is the prototypical restrictive eating disorder and carries the highest standardized mortality ratio of any psychiatric illness, driven by both medical complications of starvation and a markedly elevated suicide rate.1-2 defines it by three features: persistent restriction of energy intake leading to significantly low body weight, intense fear of weight gain or behavior interfering with weight gain, and a disturbance in how body weight or shape is experienced.3 The disorder typically begins in adolescence, affects women more often than men although male cases are under-recognized, and is frequently complicated by depression, anxiety, obsessive-compulsive features, and substance use.1,4 Treatment is medical and psychiatric in parallel: weight restoration through structured nutritional rehabilitation is the foundation, is first-line for adolescents, and no medication has established efficacy for the core illness.5-6 The bottom line is that recognition, early nutritional restoration, and management of refeeding and cardiac risk save lives that pharmacotherapy alone cannot.
Anorexia nervosa is less common than bulimia or but disproportionately consequential because of its mortality and chronicity. Population estimates have risen over the past two decades, partly from broadened DSM-5 criteria and partly from rising incidence in younger cohorts.1,4
Prevalence and incidence
- Lifetime prevalence in women is approximately 0.8-1.4% and in men approximately 0.1-0.3% in pooled community surveys.1,4
- Twelve-month prevalence in adolescent girls is approximately 0.3%.4
- Annual incidence peaks in girls aged 15-19, where it reaches roughly 100-300 per 100,000 person-years.1
Demographic and onset features
- Female-to-male ratio is approximately 10:1 in clinical samples, with community samples suggesting a narrower 3:1 ratio and frequent under-recognition in males.4
- Bimodal age of onset peaks around 14 and 18 years; onset after 25 is uncommon and should prompt scrutiny for medical mimics or atypical presentations.1
- Higher rates among elite athletes (particularly in lean-build sports), ballet dancers, and individuals in occupations emphasizing low weight.7
Comorbidity
- co-occurs in approximately 50-70% of cases over the lifetime.1,4
- , particularly social anxiety and , precede onset in many patients.1
- Substance use disorders are more common in the binge-eating/purging subtype than the restricting subtype.1
- Suicide accounts for roughly one in five deaths in anorexia nervosa.2
Key risk factors
Anorexia nervosa is best understood as a multifactorial disorder in which genetic vulnerability, neurobiological dysregulation of reward and , and sociocultural pressures interact and are then perpetuated by the neuropsychiatric consequences of starvation itself.1,9 Starvation is not just a complication; it changes cognition, mood, and decision-making in ways that lock the illness in place.10
Neurobiology
- Functional imaging shows altered activity in the , anterior cingulate, and striatal reward circuits, with abnormal interoceptive processing and a blunted reward response to palatable food.9
- Serotonergic dysregulation is implicated, with elevated cerebrospinal 5-HIAA after weight recovery suggesting a trait-related hyperserotonergic state contributing to anxiety and harm avoidance.9
- Acute starvation produces structural changes including reduced gray and white matter volume that largely, though not entirely, reverse with weight restoration.11
Genetics
- Twin studies estimate heritability at 50-60%.8
- A 2019 genome-wide association study identified eight significant loci and showed substantial genetic correlation with psychiatric disorders (OCD, depression, anxiety) and with metabolic and anthropometric traits, supporting a metabo-psychiatric conceptualization.12
Environmental and psychological factors
- Sociocultural idealization of thinness, social media exposure, and weight-based teasing increase risk in vulnerable individuals.1
- Perfectionism, cognitive rigidity, and elevated harm avoidance are stable temperament correlates.1
- Childhood adversity, including sexual abuse, raises risk nonspecifically across eating disorders.1
Integrative model
- Vulnerability (genes, temperament, sex) plus a precipitant (diet, life transition, athletic demand) initiates restriction; starvation-induced neurobiological changes and ego-syntonic reinforcement (anxiety reduction, sense of control) maintain the disorder.1,10
