Bulimia Nervosa (BN) - Adult

1. Clinical Overview

Summary

Bulimia Nervosa (BN) is a severe eating disorder characterised by recurrent episodes of binge eating followed by inappropriate compensatory behaviours designed to prevent weight gain. [1,2] Unlike Anorexia Nervosa, individuals with BN typically maintain a normal or above-normal body weight, which often delays diagnosis and allows the disorder to remain hidden for years. The condition was first formally described by Gerald Russell in 1979 as "an ominous variant of anorexia nervosa." [3]

The core psychopathology centres on an overvaluation of body shape and weight as central determinants of self-worth, driving the relentless pursuit of thinness through pathological eating behaviours. [1,2] The binge-purge cycle becomes self-perpetuating: dietary restriction triggers binge episodes, which provoke intense shame and fear of weight gain, leading to compensatory purging behaviours that provide temporary relief but ultimately perpetuate the cycle.

Bulimia Nervosa carries substantial medical morbidity, including life-threatening electrolyte disturbances (particularly hypokalaemia leading to cardiac arrhythmias), dental erosion (perimylolysis), oesophageal injury, and renal complications. [4,5] Psychiatric comorbidity is extensive, with major depression affecting 50-70% of patients and anxiety disorders present in 40-60%. [6] First-line treatment is Cognitive Behavioural Therapy for Bulimia Nervosa (CBT-BN), with high-dose fluoxetine (60mg daily) as the evidence-based pharmacological adjunct. [7,8,9]

Key Facts Card

Clinical Pearls

"Normal Weight, Hidden Disorder": Unlike Anorexia Nervosa, patients with Bulimia are typically normal weight (BMI 18.5-30). The disorder is concealed by shame - actively search for physical clues (Russell's sign, dental erosion, parotid swelling) in any patient with unexplained electrolyte abnormalities or GI complaints.

"Russell's Sign is Pathognomonic": Calluses or scars on the dorsum of the hand (metacarpophalangeal joints) from repeated trauma against the upper incisors during self-induced vomiting. First described by Gerald Russell in 1979. Present in up to 30% of patients who purge by vomiting. [3]

"Fluoxetine 60mg - Triple the Antidepressant Dose": Unlike depression where 20mg is effective, Bulimia Nervosa requires 60mg daily fluoxetine for therapeutic benefit. This is the only FDA/MHRA-approved pharmacotherapy for BN. [8,9]

"The Hypokalaemia Triad Kills": Vomiting causes loss of HCl → Hypochloraemic, Hypokalaemic Metabolic Alkalosis. Severe hypokalaemia (less than 2.5 mmol/L) causes U-waves, prolonged QT, and life-threatening ventricular arrhythmias. [4,5]

"Metabolic Fingerprints Reveal the Behaviour": Vomiting = metabolic alkalosis. Laxative abuse = metabolic acidosis. Diuretic abuse = metabolic alkalosis. The acid-base pattern reveals the compensatory behaviour even when the patient denies it.

Why This Matters Clinically

Bulimia Nervosa is often a hidden illness characterised by profound shame and secrecy. Patients may present to multiple medical specialties with dental problems, unexplained electrolyte abnormalities, chronic throat irritation, or gastrointestinal symptoms before the underlying eating disorder is identified. The average delay from symptom onset to treatment is 5-10 years. [10]

Recognition of the physical stigmata (Russell's sign, dental erosion, parotid hypertrophy), appropriate screening (SCOFF questionnaire), and sensitive but direct inquiry about eating behaviours can be life-saving. Untreated Bulimia carries elevated mortality from both medical complications and suicide. Early intervention with evidence-based treatments (CBT-BN, fluoxetine) achieves recovery in approximately half of all patients.

---

2. Epidemiology

Prevalence and Incidence

Bulimia Nervosa is the most common eating disorder presenting to clinical services, though many cases remain undiagnosed in the community. [1,10]

Demographics and At-Risk Populations

• insulin omission for weight control | | Males | Under-recognised | 10-15% of cases; often present later |

Risk Factors

Temporal Trends

Incidence of Bulimia Nervosa increased dramatically in the 1980s-1990s following its formal recognition in 1979, likely reflecting improved recognition rather than true increase. Recent data suggest stable or slightly declining incidence in Western countries, though rates are increasing in non-Western societies undergoing Westernisation. [10]

---

3. Aetiology and Pathophysiology

Aetiological Framework

Bulimia Nervosa arises from the complex interplay of genetic vulnerability, neurobiological factors, psychological traits, and sociocultural influences. The biopsychosocial model provides the most comprehensive understanding.

