Eating Disorders

Eating disorders are serious psychiatric illnesses defined by disturbed eating behaviour and a pathological relationship with body weight and shape — anorexia nervosa (restriction of intake leading to a significantly low body weight, with intense fear of weight gain and disturbance in how body weight or shape is experienced), bulimia nervosa (recurrent binge eating followed by compensatory behaviour such as self-induced vomiting, laxative misuse, or excessive exercise, typically at a normal or higher body weight), and binge eating disorder (recurrent binge eating without compensatory behaviour).^[1] All three carry genuine medical risk — electrolyte disturbances, cardiac complications, and loss of bone density are common and can become life-threatening — alongside the psychiatric illness itself. Nutritional rehabilitation and eating-disorder-focused psychotherapy are the foundation of treatment for every eating disorder; medication has a limited, adjunctive role and is not an effective stand-alone treatment for any of the three. Effective care is genuinely multidisciplinary — medicine, psychiatry, psychology, and dietetics working together — and pharmacists are positioned to catch two of the highest-stakes, most preventable pharmacotherapy errors in this population: prescribing bupropion to a patient with any eating disorder history, and missing the electrolyte and refeeding-syndrome risks of nutritional rehabilitation.^[2]

General presentation clues

Consider an eating disorder in any patient with unexplained weight loss or marked weight fluctuation, amenorrhea or menstrual irregularity, GI complaints without another clear explanation, unexplained electrolyte abnormalities, dental erosion, or a family or patient report of unusual eating patterns, food rituals, or body-image preoccupation. Presentation spans the entire weight spectrum — a patient can have clinically significant bulimia nervosa or binge eating disorder at a completely normal or elevated body weight, so a normal weight must never be used on its own to rule an eating disorder out.

Physical examination findings

• Bradycardia, orthostatic hypotension, or hypothermia from malnutrition or dehydration.
• Lanugo hair, hypercarotenemia, and dry skin with significant malnutrition.
• Parotid gland hypertrophy and dental erosion from recurrent vomiting.
• Russell sign — calluses or scarring over the knuckles from repeated self-induced vomiting.
• Peripheral edema, proximal myopathy, and neuromuscular hyperirritability (Chvostek and Trousseau signs) with advanced malnutrition or electrolyte disturbance.

• Personal or family history of an eating disorder, depression, anxiety, or obsessive-compulsive disorder.
• A history of dieting, weight-based teasing, or participation in activities that emphasize leanness or a specific body shape (e.g., certain competitive sports, dance, modelling).
• Perfectionism and rigid, all-or-nothing thinking styles.
• A history of trauma, including sexual abuse.
• Family dysfunction or a high-conflict family environment.
• For binge eating disorder specifically: a family history of addiction, and comorbid attention-deficit/hyperactivity disorder.
• Sexual and gender minority identity is associated with elevated risk across all eating disorder types.
• Type 1 diabetes mellitus, particularly for insulin omission or restriction used as a compensatory behaviour.

Differentiating the three eating disorders

Based on DSM-5-TR diagnostic criteria.^[1] A patient can transition between these presentations over time (e.g., restricting-type anorexia nervosa developing binge/purge episodes) — reassess the working diagnosis at each visit rather than assuming it is fixed.

History

• Detailed eating history: current intake pattern, any binge episodes (size, frequency, sense of control), and any compensatory behaviour (vomiting, laxative/diuretic/enema misuse, fasting, excessive exercise, or insulin restriction in a patient with diabetes).
• Menstrual history, body image, and weight- or shape-related cognitions.
• Depression, anxiety, obsessive-compulsive symptoms, suicidal ideation, substance use, and family dysfunction or trauma history.
• Symptoms of malnutrition or electrolyte disturbance: chest pain, palpitations, syncope, hematemesis, seizures, abdominal pain, muscle weakness or cramping, and episodes of confusion.
• Autonomic symptoms that increase arrhythmia risk: episodic sweating, changes in heart rate or blood pressure with position, and sudden urgency to defecate or urinate.