DSM-5-TR diagnosis requires three features and is no longer contingent on amenorrhea, a change from DSM-IV that increased recognition in men and in patients on hormonal contraception.3 The clinician's task is to operationalize "significantly low weight" using growth trajectory in young patients and BMI together with course in adults.3,5
Core DSM-5-TR criteria
- Persistent restriction of energy intake relative to requirements, producing a significantly low body weight in the context of age, sex, developmental trajectory, and physical health.3
- Intense fear of gaining weight or becoming fat, or persistent behavior that interferes with weight gain, even when at a significantly low weight.3
- Disturbance in the way one's 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.3
Subtypes (over the past three months)
- Restricting type: weight loss accomplished primarily through dieting, fasting, or excessive exercise without recurrent binge-eating or purging.3
- Binge-eating/purging type: recurrent binge-eating or purging behavior (self-induced vomiting, laxative, diuretic, or enema misuse).3
Severity (adults, based on current BMI)
- Mild: BMI greater than or equal to 17 kg/m^2.3
- Moderate: BMI 16-16.99 kg/m^2.3
- Severe: BMI 15-15.99 kg/m^2.3
- Extreme: BMI less than 15 kg/m^2.3
Course specifiers
- In partial remission: criterion A no longer met for a sustained period, but criterion B or C still present.3
- In full remission: none of the criteria met for a sustained period.3
places anorexia nervosa under "Feeding and Eating Disorders" (6B80) and uses a BMI threshold of less than 18.5 kg/m^2 in adults (or under the fifth percentile in children and adolescents) as part of its operational definition, with a separate code for "anorexia nervosa with dangerously low body weight" at BMI less than 14.13
FEED
Fear of weight gain, Energy intake restricted, Experience of body distorted, Dangerously low weight — the four-point capture of DSM-5-TR anorexia nervosa.
Presentation is rarely a chief complaint of "I have anorexia." Patients more often present with amenorrhea, syncope, bradycardia, fatigue, fertility evaluation, or are brought by a parent who has noticed weight loss and food avoidance.1,5 A high index of suspicion is required because denial and minimization are intrinsic to the illness.1
Behavioral features
- Restrictive eating patterns: rigid food rules, calorie counting, elimination of fat or carbohydrates, ritualized eating (cutting food into tiny pieces, prolonged meals).1
- Compulsive exercise, often performed in secret and continued despite injury, fatigue, or weather.1
- Purging in the binge-eating/purging subtype: self-induced vomiting, laxative, diuretic, or enema misuse.3
- Body checking (frequent weighing, mirror checking, pinching) and body avoidance.1
Cognitive and emotional features
- Overvaluation of weight and shape as the dominant determinant of self-worth.1
- Disturbed body image with distorted perception of size, often focal (abdomen, thighs).1
- Anxiety around eating; depressive symptoms that frequently improve with weight restoration alone.1,10
- Ego-syntonic illness perception, particularly early in course, complicating engagement.1
Physical findings
- Bradycardia (often less than 50 bpm), hypotension, orthostasis, and hypothermia.14
- , dry skin, brittle hair, carotenoderma (yellowing of palms and soles).14
- (callouses on the dorsum of the hand) and parotid hypertrophy in patients who induce vomiting.14
- Amenorrhea or oligomenorrhea, low libido in males, delayed puberty in pre-pubertal patients.1,14
Course
- Prodrome of dieting, perfectionistic striving, or athletic preoccupation often precedes overt restriction by months.1
- Without treatment, course is protracted; approximately 50% achieve full recovery, 30% partial recovery, and 20% develop a chronic course over long-term follow-up.15
CLINICAL SCENARIO: A 16-year-old cross-country runner is brought in by her mother after fainting at practice. Resting HR is 42, BMI 16.4, and she insists she "eats plenty" but has lost 9 kg over four months and tells you, with conviction, that her thighs are still too big. The denial, the bradycardia, and the trajectory together — not the BMI in isolation — are the diagnosis.