Genetic Factors

Twin studies demonstrate heritability of 50-83% for Bulimia Nervosa, indicating substantial genetic contribution. [12] Genome-wide association studies have identified variants in genes involved in:

• Serotonergic neurotransmission (5-HT2A receptor polymorphisms)
• Dopaminergic reward pathways
• Opioid system regulation
• BDNF (Brain-Derived Neurotrophic Factor)

First-degree relatives of individuals with BN have 4-11 times increased risk of developing an eating disorder. [12]

Neurobiological Factors

Exam Detail: Neuroimaging Findings in Bulimia Nervosa:

• fMRI: Increased activation in orbitofrontal cortex and insula to food cues; reduced prefrontal inhibitory control
• PET: Reduced 5-HT2A receptor binding in frontal and temporal cortices
• Structural MRI: Grey matter volume reductions in frontal and temporal regions (may normalize with recovery)
• These findings support the neurobiological basis for impaired inhibitory control and altered reward processing characteristic of BN.

The Binge-Purge Cycle: Detailed Pathophysiology

The binge-purge cycle is the cardinal behavioural pattern of Bulimia Nervosa. Understanding this cycle is essential for both diagnosis and treatment.

┌─────────────────────────────────────────────────────────────────┐
│                    THE BINGE-PURGE CYCLE                        │
│                                                                 │
│   ┌──────────────┐                                              │
│   │   TRIGGER    │ ← Dietary restriction / Negative emotion    │
│   │  (Hunger,    │   Stress / Interpersonal conflict          │
│   │   Stress,    │   Body dissatisfaction / "Feeling fat"     │
│   │  Negative    │                                              │
│   │   Affect)    │                                              │
│   └──────┬───────┘                                              │
│          ↓                                                      │
│   ┌──────────────┐                                              │
│   │    URGE      │ ← Intense craving; preoccupation with food  │
│   │  TO BINGE    │   Mounting tension and anxiety              │
│   └──────┬───────┘                                              │
│          ↓                                                      │
│   ┌──────────────┐                                              │
│   │    BINGE     │ ← Large quantity (> 1000-2000 kcal typical)  │
│   │   EATING     │   Discrete period (less than 2 hours usually)        │
│   │              │   LOSS OF CONTROL is defining feature       │
│   │              │   Often secretive; "forbidden" foods         │
│   └──────┬───────┘                                              │
│          ↓                                                      │
│   ┌──────────────┐                                              │
│   │   NEGATIVE   │ ← Guilt, shame, self-disgust               │
│   │   EMOTIONS   │   Fear of weight gain                       │
│   │              │   Physical discomfort (bloating, nausea)    │
│   └──────┬───────┘                                              │
│          ↓                                                      │
│   ┌──────────────┐                                              │
│   │ COMPENSATORY │ ← Vomiting (80-90% of cases)               │
│   │  BEHAVIOUR   │   Laxatives, diuretics, fasting, exercise  │
│   │  (PURGING)   │   Temporary relief from anxiety            │
│   └──────┬───────┘                                              │
│          ↓                                                      │
│   ┌──────────────┐                                              │
│   │  TEMPORARY   │ ← Reduced anxiety (negative reinforcement) │
│   │    RELIEF    │   BUT: hunger returns, guilt persists      │
│   └──────┬───────┘                                              │
│          │                                                      │
│          └──────────────→ CYCLE REPEATS                        │
│                                                                 │
└─────────────────────────────────────────────────────────────────┘

Stage-by-Stage Analysis

1. Trigger Phase

• Dietary Restriction: The most potent trigger. Biological hunger from caloric deficit creates physiological drive to eat.
• Negative Emotions: Anxiety, depression, anger, loneliness, boredom - eating provides temporary emotional regulation.
• Interpersonal Stressors: Conflict, rejection, criticism - particularly weight/appearance-related comments.
• Body Checking: Looking in mirror, trying on clothes - can trigger "feeling fat" and subsequent restriction or binge.

2. Binge Episode

• Definition: Eating an objectively large amount of food in a discrete period (typically less than 2 hours) with a sense of loss of control.
• Quantity: Typically 1,000-2,000+ kcal in a single episode; may exceed 3,000-5,000 kcal in severe cases.
• Food Type: Usually "forbidden" high-calorie, palatable foods (carbohydrates, sweets, fats) avoided during restriction.
• Setting: Usually secretive, alone, at home; may plan binge in advance (purchasing "binge foods").
• Subjective Experience: Dissociative quality ("numbing out"); eating rapidly without tasting; feeling unable to stop.
• Duration: Minutes to 2 hours typically; may be interrupted by opportunity to purge.

