Eating Disorders

Non-modifiable (biological) factors

• Family history/heritability: first-degree relatives of probands have markedly increased risk; twin heritability is high (see Pathophysiology). A relative with an eating disorder, OCD, or an anxiety disorder in the stem is the intended clue.
• Female sex and adolescence: peak onset is mid-to-late adolescence for AN and late adolescence/early adulthood for BN, coinciding with puberty-related fat redistribution and identity formation. Male cases are underdiagnosed and often present as drive for muscularity.
• Temperament: perfectionism, harm avoidance, and rigid cognitive style predispose to restrictive AN; impulsivity, affective instability, and cluster B traits cluster with BN and binge-purge behavior.
• Psychiatric comorbidity: major depression, anxiety/OCD, PTSD, and substance use disorders are strongly associated and worsen prognosis.

Modifiable / environmental factors

• Dieting and weight-loss attempts: the single most consistent behavioral antecedent — caloric restriction destabilizes reward and satiety signaling and initiates the binge–restrict cycle.
• Weight-focused activities: ballet, gymnastics, figure skating, distance running, wrestling, and modeling; sport-specific weight targets are the classic stem detail.
• Weight-related teasing, bullying, and appearance-focused social media exposure; family preoccupation with weight or dieting.
• Childhood adversity: physical or sexual abuse and neglect, particularly associated with bulimic and binge-eating presentations.
• Type 1 diabetes mellitus: insulin omission for weight control is a recognized purging behavior; the ADA Standards of Care recommend screening for disordered eating in youth and adults with diabetes when glycemic control is unexplainedly poor with recurrent DKA.
• Weight stigma and history of overweight/obesity: a risk pathway for binge eating disorder, whose behaviors then perpetuate weight gain.

Screening context

• The USPSTF (2022) concluded that evidence is insufficient to recommend universal screening for eating disorders in asymptomatic adolescents and adults, so case finding rests on the risk factors above; the AAP endorses attention to disordered eating at adolescent preventive visits.

• Genetic factors: Twin studies demonstrate 50-80% heritability; specific genes affecting serotonin, dopamine, and peptide signaling (NPY, AgRP, POMC pathways) are implicated
• Serotonin dysregulation: Reduced 5-HT1A and 5-HT2A receptor binding in prefrontal and anterior cingulate cortex; contributes to impulsivity, anxiety, and mood disturbance
• Hypothalamic-pituitary-adrenal (HPA) axis hyperactivity: Chronic stress response with elevated cortisol; suppresses appetite-stimulating neuropeptides (ghrelin, NPY) and enhances appetite-suppressing signals (leptin, CRH)
• Reward system dysfunction: Altered dopaminergic signaling in nucleus accumbens and ventral tegmental area; reduced pleasure response to food and other stimuli
• Cognitive distortions: Perfectionism, rigidity, and obsessive-compulsive traits mediated by hyperactivity in anterior insula and prefrontal regions
• Nutritional depletion effects: Starvation induces metabolic slowdown, reduced thermogenesis, electrolyte abnormalities, and multi-organ dysfunction independent of psychiatric etiology
• Hormonal alterations: Suppressed leptin, increased ghrelin resistance, low estrogen (in females), low testosterone (in males), reduced T3 from peripheral deiodination, and hypogonadotropic hypogonadism

Anorexia Nervosa (Restrictive and Binge/Purge Subtypes)

• Severe caloric restriction leading to significantly low body weight (BMI <17.5 kg/m²); relentless pursuit of thinness despite being underweight
• Intense fear of weight gain and body image disturbance; patient perceives self as overweight despite objective evidence to the contrary
• Preoccupation with food, calories, and weight; ritualistic eating behaviors; excessive exercise; food-related anxiety
• Physical signs: emaciation, lanugo (fine body hair), bradycardia, hypotension, hypothermia, amenorrhea/oligomenorrhea, constipation, abdominal distention, growth retardation (in adolescents)
• Binge/purge subtype includes compensatory behaviors (self-induced vomiting, laxative abuse, diuretic use) and may present with parotid gland enlargement, dental erosion, calluses on knuckles (Russell's sign)