Investigations

• Electrolytes, including magnesium and phosphate specifically (not always part of a routine basic metabolic panel) — critical both at baseline and, even more importantly, during nutritional rehabilitation.^[5]
• Creatinine, glucose, CBC, and liver function tests.
• ECG — assess for bradycardia, arrhythmia, and QTc prolongation.
• Vital signs, including orthostatic blood pressure and heart rate.
• Pregnancy testing where clinically relevant — amenorrhea does not exclude the possibility of pregnancy.

What not to over-rely on: a single normal serum potassium does not exclude clinically important purging behaviour or cardiac risk — purging can cause intermittent, rapidly-corrected electrolyte shifts that one sample can miss. A normal body weight or BMI does not rule out bulimia nervosa or binge eating disorder and should never be the sole basis for deciding an eating disorder assessment is unnecessary. Routine bone density (DEXA) scanning is not indicated at the initial visit — reserve it for patients who meet the duration and risk criteria described in Monitoring and Follow-up.

• Achieve and maintain medical stability — normalize vital signs, correct electrolyte disturbances, and resolve any acute medical risk.
• Restore body weight to a healthy, individualized target range in anorexia nervosa, and prevent further weight loss where restoration is not yet the immediate goal.
• Eliminate binge eating and, in bulimia nervosa, eliminate compensatory (purging) behaviour.
• Normalize eating patterns and reduce food-related rituals and avoidance.
• Treat coexisting psychiatric conditions — depression, anxiety, obsessive-compulsive symptoms, suicidality.
• Restore normal cognitive and emotional function — this generally requires nutritional rehabilitation first, since malnutrition itself impairs cognition and makes psychotherapy less effective.
• Restore menstrual function and protect bone health.
• Prevent relapse and support long-term recovery through continued multidisciplinary follow-up.

Nutritional rehabilitation (anorexia nervosa)

Structured nutritional rehabilitation, guided by an experienced dietitian, is foundational to anorexia nervosa treatment — psychological and cognitive function will not normalize until nutritional status improves. Set stepwise, individualized weight-gain targets appropriate to the treatment setting: roughly 0.9-1.8 kg per week for hospitalized or residential patients, 0.4-1.4 kg per week for partial hospitalization, and 0.4-0.9 kg per week for outpatient programs, continuing until a healthy weight and normalized growth trajectory are achieved.^[10] Oral nutritional supplements can be used when food alone cannot achieve the target rate of gain; tube feeding may be needed if oral intake fails despite structured support. Trained meal support — family members or staff present and actively engaged at mealtimes — improves adherence.

Psychotherapy

• Family-based treatment (FBT) is the best-supported approach for children and adolescents with anorexia nervosa — it trains parents to take an active role in renourishing their child and progresses through phases of parental control, gradually returning control of eating to the adolescent as recovery progresses.^[6]
• Cognitive behavioural therapy for eating disorders (CBT-ED) and specialist supportive clinical management are appropriate first-line psychotherapies for adults with anorexia nervosa.
• CBT for bulimia nervosa (CBT-BN) directly targets the binge-purge cycle and the overvaluation of shape and weight that drives it; guided self-help CBT is an accessible, effective early option for adolescents and adults with bulimia nervosa or binge eating disorder who do not have significant psychiatric comorbidity.
• CBT is the standard first-line psychotherapy for binge eating disorder; other modalities, such as dialectical behaviour therapy, are reasonable alternatives depending on therapist availability and patient fit.
• Family therapy and the involvement of all family members materially improves outcomes for children and adolescents across every eating disorder type, not anorexia nervosa alone.

General supportive measures

• Limit or supervise exercise in any medically unstable or significantly underweight patient — unrestricted exercise can worsen medical risk and interfere with weight restoration.
• Address binge/purge and laxative-misuse behaviour with explicit, gradual tapering goals rather than expecting abrupt cessation, particularly for chronic laxative misuse.
• Screen for and treat comorbid depression, anxiety, obsessive-compulsive symptoms, substance use, and suicidality — recovery from the eating disorder is unlikely without addressing these.
• Build and maintain a genuine therapeutic alliance — engagement and rapport materially affect whether a patient stays in treatment, given how often ambivalence toward treatment is itself part of the illness.

