurological signs, late onset, absence of body-image disturbance) suggest an intracranial process.⁶
• Serum gonadotropins, LH/FSH, and estradiol are not required for diagnosis; functional hypothalamic amenorrhea is expected in anorexia nervosa.²⁷

Treatment is diagnosis-specific. Anorexia nervosa is the only major eating disorder for which psychotherapy outperforms pharmacotherapy at the headline level; bulimia and binge-eating disorder respond to both. Weight restoration in anorexia is the prerequisite for everything else.

Pharmacotherapy

• Anorexia nervosa: no medication has consistently demonstrated efficacy for weight restoration or relapse prevention; SSRIs are not effective in the underweight state and are not first-line.^29-30
  • Low-dose olanzapine (2.5-10 mg/day) has shown modest benefit for weight gain in adults with anorexia nervosa in randomized trials, though effects are small and metabolic harms must be weighed.³¹
  • SSRIs may be used for comorbid mood or anxiety disorders after weight restoration is underway, where their efficacy returns.^29-30
• Bulimia nervosa: fluoxetine 60 mg/day is FDA-approved and reduces binge-purge frequency by approximately 50-70%; this is the only psychotropic with an FDA indication for bulimia.^29,32
  • Other SSRIs, SNRIs, and topiramate have demonstrated benefit in smaller trials but lack FDA approval.^29,32
  • Bupropion is contraindicated in patients with bulimia nervosa or anorexia nervosa due to elevated seizure risk.³³
• Binge-eating disorder: lisdexamfetamine (50-70 mg/day) is FDA-approved for moderate-to-severe BED in adults and reduces binge frequency; topiramate also reduces binge frequency but is limited by adverse effects.^29,34
  • SSRIs reduce binge frequency modestly but do not produce meaningful weight loss.²⁹
• ARFID, pica, rumination disorder: no FDA-approved pharmacotherapy; case reports support specific agents in particular subtypes.⁴

Psychotherapy

• Anorexia nervosa in adolescents: family-based treatment (FBT, Maudsley method) is the first-line intervention, with strong evidence for weight restoration at 12 months versus individual therapies.^35-36
  • FBT proceeds in three phases: parental control of refeeding, gradual return of control to the adolescent, and establishment of healthy adolescent identity.³⁵
• Anorexia nervosa in adults: evidence is more modest, with CBT-E (enhanced cognitive behavioral therapy), MANTRA (Maudsley model for adults), and SSCM (specialist supportive clinical management) showing comparable outcomes in head-to-head trials.³⁷
• Bulimia nervosa: CBT-BN (or CBT-E) is the first-line intervention, with the largest effect sizes for symptom reduction and durable remission.^38-39
  • Interpersonal psychotherapy (IPT) is a comparably effective second-line option, with slower onset of action.³⁸
• Binge-eating disorder: CBT and IPT both demonstrate strong efficacy; CBT-E is broadly considered first-line.^38,40
• ARFID: cognitive behavioral therapy adapted for ARFID (CBT-AR) and family-based interventions show promise; evidence base remains limited.⁴

Neuromodulation

• Repetitive transcranial magnetic stimulation (rTMS) targeting the dorsolateral prefrontal cortex has shown small effects on eating-disorder symptoms in early trials but is not standard of care.⁴¹
• Deep brain stimulation for severe and enduring anorexia nervosa remains investigational.⁴¹
• ECT is not indicated for eating disorders themselves and is reserved for severe comorbid depression with standard indications.⁴²

Adjunctive

• Medical stabilization and refeeding: inpatient or partial hospital level of care for any patient meeting acute medical criteria.²⁴
  • Initial refeeding caloric prescription has historically been conservative (1,000-1,200 kcal/day) but contemporary evidence supports more aggressive starts (1,500-2,000 kcal/day) in non-extreme malnutrition with vigilant electrolyte monitoring.^28,43
  • Phosphate supplementation is recommended prophylactically when serum phosphate is in the low-normal range or trending down.²⁸
• Nutritional rehabilitation by a registered dietitian with eating-disorder expertise is essential across diagnoses.²⁴
• Bone health: weight restoration is the most effective intervention for bone density in anorexia; transdermal estradiol with cyclic progestin has demonstrated efficacy in adolescents, whereas oral contraceptives have not.⁴⁴
• Treatment of comorbid mood, anxiety, OCD, and substance use disorders proceeds in parallel.⁶

Eating disorders carry medical risks that rival any condition in psychiatry, and the treatments themselves require careful monitoring. The evidence base is also more limited than the clinical urgency of these disorders would suggest.

