Eating Disorders — Psychiatric Perspective

Non-modifiable (biological) risk

• Genetic loading: first-degree relatives of probands with anorexia nervosa have markedly increased risk; twin heritability is high (see Pathophysiology). Family history of mood, anxiety, or obsessive-compulsive disorder is the association examiners plant most often.
• Female sex and adolescence: peak incidence spans puberty through young adulthood, when estrogen-related changes in serotonin signaling, body composition, and peer comparison converge. Males are affected and systematically underdiagnosed.
• Temperament: harm avoidance, perfectionism, and cognitive rigidity precede illness onset and persist after weight restoration, arguing they are traits rather than starvation effects.
• Type 1 diabetes mellitus: insulin omission for weight control ("diabulimia") is a high-yield, frequently missed presentation; suspect it with recurrent DKA plus poor glycemic control in a young woman.

Modifiable / environmental precipitants

• Dieting and energy restriction: the single strongest modifiable predictor. Restriction destabilizes hypothalamic appetite signaling and sets up the binge–restrict cycle in bulimia nervosa and binge eating disorder.
• Leanness-focused activities: ballet, gymnastics, wrestling, figure skating, distance running, and modeling. Recognize the female athlete triad / relative energy deficiency in sport — low energy availability, menstrual dysfunction, and low bone density.
• Weight-based teasing and appearance-focused social media exposure: repeatedly cited in adolescent stems; internalization of the thin (or, in males, muscular) ideal mediates the effect.
• Childhood adversity: sexual or physical abuse, neglect, and bullying raise risk broadly for bulimia nervosa and binge eating disorder, often with comorbid PTSD or borderline personality traits.
• Family environment: critical or enmeshed interaction patterns and parental dieting behavior. Note the framing endorsed by the American Academy of Pediatrics — families are not the cause and should be enlisted as treatment allies, not blamed.

• Serotonin dysregulation: Altered 5-HT neurotransmission in the hypothalamus and prefrontal cortex affects appetite regulation, impulse control, and mood; SSRIs show modest efficacy suggesting monoamine involvement
• Hypothalamic dysfunction: The lateral hypothalamus (appetite center) and ventromedial hypothalamus (satiety center) show disrupted signaling; orexigenic (NPY, AgRP) and anorexigenic (POMC, CRH) neuropeptides are dysregulated in restriction states
• Genetic predisposition: 56-83% heritability for AN; genome-wide association studies implicate genes related to energy homeostasis, psychiatric comorbidity, and metabolic regulation
• Reward system abnormalities: Altered dopamine signaling in the nucleus accumbens and striatum; dysregulated response to food cues with heightened salience of body-related stimuli
• HPA axis hyperactivation: Elevated cortisol, CRH, and ACTH contribute to restrictive behaviors; cortisol remains elevated even after weight restoration in some cases
• Cognitive distortions: Perfectionism, need for control, and distorted body image involve prefrontal-limbic circuit dysfunction and interoceptive insensitivity
• Sociocultural factors: Media-driven thin ideal, peer influence, and diet culture interact with biological vulnerability to precipitate illness
• Comorbid psychiatric conditions: Up to 80% have concurrent major depression, anxiety disorders, or obsessive-compulsive spectrum disorders that share neurobiological substrates

Anorexia Nervosa (AN) — Restrictive Type vs. Binge-Eating/Purging Type

• Severe restriction of food intake with body weight <85% of expected (or BMI typically <17.5); intense fear of weight gain despite being underweight; distorted body image with denial of illness severity
• Restrictive subtype: Weight loss through caloric restriction and/or excessive exercise; no regular binge-eating or purging behaviors
• Binge-eating/purging subtype: Regular episodes of binge eating and/or purging (self-induced vomiting, laxative abuse, diuretic misuse) despite overall caloric restriction
• Physical signs: Lanugo (fine body hair), bradycardia, hypotension, hypothermia, amenorrhea or oligomenorrhea (in females; delayed puberty in adolescents), downy hair on face/arms, pallor, dry skin, brittle nails, parotid gland enlargement (from vomiting)
• Psychological features: Perfectionism, rigidity, obsessive-compulsive traits, social withdrawal, irritability, depression, anxiety about eating situations, ritualistic eating behaviors
• Laboratory findings: Hypokalemia, hyponatremia, hypomagnesemia (especially with purging), elevated BUN/creatinine ratio (dehydration), anemia, leukopenia, hypoglycemia, elevated LFTs, low T3 syndrome, low cortisol with blunted ACTH response

Bulimia Nervosa (BN)