Pregnancy

Amenorrhea does not reliably prevent pregnancy in anorexia nervosa — ovulation can occur even while a patient remains amenorrheic, so effective contraception counselling is still needed for any sexually active patient who does not wish to conceive.^[10] If pregnancy occurs, follow it as a high-risk pregnancy unless the eating disorder is genuinely mild, involve a dietitian for nutrition and supplement recommendations, and reassess every medication for pregnancy risk rather than assuming continuation is safe — use an individualized risk-benefit approach and favour non-pharmacologic measures where possible. Eating disorder symptoms can improve or worsen during pregnancy in different patients, so ongoing reassessment through pregnancy and the postpartum period, including for anxiety, depression, and suicidality, is required regardless of the pre-pregnancy course.

Breastfeeding

Most patients with an eating disorder, including anorexia nervosa, can successfully breastfeed; severe, unremitted anorexia nervosa can reduce milk supply. Refer to a dietitian to optimize both maternal and infant nutrition during lactation.

Children and adolescents

Family-based treatment is the best-supported first-line psychotherapy for adolescent anorexia nervosa and involves the whole family, not just the patient.^[6] Weight targets in growing children and adolescents should be set against an appropriate growth-chart trajectory rather than a fixed adult BMI threshold. Medication evidence in this age group is more limited than in adults — reserve pharmacotherapy for the same specific situations as in adults (e.g., persistent anxiety or rigid cognitions limiting nutritional rehabilitation in anorexia nervosa) and involve a clinician experienced in pediatric psychopharmacology.

Renal and hepatic considerations

Adjust electrolyte and phosphate repletion doses to renal function, and monitor renal function closely when repleting phosphate or potassium in a patient with reduced renal clearance. Topiramate increases nephrolithiasis risk — ensure adequate hydration and use caution with a personal history of kidney stones or significant renal impairment. Monitor liver function periodically with olanzapine.

Older adults

Eating disorders are underrecognized in older adults but do occur, including late-onset and long-standing chronic presentations; the same medical risks apply and are often compounded by reduced physiologic reserve, so the threshold for medical escalation should be lower in this group.

Medical monitoring

• Vital signs, including orthostatic blood pressure and heart rate, at every visit during active treatment, more frequently in a higher-risk or recently-hospitalized patient.
• Weight, tracked against the individualized target trajectory (not just a single target number) in anorexia nervosa.
• Electrolytes — potassium, phosphate, and magnesium specifically — checked daily for at least the first several days of nutritional rehabilitation in a higher-risk patient, then at a reduced frequency once stable.^[3]
• ECG for any patient with significant bradycardia, electrolyte disturbance, or other cardiac risk features.
• Bone density (DEXA) after roughly 1 year of sustained low weight in children and adolescents, or 2 years in adults — repeat no more often than yearly unless new bone pain or a fracture occurs.^[11]
• Return of menstrual function as a marker of physiologic recovery in anorexia nervosa.

Medication-specific monitoring

• Olanzapine: weight, fasting glucose/lipids, and extrapyramidal symptoms; reassess at the planned 3-4 month mark whether continued therapy is still needed.
• Fluoxetine (bulimia nervosa dose): response (binge/purge frequency), mood and suicidality (particularly early in treatment and in younger patients), and GI bleeding risk if combined with an NSAID or antiplatelet agent.
• Lisdexamfetamine: heart rate, blood pressure, appetite/weight trend, sleep, and mood; monitor growth in adolescents; screen for misuse given its stimulant/controlled-substance status.
• Topiramate: cognitive or word-finding complaints, mood, weight, and adequate hydration/renal stone symptoms.

Psychological monitoring

Track binge/purge frequency, body-image cognitions, mood, anxiety, and suicidality at every visit — improvement in weight or medical parameters alone does not confirm psychological recovery, and relapse risk remains significant even after apparent improvement.