Common adverse effects of treatment

• SSRIs: nausea, sexual dysfunction, weight gain or loss, insomnia, and discontinuation symptoms.²⁹
• Olanzapine: weight gain, sedation, dyslipidemia, hyperglycemia, and rare extrapyramidal symptoms.³¹
• Lisdexamfetamine: insomnia, decreased appetite, headache, tachycardia, and elevated blood pressure.³⁴
• Topiramate: cognitive dulling (word-finding difficulty), paresthesias, weight loss, kidney stones, and metabolic acidosis.³²

Serious or rare adverse effects

• Refeeding syndrome with cardiac arrhythmia, heart failure, and death if electrolytes are not monitored aggressively.²⁸
• SSRI-associated suicidality in adolescents — the FDA black-box warning applies.²⁹
• Stimulant misuse and diversion with lisdexamfetamine, particularly in patients with comorbid substance use.³⁴
• QTc prolongation with multiple eating disorder medications combined with the baseline QT prolongation of severe anorexia.²⁴

Monitoring and discontinuation

• Daily weight, vital signs, and electrolytes during inpatient refeeding; weekly during the first month of outpatient treatment.^24,28
• Bone density (DXA) every 1-2 years in patients with persistent low weight or amenorrhea.²⁷
• Cardiac monitoring (ECG, telemetry) in severe malnutrition.²⁴
• SSRI discontinuation should be gradual to avoid discontinuation syndrome.²⁹

Limitations of the evidence base

• Long-term outcome data beyond 5 years are sparse for all eating disorders.³⁶
• Anorexia nervosa trials are limited by small samples, high dropout rates, and challenges in blinding nutritional interventions.³⁶
• Most psychotherapy trials enroll female participants; generalizability to males, transgender individuals, and racial/ethnic minorities is limited.⁷
• ARFID treatment evidence is in its infancy, with few RCTs available.⁴

Pediatric and adolescent

• Anorexia nervosa in prepubertal children may present with growth failure rather than weight loss; expected weight for height must be calculated from growth curves.²⁴
• FBT is the dominant evidence-based intervention; adolescent-focused therapy is an alternative when family involvement is impossible.³⁵
• Bone health is a particular concern given peak bone mass accrual occurs during adolescence; transdermal estradiol replacement is favored over oral contraceptives in this population.⁴⁴

Geriatric

• Late-onset eating disorders do occur and are often missed; midlife and older-adult presentations may be triggered by bereavement, divorce, or medical illness.⁶
• Weight loss in older adults must be differentiated from malignancy, dementia-related anorexia, and depression with weight loss.⁶

Perinatal

• Pregnancy may transiently suppress or exacerbate eating disorder symptoms; postpartum relapse rates are high.⁴⁵
• Active eating disorder in pregnancy is associated with hyperemesis, intrauterine growth restriction, preterm delivery, and postpartum depression.⁴⁵
• SSRIs and other psychotropics in pregnancy require individualized risk-benefit discussion.⁴⁵

Comorbid medical illness

• Type 1 diabetes with insulin omission ("diabulimia") confers very high mortality and accelerated microvascular complications; collaborative endocrine-psychiatric care is essential.¹³
• Inflammatory bowel disease, celiac disease, and gastroparesis can co-occur with ARFID-like avoidance and complicate management.⁴

Comorbid substance use

• Bulimia nervosa carries the highest rates of comorbid substance use among eating disorders; integrated treatment is recommended.^2,9
• Stimulant-use disorders may emerge from misuse of prescribed stimulants for binge-eating disorder.³⁴

Cultural and identity considerations

• Eating disorders occur across all racial, ethnic, and socioeconomic groups; symptom expression may differ (less explicit fat-phobia in some non-Western cohorts).⁷
• Sexual and gender minority youth, particularly transgender adolescents, experience elevated rates of disordered eating, with gender dysphoria sometimes intertwined with body-image disturbance.^7-8

Long-term outcomes for eating disorders span a wide range, from full recovery to chronic disability and death. Anorexia nervosa carries the highest mortality of any psychiatric disorder, and bulimia and binge-eating disorder follow chronic relapsing-remitting courses.

Anorexia nervosa

• Approximately 50% of patients achieve full recovery, 30% partial recovery, and 20% develop a chronic course over 10-20 year follow-up.⁴⁶
• Crude mortality rate is approximately 5% per decade of illness, with standardized mortality ratio approximately 5-6 times the general population.^11,46
• About half of deaths are from medical complications and approximately one-quarter from suicide.¹¹
• Predictors of poor outcome include long illness duration before treatment, very low weight at presentation, binge-purge subtype, comorbid OCD, and adult (vs. adolescent) onset.⁴⁶

Bulimia nervosa

• Approximately 45-55% achieve full recovery, 30% partial recovery, and 20% develop a chronic course.⁴⁷
• Crude mortality is lower than anorexia but elevated over the general population.⁴⁷
• Diagnostic crossover is common; up to one-third migrate to other eating disorder diagnoses over a decade.⁴⁷

Binge-eating disorder

• Course is generally chronic with periods of remission; spontaneous remission is more common than in AN or BN.³
• Long-term outcomes are heavily influenced by comorbid obesity and metabolic complications.^3,10

ARFID:

• Course is variable; some children outgrow restrictive patterns while others persist into adulthood, particularly the sensory subtype.⁴
• Long-term outcome data are limited.⁴

Recognizing the unstable eating-disorder patient is a core competency. Several presentations require immediate medical hospitalization, not outpatient referral.