The two diagnostic questions are: is this another eating or feeding disorder, and is this a medical illness producing weight loss without the cognitive features of anorexia nervosa.1,5 The cognitive triad — fear of weight gain, body image disturbance, and overvaluation of weight — is what separates anorexia nervosa from medical mimics.3
Other psychiatric disorders
- : recurrent binge eating with compensatory behaviors, but body weight is typically in the normal or overweight range; if criteria for anorexia nervosa are met, anorexia takes precedence.3
- (): food restriction without fear of weight gain or body image disturbance, often driven by sensory aversion, fear of aversive consequences (choking, vomiting), or lack of interest in eating.3
- Major depressive disorder: weight loss may occur, but is secondary to reduced appetite and absent the cognitive overvaluation of weight.3
- Obsessive-compulsive disorder: food-related can mimic restriction, but the content is contamination or symmetry rather than weight or shape.1
- : preoccupation with appearance flaws other than weight, without restrictive eating driving weight loss.3
- or other psychotic disorders: delusional food refusal (e.g., paranoid beliefs about poisoning) lacks the weight-and-shape framing.1
Medical mimics (must be excluded in atypical presentations, late onset, or absence of cognitive features):
- Endocrine: hyperthyroidism, adrenal insufficiency, type 1 diabetes mellitus, hypopituitarism.14
- Gastrointestinal: celiac disease, inflammatory bowel disease, achalasia, superior mesenteric artery (which is also a complication of severe weight loss).14
- Malignancy: lymphoma, gastric and pancreatic cancers — particularly in older patients or rapid weight loss without psychological features.14
- Infectious: HIV, tuberculosis, chronic infection.14
- Neurologic: hypothalamic tumors, Addison disease, frontotemporal dementia in older adults presenting with eating changes.14
- Medication or substance effects: stimulants, , topiramate, methylphenidate misuse.1,14
New-onset food restriction in a patient over 40 should prompt a thorough medical workup before settling on a primary eating disorder diagnosis.5
Assessment is simultaneously psychiatric and medical, and a single missed potassium can be the difference between an outpatient referral and an ICU admission.5,14 The interview should be conducted with the patient alone for at least part of the visit; collateral from family is essential, particularly in adolescents.5
Mandatory history
- Weight history: highest and lowest adult weight, rate and timing of recent loss, growth charts in pediatric patients.5
- Eating patterns: typical day's intake, food rules, fluid intake, "safe" and "forbidden" foods.5
- Compensatory behaviors: vomiting, laxative, diuretic, enema use; exercise type, duration, and intensity.5
- Menstrual history including age of menarche or arrest, contraception (which masks amenorrhea).5
- Psychiatric review including mood, anxiety, OCD features, suicide and self-injury, substance use.5
- Family history of eating disorders, mood disorders, and obesity.1
Physical examination
- Vital signs supine and standing (orthostasis), temperature, weight, height, BMI, growth percentiles.5
- Cardiovascular: bradycardia, murmurs, peripheral perfusion.14
- Skin: lanugo, carotenoderma, Russell's sign, scars, edema.14
- Oral: dental erosion (), parotid hypertrophy.14
- Tanner staging in adolescents to assess pubertal arrest.5
Laboratory and other studies
- CBC (leukopenia, anemia, thrombocytopenia common at low weight).14
- Comprehensive metabolic panel including magnesium and phosphate; phosphate is the single most important refeeding-risk lab.14
- TSH, glucose, liver enzymes.14
- EKG: look for bradycardia, prolonged QTc, low voltage, and signs of electrolyte disturbance.14
- DEXA scan after 6-12 months of amenorrhea or low weight to assess for osteoporosis.5
- Urinalysis (specific gravity flags water-loading); urine pregnancy test where applicable.5
Validated rating scales
- and EDE-Q for symptom severity.5
- as a brief 5-item screen (>=2 positives suggests an eating disorder).16
- Eating Attitudes Test (EAT-26) for screening at-risk populations.5
- MINI or SCID modules to confirm comorbid mood, anxiety, and OCD diagnoses.5
SCOFF
Sick (made yourself), Control (lost over eating), One stone (>14 lb lost in 3 months), Fat (believe yourself to be when others say not), Food (dominates life) — two or more positives warrant further evaluation.16