• Recurrent binge episodes (consuming large amounts of food with loss of control) followed by compensatory behaviors: self-induced vomiting (80-90% of cases), laxative abuse, diuretics, enemas, fasting, or excessive exercise
• Binge episodes typically occur 1-5+ times weekly; marked distress and shame following episodes; normal or near-normal body weight (often BMI 19-25), making diagnosis less obvious
• Purging subtype: Regular self-induced vomiting or laxative/diuretic abuse
• Non-purging subtype: Compensatory fasting or excessive exercise without purging
• Physical signs: Dental erosion and enamel pitting from gastric acid; calluses/scarring on dorsal hand (Russell's sign) from repeated induction of vomiting; parotid enlargement; esophageal reflux symptoms
• Electrolyte abnormalities: Severe hypokalemia (from vomiting or laxative abuse) → cardiac arrhythmias, muscle weakness; metabolic alkalosis (from vomiting) or metabolic acidosis (from laxative abuse); hypochloremia
• Psychological features: Perfectionism, low self-esteem, guilt and shame about eating behaviors, anxiety, depression, impulsivity, higher rates of substance abuse and personality disorders (especially borderline)

Binge Eating Disorder (BED)

• Recurrent binge episodes (at least 1-3 times weekly for ≥3 months) without regular compensatory purging; marked distress about loss of control during binges
• Associated with obesity in ~30-40% of cases, but can occur at any weight; often preceded by strict dieting
• Psychological features: Greater depression and anxiety than general population; lower body dissatisfaction than AN/BN but still significant; associated with impulsivity and emotion dysregulation

General Clinical Pearls

• Amenorrhea in females is now NOT required for AN diagnosis (DSM-5 change), though it remains common in severe restriction
• Eating disorders frequently co-occur with anxiety disorders (particularly social anxiety and generalized anxiety), major depression, OCD, and ADHD
• Males are underdiagnosed due to focus on appearance ideals (muscularity vs. thinness) and less help-seeking behavior
• Age of onset typically 16-20 years for AN and BN; BED often begins in late 20s-30s

DSM-5 Diagnostic Criteria Approach

• Anorexia Nervosa: (1) Restriction of energy intake leading to significantly low body weight; (2) intense fear of weight gain or persistent behaviors that interfere with weight gain; (3) disturbance in perception of body weight/shape, with undue influence on self-evaluation or denial of seriousness of illness. Severity specifier based on BMI: Mild (BMI ≥17), Moderate (16-16.9), Severe (15-15.9), Extreme (<15)
• Bulimia Nervosa: (1) Recurrent binge eating episodes; (2) recurrent compensatory behaviors (purging or non-purging); (3) behavior occurs ≥1x/week for ≥3 months; (4) self-evaluation unduly influenced by body shape/weight; (5) NOT occurring exclusively during AN episodes. Severity specifier based on compensatory behavior frequency: Mild (1-3x/week), Moderate (4-7x/week), Severe (8-13x/week), Extreme (≥14x/week)
• Binge Eating Disorder: (1) Recurrent binge episodes (loss of control + eating large amounts); (2) associated with ≥3 of: rapid eating, eating to discomfort, eating large amounts when not hungry, eating alone, feeling guilty/disgusted/depressed after; (3) marked distress; (4) ≥1x/week for ≥3 months; (5) NOT occurring exclusively during AN/BN/ARFID

Laboratory and Imaging Investigations

• Electrolyte panel (critical): Assess for hypokalemia (K <3.5 mEq/L), hyponatremia, hypomagnesemia, hypocalcemia, hypophosphatemia; hypokalemia is most dangerous and correlates with purging severity
• ECG: Mandatory in all eating disorder patients, especially those with hypokalemia or purging behaviors; assess for prolonged QT interval, ST-segment depression, T-wave inversions, ar

Step 1 — Decide the level of care (medical stabilization first)

• Hospitalize for physiologic instability, per American Psychiatric Association and Society for Adolescent Health and Medicine criteria: marked bradycardia, hypotension, orthostatic vital sign changes, hypothermia, arrhythmia or prolonged QTc, severe electrolyte derangement, hypoglycemia, severe/rapid weight loss, food refusal, or acute suicide risk. Weight alone does not exclude instability — a normal-weight purging patient with hypokalemia is an emergency.
• Correct electrolytes and volume before anything else: replete potassium, and always replete magnesium, since hypomagnesemia makes hypokalemia refractory. Give thiamine before carbohydrate to avoid precipitating Wernicke encephalopathy.
• Refeed low and advance slowly with daily phosphorus, potassium, and magnesium monitoring (ASPEN consensus on refeeding syndrome). Nasogastric feeding if oral intake fails.

Step 2 — Definitive treatment is psychotherapy, not medication

• **Family-based treatment (Maudsley method)**: first-line for adolescents with anorexia nervosa; parents take temporary control of refeeding, then autonomy is returned.
• Enhanced cognitive behavioral therapy (CBT-E): first-line for bulimia nervosa and binge eating disorder in adolescents and adults, and the leading psychotherapy for adult anorexia nervosa along with specialist supportive clinical management.