Criteria for medical hospitalization in anorexia nervosa:

• Heart rate <40 bpm in adults or <50 bpm in adolescents, or symptomatic bradycardia.²⁴
• Systolic BP <80 mmHg in adults, <90 in adolescents, or orthostatic drop >20 mmHg.²⁴
• Hypothermia (<35.5°C), hypoglycemia, or significant electrolyte abnormality.²⁴
• BMI <15 in adults, <75% of expected body weight in children and adolescents.²⁴
• Acute medical complication (syncope, seizure, cardiac arrhythmia, hematemesis).²⁴
• Failure of outpatient treatment with continued weight loss.²⁴

Criteria for psychiatric hospitalization

• Active suicidal ideation with plan or intent.⁶
• Inability to break severe binge-purge cycle in outpatient or partial hospital setting.⁶
• Severe comorbid psychiatric illness requiring inpatient care.⁶

Agitation and refeeding distress

• Refeeding can provoke intense anxiety, body-image distress, and behavioral resistance.²⁰
• Behavioral plans (meal supervision, post-meal monitoring, validation-based intervention) take priority over PRN anxiolytics; benzodiazepines are not first-line for refeeding anxiety.²⁴
• Involuntary treatment is occasionally necessary for life-threatening anorexia and is supported by case law and specific statutes in many jurisdictions, though ethical considerations are substantial.⁴⁸

Suicide risk

• Suicide is the second leading cause of death in anorexia nervosa and a major cause in bulimia nervosa.¹¹
• Routine suicide risk assessment is mandatory at every clinical encounter.⁶

Several debates shape contemporary eating disorder practice, and trainees should be conversant with them.

Atypical anorexia and weight criteria

• DSM-5-TR retains "significantly low weight" as a criterion for anorexia nervosa, but atypical anorexia (OSFED) — with all anorexia features at higher weights — carries comparable medical and psychiatric morbidity.⁴⁹
• Whether weight criteria should be removed from anorexia altogether remains debated.⁴⁹

Refeeding pace

• Historical "start low, go slow" guidance is being challenged by RCTs supporting more aggressive caloric initiation with intensive monitoring.^28,43
• Optimal refeeding rates in extreme malnutrition (BMI <13) remain less well established.²⁸

Pharmacotherapy in anorexia nervosa

• The role of olanzapine remains contested; modest weight benefit must be weighed against metabolic risks in young patients facing lifelong cardiometabolic exposure.³¹
• No medication has emerged as a clear first-line agent.^29-30

Severe and enduring anorexia nervosa (SE-AN)

• Whether to pursue palliative or harm-reduction approaches for patients with decade-long refractory illness is among the most ethically charged questions in eating disorder care, with no consensus on criteria for transitioning from curative to palliative goals.⁵⁰

Diagnostic boundaries

• The distinction between binge-eating disorder and obesity with overeating, and between ARFID and "picky eating" or autism-related selectivity, remains clinically and conceptually fuzzy in clinical practice.^4,21

Emerging therapies

• Psychedelic-assisted therapy (psilocybin, MDMA) for anorexia nervosa is in early-phase trials with no established efficacy or safety profile in this population.⁵¹
• Neuromodulation approaches (rTMS, DBS) remain investigational.⁴¹

• Anorexia nervosa has the highest mortality rate of any psychiatric disorder, with crude mortality of approximately 5% per decade and SMR of about 5-6.^11,46
• DSM-5-TR removed amenorrhea as a criterion for anorexia nervosa.²¹
• Fluoxetine 60 mg/day is the only FDA-approved psychotropic for bulimia nervosa.³²
• Lisdexamfetamine is the only FDA-approved psychotropic for moderate-to-severe binge-eating disorder in adults.³⁴
• Bupropion is contraindicated in patients with bulimia nervosa or anorexia nervosa due to seizure risk.³³
• Family-based treatment (Maudsley method) is first-line for adolescent anorexia nervosa.^35-36
• CBT-E is first-line for bulimia nervosa and binge-eating disorder.^38-39
• Refeeding syndrome features hypophosphatemia, hypokalemia, hypomagnesemia, thiamine deficiency, and fluid overload, and can be fatal.²⁸
• Russell sign — knuckle calluses from self-induced vomiting — is a physical clue to purging behavior.²³
• Suicide is the second leading cause of death in anorexia nervosa.¹¹
• ARFID, unlike anorexia nervosa, does not involve body-image disturbance or fear of weight gain.²¹
• Atypical anorexia (OSFED) carries comparable medical risk to anorexia nervosa despite normal or elevated weight.⁴⁹
• The Minnesota Starvation Experiment demonstrated that starvation alone produces obsessionality, food preoccupation, and mood symptoms — supporting weight restoration as foundational treatment.²⁰
• Olanzapine has modest evidence for weight gain in anorexia nervosa but is not first-line.³¹
• Diabulimia — insulin omission in type 1 diabetes — carries very high mortality and accelerated microvascular complications.¹³

No external funding. No conflicts of interest declared. Peer-review status: pending.