What NOT to order routinely
Treatment is built around two non-negotiables: medical stabilization and weight restoration.5-6 No medication has established efficacy for the core illness, and psychotherapy without nutritional rehabilitation does not work in a severely underweight patient because starvation itself impairs cognition and the capacity to engage.6,10 Treatment setting (outpatient, partial hospitalization, residential, inpatient medical, inpatient psychiatric) is determined by medical stability, weight, rate of loss, comorbidities, and prior treatment response.5
Pharmacotherapy
- No medication is FDA-approved for the treatment of anorexia nervosa, and evidence for the core syndrome is consistently negative or weak.6,17
- Olanzapine has the strongest evidence among pharmacologic options, with limited evidence suggesting modest weight gain and reductions in obsessive thinking about weight in adults; the 2019 trial by Attia and colleagues demonstrated a small but statistically significant weight benefit over placebo.18
- SSRIs do not improve weight or core eating disorder symptoms in the underweight state; they are used to treat persistent comorbid depression or anxiety after partial weight restoration.6,17
- Bupropion is contraindicated because of seizure risk in patients with eating disorders, particularly those who purge.19
- may be used for pre-meal anxiety but have no disease-modifying role and carry dependence and falls risk.5
Psychotherapy
- Family-based treatment (FBT, the Maudsley approach) is first-line for adolescents and young adults still living with caregivers; strong evidence supports its effect on weight restoration in this group.20
- Enhanced (CBT-E) is recommended for adults; evidence suggests benefit for weight maintenance and reduction in eating disorder cognitions among those who are medically stable enough to engage.21
- The Maudsley Anorexia Nervosa Treatment for Adults (MANTRA) and Specialist Supportive Clinical Management (SSCM) have moderate evidence in adult populations and are recommended by NICE alongside CBT-E.22
- Adolescent-focused therapy (AFT) is an alternative when FBT is not feasible; some experts recommend it for older adolescents with more autonomous functioning, though high-quality evidence is lacking.20
Neuromodulation
- has no role in the treatment of anorexia nervosa per se and is reserved for severe comorbid depression or .5
- and targeting the subcallosal cingulate or nucleus accumbens are investigational; limited evidence suggests possible benefit in severe and enduring anorexia nervosa, but they remain outside routine care.23
Adjunctive
- Nutritional rehabilitation by a registered dietitian, with structured meal plans and supervised meals where feasible, is the operational core of treatment.5
- Bone health: calcium and vitamin D supplementation are recommended; transdermal estradiol with cyclic progesterone improves bone mineral density in adolescents with persistent amenorrhea, whereas oral contraceptive pills do not.24
- Multidisciplinary involvement: psychiatrist, primary care or adolescent medicine, dietitian, therapist, and family members coordinated across settings.5
Refeeding strategy
- Start low and go slow in severely underweight patients (BMI less than 15) to mitigate refeeding syndrome, although more recent evidence suggests that "start low, go slow" can prolong undernutrition and that moderately higher initial calories with close electrolyte monitoring are safe in less-severe presentations.25
- Monitor phosphate, magnesium, and potassium daily during the first week of refeeding; supplement prophylactically when initial phosphate is borderline.14,25
- Cardiac monitoring during initial refeeding in patients with bradycardia, prolonged QTc, or BMI less than 14.14
Refeeding syndrome — characterized by hypophosphatemia, hypokalemia, hypomagnesemia, fluid shifts, and cardiac decompensation — typically occurs in the first 5-7 days of refeeding and is the leading inpatient mortality cause if calories are advanced without electrolyte monitoring.14,25
Treat the starvation, not the depression, first. Mood and anxiety symptoms in underweight patients improve substantially with weight restoration alone, and antidepressant response is poor below approximately 85% of ideal body weight.10