3. Compensatory Behaviours (Purging)

Clinical Pearl: The Ineffectiveness of Purging: Self-induced vomiting only eliminates approximately 50% of calories consumed during a binge (range 30-75%). Laxatives are even less effective - they act on the large intestine AFTER caloric absorption in the small intestine. Patients often do not understand this and believe purging "undoes" the binge. Education about this can be therapeutically useful.

4. Reinforcement and Maintenance The cycle is maintained by both positive and negative reinforcement:

• Positive Reinforcement: Pleasurable sensations during binge (taste, fullness, "numbing")
• Negative Reinforcement: Purging reduces anxiety and fear of weight gain
• Cognitive Factors: Overvaluation of shape/weight maintains drive for thinness
• Dietary Restriction: Post-purge restriction re-primes the cycle through hunger

Psychological Factors

---

4. Clinical Presentation

Behavioural Features

Physical Signs

Pathognomonic and Characteristic Signs

Systemic Signs by Body System

Exam Detail: Russell's Sign - Detailed Clinical Examination:

• Location: Dorsum of dominant hand, over metacarpophalangeal joints (knuckles)
• Appearance: Calluses, hyperkeratosis, scars, or healed abrasions
• Mechanism: Upper incisors repeatedly traumatise the hand during self-induced vomiting
• Named After: Gerald Russell, who described this sign in his 1979 paper defining bulimia nervosa [3]
• Sensitivity: Low (25-35%) - many patients vomit without hand contact, or have "learned vomiting"
• Specificity: High - few other causes for this specific distribution
• Differential: Cutaneous lupus; lichen planus; occupational calluses (rare in this distribution)
• Clinical Significance: When present, virtually pathognomonic for self-induced vomiting

Symptoms and Complications Patients May Report

---

5. Diagnosis

DSM-5 Diagnostic Criteria for Bulimia Nervosa

DSM-5 Severity Specifiers

Severity can be increased based on functional impairment and medical complications, even if frequency is lower.

ICD-11 Diagnostic Guidelines

ICD-11 (6B81) criteria are similar to DSM-5:

• Recurrent binge eating (loss of control, large amount)
• Repeated inappropriate compensatory behaviours
• Preoccupation with body weight/shape unduly influencing self-evaluation
• Not better accounted for by AN (not significantly underweight)

Screening Tools

SCOFF Questionnaire

Quick 5-question screening tool for eating disorders. [15]

Scoring: ≥2 positive responses indicates likely eating disorder. Performance: Sensitivity 97-100%; Specificity 87-94% for eating disorders. [15]

Other Validated Instruments

Differential Diagnosis

---

6. Investigations

Rationale

Investigations in Bulimia Nervosa serve to:

1. Assess medical complications (especially electrolytes, cardiac)
2. Stratify risk and guide intensity of treatment
3. Exclude differential diagnoses
4. Monitor during treatment

Laboratory Investigations

Essential Blood Tests

Exam Detail: Electrolyte Disturbances in Bulimia Nervosa - Detailed Mechanisms:

Self-Induced Vomiting:

1. Loss of gastric HCl → Hypochloraemia
2. Loss of H+ → Metabolic Alkalosis
3. Alkalosis drives K+ into cells → Hypokalaemia
4. Volume depletion activates RAAS → Secondary hyperaldosteronism → Further K+ loss
5. Classic Triad: Hypokalaemia + Hypochloraemia + Metabolic Alkalosis

Laxative Abuse:

1. Loss of HCO3- and K+ in stool → Metabolic Acidosis + Hypokalaemia
2. Volume depletion → RAAS activation → Secondary hyperaldosteronism
3. Pattern: Hypokalaemia + Metabolic Acidosis (Non-anion gap)

Diuretic Abuse:

1. Renal K+ and Na+ loss
2. Volume depletion → RAAS activation
3. Pattern: Hypokalaemia + Hyponatraemia + Metabolic Alkalosis (loop/thiazide)

Additional Investigations (As Indicated)

ECG Findings in Hypokalaemia

Clinical Pearl: The U-Wave: U-waves (positive deflection after T-wave) are characteristic of hypokalaemia. As K+ falls, U-waves become more prominent and may fuse with the T-wave, creating apparent QT prolongation (actually QU prolongation). Always measure K+ when you see U-waves.