1. Confirm genuine engagement with nutritional rehabilitation and psychotherapy before attributing a lack of progress to medication — medication cannot substitute for either.
2. For anorexia nervosa not achieving the expected rate of weight gain: reassess for undisclosed compensatory behaviour (purging, excessive exercise, water-loading before weigh-ins, discarding food), and escalate the level of care (day program, inpatient, or residential treatment) if outpatient management is failing or the patient is medically unstable.
3. For bulimia nervosa or binge eating disorder with an inadequate response to fluoxetine: confirm the dose is adequate (60 mg/day for bulimia nervosa) and the trial has run long enough, then consider switching to an alternative agent (another SSRI, venlafaxine, or trazodone) rather than simply increasing beyond the studied dose — never add a second antidepressant to fluoxetine, since there is no proven benefit and adverse effects and cost both increase.
4. For binge eating disorder with an inadequate response to lisdexamfetamine at the maximum tolerated or target dose: consider a trial of topiramate, and reassess whether comorbid ADHD, depression, or anxiety is driving the binge pattern and needs separate treatment.
5. Reassess psychotherapy modality and intensity before or alongside any medication change — a medication change without addressing psychotherapy engagement rarely succeeds on its own.
6. Persistent medical instability at any point — regardless of psychiatric readiness for a lower level of care — takes priority and should trigger escalation to a higher level of care or a specialist eating disorder team.

• Prescribing bupropion to a patient with any current or past eating disorder diagnosis — this carries a materially increased seizure risk and is never appropriate in this population, regardless of the indication being treated.
• Treating any eating disorder with medication alone, without nutritional rehabilitation and psychotherapy — medication is an adjunct, not a substitute.
• Dosing fluoxetine for bulimia nervosa the same way as for depression — the bulimia nervosa dose (60 mg/day) is substantially higher than typical antidepressant dosing.
• Missing refeeding syndrome risk when reintroducing nutrition too quickly in a patient with minimal recent intake — check phosphate, potassium, and magnesium specifically (not just a routine electrolyte panel) and give thiamine before or at the start of feeding.
• Assuming a normal or above-normal body weight excludes bulimia nervosa or binge eating disorder — both occur across the full weight spectrum.
• Failing to ask directly and specifically about purging, laxative or diuretic misuse, and compensatory exercise — patients rarely volunteer this information unprompted.
• Relying on a single normal potassium or ECG to exclude ongoing cardiac risk in a patient who purges intermittently.
• Starting lisdexamfetamine or topiramate for binge eating disorder without also arranging psychotherapy — medication alone is not the standard of care.
• Overlooking bone health — not arranging DEXA screening when duration/severity criteria are met, or assuming bone loss will fully reverse once weight is restored.
• Attributing GI, cardiac, or neurologic symptoms in a patient with a known eating disorder to anxiety without an appropriate medical work-up.

How to use this table: Doses are adult doses and require patient-specific confirmation, including renal/hepatic adjustment and, in children and adolescents, weight-based dosing under specialist direction. Select any drug name to open its complete Pharmasist Drug Database page.

Second-generation antipsychotics — anorexia nervosa

Adjunctive only, used selectively during nutritional rehabilitation — never a routine or stand-alone treatment.

Antidepressants

Fluoxetine is the only medication with a formal indication for an eating disorder in this class (bulimia nervosa); the others are reasonable alternatives when fluoxetine is not tolerated or not effective.

Amphetamine-based agent — binge eating disorder

The only medication with a Health Canada-approved indication specifically for binge eating disorder.

Anticonvulsant — binge eating disorder (off-label)

A reasonable off-label alternative when lisdexamfetamine is contraindicated, not tolerated, or inappropriate; evidence supports efficacy, but adverse effects limit its use as a routine first choice.

Refeeding syndrome and nutritional rehabilitation

Applies across all eating disorder types whenever a patient with minimal recent intake begins nutritional rehabilitation — hypophosphatemia is the hallmark of refeeding syndrome, and its correction alongside cautious caloric advancement is the core of prevention.