Bupropion lowers seizure threshold and is contraindicated in active eating disorders; verify any patient on bupropion does not have an undisclosed eating disorder history before continuation.19
| Intervention | Evidence base/Comparator | Benefits | Harms | Certainty | Notes |
|---|---|---|---|---|---|
| Family-based treatment (FBT) | RCTs vs adolescent-focused therapy and treatment-as-usual in adolescents | Higher weight restoration and remission at end-of-treatment in adolescents living with family | Family burden; not feasible in high-conflict households | moderate | First-line for adolescents per APA and NICE [5,20] |
| CBT-E | RCTs in medically stable adults vs other psychotherapies | Reduction in eating disorder cognitions; modest weight gain in those who engage | High dropout in severely underweight patients | moderate | Recommended adult first-line option [21,22] |
| MANTRA | RCTs vs SSCM in adults | Comparable outcomes to SSCM and CBT-E in adults | Specialist availability limited | moderate | NICE-recommended adult option [22] |
| SSCM | RCTs vs CBT-E and MANTRA in adults | Comparable adult outcomes; structured supportive framework | Less manualized than alternatives | moderate | NICE-recommended adult option [22] |
| Olanzapine | RCT (Attia 2019) and earlier small trials vs placebo in adults | Small but statistically significant weight gain; reduction in obsessional thinking about weight | Metabolic effects, sedation, EPS | low to moderate | Off-label; not a substitute for nutritional rehabilitation [18] |
| SSRIs (acute underweight) | RCTs vs placebo | No benefit for weight or core symptoms in underweight state | Standard SSRI adverse effect profile | moderate | Reserve for persistent comorbid depression or anxiety after weight gain [6,17] |
| Inpatient weight restoration | Cohort and quasi-experimental data | Reliable weight gain; medical stabilization | Refeeding syndrome risk; institutional dependency | moderate | Indicated for medical instability or failure of outpatient care [5,14] |
| Bone health: transdermal estradiol with cyclic progesterone (adolescents) | RCT data in adolescents with persistent amenorrhea | Improved bone mineral density vs oral contraceptives or no hormonal therapy | Hormonal side effects; does not address weight | moderate | Preferred over oral contraceptives for bone protection [24] |
Anorexia nervosa carries the highest mortality of any psychiatric disorder, with deaths split between medical complications of starvation and suicide.2 The evidence base for treatment, while improving, remains thinner than for mood and anxiety disorders, with persistent gaps for adults, males, and severe and enduring presentations.6,17
Common adverse effects of the illness
- Bradycardia, hypotension, and orthostasis with risk of syncope and cardiac arrhythmia.14
- Electrolyte derangements: hypokalemia and metabolic alkalosis from purging; hypophosphatemia during refeeding.14
- Amenorrhea, infertility, and pubertal arrest.1,14
- Osteoporosis, with elevated fracture risk persisting after recovery.24
- Gastroparesis, constipation, and superior mesenteric artery syndrome.14
- Leukopenia with paradoxically low rates of serious infection despite low counts.14
Serious or rare complications
- Cardiac arrhythmia and sudden cardiac death, particularly with prolonged QTc or refeeding-related shifts.14
- Refeeding syndrome with cardiac failure and Wernicke encephalopathy in the absence of thiamine repletion.25
- Suicide, accounting for approximately 20% of deaths.2
Monitoring, withdrawal, and discontinuation considerations
- Olanzapine should be tapered if discontinued and metabolic parameters monitored throughout use.18
- SSRIs require standard discontinuation tapers if started for comorbid depression.5
- Long-term follow-up is required after weight restoration; relapse rates within one year exceed 30% in many series.15
Limitations of the evidence base
- Most psychotherapy trials enrolled adolescent or young-adult women, limiting generalizability to males and older adults.6,20
- Pharmacotherapy trials have been small, short, and confounded by concurrent psychotherapy and weight gain.17-18
- Severe and enduring anorexia nervosa is under-represented in trial samples that exclude patients below BMI thresholds.6
- Long-term outcome data beyond 5-10 years are sparse for newer interventions.15
The diagnostic and management framework holds across groups, but execution differs meaningfully by age, sex, pregnancy status, and medical comorbidity.5
Pediatric and adolescent