Dental Examination

Referral to dentist recommended for all patients with vomiting behaviour. [14]

---

7. Medical Complications

Complications by Purging Behaviour

Self-Induced Vomiting Complications

Exam Detail: Boerhaave Syndrome (Spontaneous Oesophageal Rupture):

• Definition: Full-thickness tear of the oesophagus, usually distal left posterolateral wall
• Mechanism: Sudden increase in intra-oesophageal pressure against closed cricopharyngeus during forceful vomiting
• Presentation: Severe retrosternal chest pain after vomiting; dysphagia; subcutaneous emphysema (crepitus); Hamman's sign (mediastinal crunch on auscultation); systemic sepsis
• Diagnosis: CT chest with oral contrast (pneumomediastinum, pleural effusion, extraluminal contrast); CXR may show pneumomediastinum
• Management: Surgical emergency - thoracotomy and repair vs. conservative (contained, stable) vs. endoscopic stenting
• Mortality: 20-40% even with treatment; higher if delayed diagnosis
• In Bulimia: Rare but well-documented; must be considered in any patient with severe chest pain after purging

Laxative Abuse Complications

Diuretic Abuse Complications

Complications of Binge Eating

Long-Term Medical Sequelae

---

8. Psychiatric Comorbidity

Prevalence of Comorbid Disorders

Suicide Risk

Bulimia Nervosa carries significantly elevated mortality from suicide. [6]

• Standardised Mortality Ratio (SMR) for suicide: approximately 7.5 (i.e., 7.5× general population risk)
• All patients must be assessed for suicidal ideation and self-harm
• Risk factors: comorbid depression, substance abuse, personality disorder, history of trauma, severe symptoms

Clinical Pearl: Multi-Impulsive Bulimia: A subtype characterised by not only binge-purge behaviours but also impulsivity in other domains: self-harm, substance abuse, shoplifting, sexual impulsivity. Often associated with Borderline Personality Disorder. These patients may require longer, more intensive treatment addressing the broader pattern of impulsivity.

---

9. Management

Principles of Treatment

1. Multi-Disciplinary Team (MDT): Psychiatry, Psychology, Dietitian, GP, Dentist (± Physician if medical complications)
2. Medical Stabilisation First: Correct electrolytes; manage cardiac risk
3. Psychological Therapy: CBT-BN is first-line for adults [7]
4. Pharmacotherapy: Fluoxetine 60mg as adjunct [8,9]
5. Nutritional Rehabilitation: Regular eating pattern; stop restriction
6. Treat Comorbidities: Depression, anxiety, personality disorder
7. Outpatient as Default: Most can be treated as outpatients; inpatient for severe medical/psychiatric risk

Stepped Care Model (NICE NG69)

┌─────────────────────────────────────────────────────────────────┐
│                    STEPPED CARE FOR BULIMIA                     │
│                                                                 │
│  STEP 1: Recognition, Assessment, Referral                     │
│  ├── Primary Care: Identify; SCOFF screening; bloods           │
│  └── Refer to specialist Eating Disorders Service              │
│                                                                 │
│  STEP 2: Evidence-Based Psychological Treatment                │
│  ├── FIRST LINE: CBT-BN (individual, 16-20 sessions)          │
│  ├── OR: Guided Self-Help (GSH) based on CBT principles       │
│  └── ADOLESCENTS: BN-focused Family Therapy (FT-BN)            │
│                                                                 │
│  STEP 3: Add Pharmacotherapy if Needed                         │
│  └── Fluoxetine 60mg daily as adjunct to psychological Rx      │
│                                                                 │
│  STEP 4: Intensified Treatment                                 │
│  ├── Increased session frequency                               │
│  ├── Day Programme                                              │
│  └── Consider alternative psychological approaches (IPT)       │
│                                                                 │
│  STEP 5: Inpatient / Specialist Residential                    │
│  ├── Severe medical compromise (electrolyte, cardiac)          │
│  ├── High suicide risk                                          │
│  └── Failed community treatment                                 │
│                                                                 │
└─────────────────────────────────────────────────────────────────┘

Psychological Therapies

CBT-BN / CBT-ED (Cognitive Behavioural Therapy for Bulimia Nervosa)

Evidence Base: CBT-BN is the most extensively studied treatment for Bulimia Nervosa with robust RCT evidence demonstrating superiority to waiting list, other psychotherapies, and pharmacotherapy alone. [7,16]

Components of CBT-BN:

Exam Detail: Enhanced CBT (CBT-E): CBT-E is a "transdiagnostic" version of CBT for eating disorders developed by Christopher Fairburn. It addresses eating disorder psychopathology regardless of specific diagnosis (AN, BN, BED, OSFED). It has four modules that can be added for complex cases:

1. Core Module: As above for CBT-BN
2. Mood Intolerance Module: For those using binge eating for emotion regulation
3. Clinical Perfectionism Module: For rigid perfectionism maintaining disorder
4. Interpersonal Difficulties Module: For interpersonal problems maintaining disorder CBT-E has become the dominant form of CBT for eating disorders in specialist services. [16]

Other Psychological Therapies

Pharmacotherapy

Fluoxetine

Why 60mg?