Step 3 — Pharmacotherapy (adjunctive)

• SSRI — fluoxetine, 60 mg/day: the only FDA-approved drug for bulimia nervosa; the antibulimic dose is higher than the usual antidepressant dose.
• Stimulant prodrug — lisdexamfetamine: FDA-approved for moderate-to-severe binge eating disorder; not for weight loss.
• Atypical antipsychotic — olanzapine: APA suggests it may be considered in anorexia nervosa for weight gain and ruminative preoccupation; effect is modest.
• No drug is approved for anorexia nervosa; antidepressants are ineffective in the malnourished state and should target comorbidity after weight restoration.

Emergencies

• Refeeding syndrome ⚠️: carbohydrate load → insulin surge → intracellular shift of phosphate, potassium, and magnesium plus expansion of extracellular fluid. Signaled by falling serum phosphorus within the first days of refeeding, then heart failure, arrhythmia, rhabdomyolysis, seizures, and hemolysis. Thiamine depletion adds Wernicke encephalopathy. Prevent with slow advancement and electrolyte repletion (ASPEN).
• Hypokalemia-driven arrhythmia ⚠️: from vomiting (hypokalemic, hypochloremic metabolic alkalosis) or laxatives (non-anion-gap metabolic acidosis). QT prolongation → torsades. ECG is mandatory.
• Boerhaave syndrome ⚠️: transmural esophageal rupture from forceful vomiting — chest pain, subcutaneous emphysema, pneumomediastinum. Mallory-Weiss tear is the milder mucosal cousin, presenting with hematemesis.
• Bradyarrhythmia and sudden cardiac death ⚠️: increased vagal tone plus myofibrillar atrophy; bradycardia, hypotension, and pericardial effusion on echo. Suicide is the other leading cause of death.

Chronic disease complications

• Osteopenia/osteoporosis: hypoestrogenemia, hypercortisolemia, and low IGF-1 uncouple bone turnover; stress fractures and low DXA Z-score. Only partially reversible; oral contraceptives do not reliably restore bone.
• Functional hypothalamic amenorrhea and delayed puberty: low leptin → suppressed GnRH pulsatility → low FSH/LH.
• Euthyroid sick (low T3) syndrome: adaptive downregulation, not hypothyroidism — do not treat with levothyroxine.
• Gastroparesis, constipation, superior mesenteric artery syndrome: loss of the aortomesenteric fat pad causes postprandial vomiting and duodenal obstruction.
• **Dental erosion, parotid hypertrophy with elevated salivary amylase, *Russell's sign***: acid and mechanical trauma from purging.
• Pseudo-Bartter syndrome with rebound edema: chronic volume depletion drives hyperaldosteronism; abrupt cessation of purging produces alarming edema that is not treatment failure.
• Cytopenias and gelatinous marrow transformation; hypoglycemia from depleted glycogen and gluconeogenic substrate.

• **Refeeding syndrome is a hypophosphatemia question.** Underweight patient started on nutrition, then confusion, weakness, arrhythmia — the single best next step is check and replete phosphorus (with magnesium and potassium), and give thiamine before glucose. Prevention is slow caloric advancement, not delayed feeding.
• Fluoxetine 60 mg/day is the FDA-approved drug for bulimia nervosa, and the dose is deliberately higher than the depression dose. Bupropion is contraindicated in purging or underweight patients because of seizure risk — that is the classic distractor.
• Lisdexamfetamine is approved for moderate-to-severe binge eating disorder; do not choose it for weight loss or for anorexia nervosa.
• **Adolescent anorexia nervosa → family-based (Maudsley) treatment; bulimia nervosa and binge eating disorder → CBT-E**. No medication is approved for anorexia nervosa, and antidepressants do not work in the starved state.
• Normal BMI does not exclude a life-threatening eating disorder. Bulimia nervosa patients are typically normal weight; hypokalemia and QT prolongation kill them. Russell's sign, dental enamel erosion, parotid hypertrophy, and elevated salivary amylase are the giveaways.
• Vomiting → hypokalemic hypochloremic metabolic alkalosis; laxative abuse → non-anion-gap metabolic acidosis. Persistent hypokalemia that will not correct means unreplaced magnesium.
• Amenorrhea is no longer a DSM-5 criterion for anorexia nervosa, and the diagnosis requires significantly low weight, not a fixed BMI number — a common trap in updated question banks.
• Anorexia nervosa has the highest mortality of any psychiatric illness, split between cardiac/medical causes and suicide. Screen explicitly for suicidal ideation at every visit (American Psychiatric Association).
• Rebound edema after stopping purging reflects pseudo-Bartter physiology, not overfeeding or heart failure — reassure and taper fluids rather than diurese.