- Use growth charts to define "significantly low weight"; a child who has fallen across percentiles may meet criteria at a BMI above adult thresholds.5
- FBT is first-line; parents are coached to take charge of refeeding initially and transfer control back as recovery progresses.20
- Pubertal arrest and growth failure are reversible only with timely weight restoration.5
- Hospitalize at lower thresholds than adults: heart rate less than 50 daytime or less than 45 nocturnal, orthostatic changes, electrolyte disturbance, or rapid weight loss warrant admission.26
Geriatric
- New-onset restriction in older adults should prompt an exhaustive medical workup before psychiatric attribution.5
- Late-life anorexia nervosa, when present, is often a continuation or recurrence of earlier illness rather than de novo onset.1
- Higher osteoporosis and fall risk amplify the consequences of even moderate weight loss.14
Perinatal
- Active anorexia nervosa increases risk of miscarriage, preterm birth, low birthweight, and small-for-gestational-age infants.27
- Many patients experience symptom reduction during pregnancy followed by postpartum relapse; vigilant follow-up across the perinatal period is required.27
- Olanzapine carries a known pregnancy risk profile (gestational diabetes, large-for-gestational-age); discuss in shared decision-making.5
Comorbid medical illness
- Type 1 diabetes mellitus with insulin restriction ("diabulimia") is associated with markedly elevated mortality and microvascular complications; screen with hemoglobin A1c trends and DKA history.5,14
- Inflammatory bowel disease can confound diagnosis; cognitive features of anorexia nervosa must be present to make the comorbid diagnosis.14
Males
- Often present later and with greater illness severity due to delayed recognition.4
- Drive may emphasize leanness or muscularity rather than thinness alone; consider muscle dysmorphia overlap.1
- Hormonal sequelae include low testosterone, reduced libido, and reduced bone density.14
Cultural considerations
- "Non-fat-phobic" presentations are reported in some non-Western settings, where weight restriction is justified by somatic complaints (bloating, no appetite) rather than fear of fatness; DSM-5-TR accommodates this through behavioral interference with weight gain as an alternative to explicit fear.3
Outcome over the long term is heterogeneous, with a sizable minority recovering fully and a smaller, important group developing a chronic and treatment-resistant course.15
Natural history and recovery
- Pooled long-term follow-up suggests approximately 50% achieve full recovery, 30% partial recovery, and 20% have a chronic course.15
- Adolescents have better outcomes than adults at any given duration of illness, supporting the case for early identification.15,20
- Duration of illness greater than 5-7 years is a poor prognostic indicator and informs the "severe and enduring" framework.6
Relapse
- One-year relapse after inpatient weight restoration exceeds 30% in many series; structured outpatient follow-up reduces this risk.15
- Discharge weight closer to 95% of expected weight reduces short-term relapse compared to lower thresholds.5,26
Mortality
- Standardized mortality ratio is approximately 5-6 in pooled meta-analyses, the highest of any psychiatric disorder.2
- Causes of death are roughly half medical (cardiac, refeeding-related, infection) and one-fifth suicide; the remainder are mixed.2
- Mortality rises with longer illness duration, lower BMI nadir, and comorbid substance use.2
Functional outcome
The two acute questions are: does this patient need a medical bed, and does this patient need a psychiatric bed.5,26 Both can be true at once, and a patient does not need to be at extreme BMI to be in physiologic danger.14
Criteria for medical inpatient admission (one or more):
- Heart rate less than 40 daytime or hemodynamic instability.26
- Hypotension (systolic less than 90 mmHg adult, less than 80 child) or marked orthostasis.26
- Temperature less than 35.5 C (95.9 F).26
- Electrolyte disturbance (potassium less than 3.0, phosphate less than 2.5, magnesium derangement) or arrhythmia.14,26
- BMI less than 15 in adults; weight less than 75% of expected in pediatric patients.5,26
- Rapid weight loss (greater than 1 kg/week sustained), syncope, or acute food refusal.26
- Refusal of all oral intake.26
Suicide risk
- Lifetime suicide attempt rates approach 20-25% in anorexia nervosa.2