Bulimia Nervosa

• Recurrent binge episodes (eating large quantities of food with loss of control) followed by purging behaviors (vomiting, laxatives, diuretics, enemas) or non-purging compensation (excessive exercise, fasting)
• Weight may be normal or slightly elevated; extreme concern with weight and shape despite absence of severe underweight
• Episodes typically occur in secret; shame and guilt accompany binges
• Physical findings: dental erosion from acid exposure, parotid enlargement, perimylolysis, electrolyte abnormalities (hypokalemia, hyponatremia, metabolic alkalosis), esophageal complications
• May have calluses on hands and knuckles; prone to impulsive behaviors and mood instability

Binge Eating Disorder

• Regular binge episodes without compensatory purging; sense of loss of control during eating
• Associated with obesity (BMI often >30 kg/m²) and psychological distress about binge episodes
• Unlike BN, no regular use of purging, fasting, or excessive exercise
• Patients often report feeling emotionally triggered to binge; distress about body image but typically less severe than in AN or BN

Important Presentation Variants

• Atypical AN: Same psychological features as AN but weight remains in normal range despite significant weight loss; carries serious medical risk
• Male patients: May present with body dysmorphia focused on muscularity rather than thinness; compulsive exercise; less likely to report body dissatisfaction
• Pediatric presentations: Growth faltering, delayed puberty, behavioral rigidity around meals
• Medical complications can be the presenting complaint (syncope, seizure from electrolytes, acute pancreatitis)

• DSM-5 diagnostic criteria for AN: (1) Restriction of energy intake leading to significantly low body weight; (2) Intense fear of weight gain or persistent behavior that interferes with weight gain; (3) Disturbance in the way body weight/shape is experienced (e.g., undue influence on self-evaluation, denial of seriousness)
• DSM-5 diagnostic criteria for BN: (1) Recurrent episodes of binge eating (at least 1x/week for 3 months); (2) Recurrent inappropriate compensatory behaviors (purging/non-purging); (3) Self-evaluation unduly influenced by body shape/weight
• DSM-5 diagnostic criteria for BED: (1) Recurrent binge episodes (at least 1x/week for 3 months); (2) Associated features of loss of control; (3) Marked distress; (4) No regular compensatory behaviors
• Laboratory assessment: Comprehensive metabolic panel (electrolytes, glucose, liver/renal function), phosphate (risk for refeeding syndrome), magnesium, albumin/prealbumin (nutritional markers), lipid panel, CBC, TSH, ECG (QTc prolongation, arrhythmia risk), bone density scan if prolonged AN (risk for osteoporosis)
• Psychometric screening: Eating Disorder Examination-Questionnaire (EDE-Q), SCOFF questionnaire (4 or 5 positive responses suggests eating disorder)
• Differential diagnosis considerations: Inflammatory bowel disease, celiac disease, hyperthyroidism, malabsorption syndromes, depression with appetite loss, obsessive-compulsive disorder; eating disorder behavior is ego-syntonic whereas in other conditions patient seeks to stop the behavior

First-Line Psychotherapeutic Interventions

• Cognitive-behavioral therapy (CBT): Gold standard for BN and BED; targets dysfunctional thoughts about weight/shape and teaches behavioral strategies to interrupt binge-purge cycles; 16-20 sessions typically
• Family-based treatment (FBT): First-line for adolescent AN; parents guide refeeding under therapist supervision; 12-20 sessions over 6-12 months
• Acceptance and commitment therapy (ACT): Emerging evidence in AN; focuses on psychological flexibility rather than direct symptom reduction

Nutritional Rehabilitation

• Refeeding protocol for AN: Initiate cautiously with 30-40 kcal/kg/day, increasing gradually by 200 kcal every 3-7 days to target 2000-3500 kcal/day depending on baseline deficit
• Monitor for refeeding syndrome: Risk especially in severely malnourished patients (BMI <14 kg/m²); phosphate, magnesium, and thiamine depletion leads to cardiac arrhythmias, respiratory failure, and seizures—provide supplementation and monitor electrolytes closely during first 5-7 days
• Registered dietitian counseling on balanced macronutrient intake; avoid restriction-based advice that may trigger anxiety
• Oral intake preferred; nasogastric feeding if unable to consume adequate calories (less common in adolescents, more often needed in severe adult AN)

Pharmacotherapy

• SSRIs: Limited evidence in AN; fluoxetine (up to 80 mg/day) may help with comorbid depression/anxiety and prevent relapse after weight

Cardiovascular (highest mortality contributor)

• Sinus bradycardia, hypotension, orthostasis: increased vagal tone plus loss of myocardial mass from catabolism. Marked bradycardia, orthostatic change, or hypothermia are admission criteria under the APA and Society for Adolescent Health and Medicine guidance — an emergency for inpatient medical stabilization.
• QTc prolongation and ventricular arrhythmia: driven by hypokalemia and hypomagnesemia from purging; torsades de pointes and sudden cardiac death are the feared endpoints. Emergency.
• Ipecac-induced cardiomyopathy: emetine is a direct myocardial toxin; presents as heart failure in a chronic purger.

Electrolyte and acid–base

• Vomiting: hypokalemic, hypochloremic metabolic alkalosis with low urine chloride and secondary hyperaldosteronism (pseudo-Bartter).
• Laxative abuse: classically a non–anion-gap metabolic acidosis from stool bicarbonate loss with hypokalemia, but significant volume depletion and secondary hyperaldosteronism can instead produce a hypokalemic metabolic alkalosis — so acid–base pattern alone is not fully specific, and urine chloride plus vomiting stigmata help distinguish. Chronic anthraquinone use causes melanosis coli.
• Hyponatremia: water loading before weigh-ins or SIADH; seizure risk.

Treatment complications

• Refeeding syndrome: insulin surge drives phosphate, potassium, and magnesium intracellularly, precipitating arrhythmia, rhabdomyolysis, respiratory failure, and seizures; thiamine depletion can unmask Wernicke encephalopathy. Emergency — falling phosphate is the earliest signal.
• Refeeding edema from sodium and fluid retention; benign but frightening to patients.
• Bupropion: contraindicated in patients with a current or prior diagnosis of bulimia nervosa or anorexia nervosa (any subtype) because of markedly increased seizure risk in the setting of electrolyte disturbance and low weight.

• Amenorrhea is no longer a criterion: DSM-5 removed amenorrhea as a criterion for anorexia nervosa (retained in DSM-5-TR), and a specific BMI number is not required — "significantly low weight" plus fear of weight gain and body-image disturbance suffices. A menstruating underweight patient still has AN.
• Weight does not distinguish AN from BN — behavior does: normal or above-normal weight with binge–purge cycling is bulimia nervosa; the binge/purge subtype of AN is defined by the low weight, not the purging.
• Check phosphate before and during refeeding: in a severely malnourished patient started on calories who develops confusion, weakness, or arrhythmia, the single best next step is serum phosphate (with magnesium and potassium) and repletion, plus thiamine before glucose.
• Acid–base helps fingerprint the purging method, imperfectly: hypokalemic, hypochloremic metabolic alkalosis with low urine chloride points to self-induced vomiting; non–anion-gap metabolic acidosis with hypokalemia points to laxative abuse — though volume-depleted laxative abusers may also be alkalotic, so use the physical stigmata. Russell's sign, dental enamel erosion, and painless parotid hypertrophy are the vomiting stigmata; lanugo, bradycardia, and hypothermia belong to starvation.
• The one drug rule examiners love: bupropion is contraindicated in patients with a current or prior diagnosis of bulimia nervosa or anorexia nervosa (any subtype) because of markedly increased seizure risk in the setting of electrolyte disturbance and low weight. Fluoxetine at 60 mg/day is the FDA-approved SSRI for bulimia nervosa; lisdexamfetamine is FDA-approved for moderate-to-severe binge eating disorder. No medication is approved for anorexia nervosa — weight restoration comes first.
• First-line psychotherapy by patient: family-based treatment for the adolescent with AN, CBT for BN and BED (consistent with APA practice guidance).
• Bone loss is treated with calories, not estrogen: per the Endocrine Society, weight restoration and resumption of menses restore density; combined oral contraceptives mask amenorrhea without protecting bone, and bisphosphonates are not routine in young women.
• Common distractor: attributing the emaciation to hyperthyroidism, malignancy, or IBD. Eating-disorder behavior is ego-syntonic — the patient defends the restriction rather than seeking relief from weight loss.