- Higher risk in binge-eating/purging subtype, comorbid depression, substance use, and prior attempts.2
- Standard suicide assessment applies; ego-syntonic restriction does not exclude active suicidal ideation, which should be screened explicitly.2
Agitation and capacity
- Severe malnutrition can impair decision-making capacity for treatment refusal; involuntary nutritional treatment may be ethically and legally indicated when capacity is compromised and risk is imminent.5
- Verbal de-escalation and minimal restraint apply; pharmacologic restraint should account for QTc and bradycardia.14
Decision-support and risk-stratification tools do not substitute for clinical judgment in determining suicide or medical risk in anorexia nervosa; the patient with a BMI of 16 and a normal EKG can still die overnight of a refeeding arrhythmia.2,14
Several areas remain contested in eating disorder care, and trainees should be able to discuss the controversies as well as the consensus.6
- Refeeding pace: traditional "start low, go slow" guidance (10-20 kcal/kg/day) is being challenged by trials suggesting that higher initial calorie prescriptions with close electrolyte monitoring are safe in less-severe patients and reduce length of stay; very-low-BMI patients still require conservative initiation.25
- Severe and enduring anorexia nervosa (SE-AN): debate persists over palliative versus curative framing, when to prioritize quality of life over weight restoration, and the ethics of withdrawing aggressive treatment in long-standing illness; consensus criteria have been proposed but are not universally adopted.6
- Olanzapine: the most recent multicenter trial showed a small but statistically significant weight benefit, but effect sizes are modest and routine use is debated given metabolic risks.18
- Compulsory treatment: ethical and legal frameworks vary widely; some experts recommend involuntary nutritional treatment in capacity-impaired patients with imminent risk, though high-quality outcome data are lacking.5-6
- Diagnostic boundary with ARFID: differentiation rests on the cognitive features of anorexia nervosa, but symptom overlap (low weight, restriction) can cause misclassification.3
- Digital and remote-delivered FBT and CBT-E: pandemic-era data suggest non-inferiority for some outcomes, but durability is uncertain.5-6
- Psilocybin and other psychedelics: early open-label trials in anorexia nervosa have shown feasibility but no efficacy signal yet; it is uncertain whether psychedelics have a role.5
- Anorexia nervosa has the highest standardized mortality ratio of any psychiatric disorder, approximately 5-6.2
- DSM-5-TR no longer requires amenorrhea for diagnosis.3
- The two DSM-5-TR subtypes are restricting and binge-eating/purging; subtype is assigned based on the past three months.3
- BMI thresholds for severity in adults are mild (>=17), moderate (16-16.99), severe (15-15.99), and extreme (<15).3
- Family-based treatment (Maudsley approach) is first-line for adolescents.5,20
- Olanzapine has the strongest pharmacologic evidence in adults, with a small effect on weight gain.18
- Bupropion is contraindicated in active eating disorders due to seizure risk.19
- Refeeding syndrome features hypophosphatemia, hypokalemia, hypomagnesemia, and fluid overload, typically in the first week of refeeding.25
- Russell's sign refers to callouses on the dorsum of the hand from self-induced vomiting.14
- Approximately 20% of deaths in anorexia nervosa are due to suicide.2
- Heritability estimates from twin studies range from 50-60%.8
- Bradycardia less than 40 bpm or BMI less than 15 are indications for medical hospitalization.26
- Transdermal estradiol with cyclic progesterone, not oral contraceptives, improves bone mineral density in adolescents with amenorrhea.24
- SSRIs do not improve weight or core eating disorder symptoms in underweight patients.6,17
- The is a 5-item screener with a positive threshold of two or more affirmative answers.16
No external funding. No conflicts of interest declared. Peer-review status: pending.
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- 12.Watson HJ, Yilmaz Z, Thornton LM, et al. Genome-wide association study identifies eight risk loci and implicates metabo-psychiatric origins for anorexia nervosa. Nat Genet. 2019;51(8):1207-1214. doi:10.1038/s41588-019-0439-2. PMID: 31308545.PMID: 31308545doi:10.1038/s41588-019-0439-2
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