• Lower doses (20-40mg) shown to be less effective for BN than for depression
• May relate to greater 5-HT dysregulation in BN requiring higher receptor occupancy
• The original FDA approval trials used 60mg [8]

Clinical Pearl: Fluoxetine 60mg - Not 20 mg: This is a common exam question. Unlike depression, Bulimia Nervosa requires high-dose fluoxetine for efficacy. Prescribing 20mg is a clinical error that will be marked wrong in exams.

Other Pharmacological Options

Drugs to AVOID in Bulimia Nervosa:

• ❌ Bupropion: Lowers seizure threshold; contraindicated in eating disorders
• ❌ TCAs: Cardiac conduction effects dangerous with electrolyte disturbance
• ❌ MAOIs: Risk of hypertensive crisis with binge eating

Nutritional Management

Dental Advice

Management of Medical Complications

Electrolyte Replacement

Clinical Pearl: Magnesium Must Be Replaced First: Hypokalaemia is often refractory to potassium replacement if concurrent hypomagnesaemia is not corrected. Magnesium is required for the Na+/K+-ATPase pump function. Always check and correct magnesium when treating hypokalaemia.

Indications for Inpatient Admission

---

10. Prognosis and Outcomes

Natural History and Recovery

Data from longitudinal studies with 10-20 year follow-up. [11]

Mortality

Prognostic Factors

Relapse and Maintenance

• Relapse is common (30-50% within first year after treatment)
• Relapse prevention strategies are integral to CBT-BN
• Long-term follow-up recommended
• Prompt re-referral if symptoms recur

---

11. Special Populations

Adolescents

Males

Pregnancy

Type 1 Diabetes ("Diabulimia")

Athletes

---

12. Exam Focus: Viva Points and Model Answers

Opening Statement for Viva

"Bulimia Nervosa is a serious eating disorder characterised by recurrent episodes of binge eating followed by inappropriate compensatory behaviours to prevent weight gain. Unlike Anorexia Nervosa, patients typically maintain normal body weight. Key physical signs include Russell's sign, dental erosion, and parotid hypertrophy. The most dangerous complication is hypokalaemia leading to cardiac arrhythmias. First-line treatment is CBT-BN for adults, with high-dose fluoxetine (60mg) as pharmacological adjunct."

Common Exam Questions and Model Answers

Q1: What is Russell's Sign and what is its significance?

"Russell's Sign refers to calluses or scars on the dorsum of the hand, typically over the metacarpophalangeal joints. It is caused by repeated abrasion of the skin against the upper incisors during self-induced vomiting. It was first described by Gerald Russell in 1979. While only present in 25-35% of patients who vomit, it is highly specific and virtually pathognomonic for self-induced vomiting when present."

Q2: What are the electrolyte disturbances associated with different purging behaviours?

"Self-induced vomiting causes loss of gastric HCl leading to hypochloraemia, hypokalaemia, and metabolic alkalosis. Laxative abuse causes loss of potassium and bicarbonate from the GI tract, leading to hypokalaemia and metabolic acidosis. Diuretic abuse causes renal potassium loss and metabolic alkalosis. The pattern of acid-base disturbance can reveal the purging behaviour even when the patient denies it."

Q3: Why is fluoxetine dosed at 60mg for Bulimia rather than 20mg?

"Randomised controlled trials have consistently shown that the higher dose of 60mg daily is required for efficacy in Bulimia Nervosa, unlike depression where 20mg is effective. This may relate to the greater degree of serotonin dysregulation in BN requiring higher receptor occupancy. The 60mg dose is the only FDA and MHRA approved dose for this indication."

Q4: What is the first-line psychological treatment for Bulimia Nervosa in adults?

"CBT-BN, or Cognitive Behavioural Therapy for Bulimia Nervosa, is the first-line treatment recommended by NICE NG69. It typically involves 16-20 individual sessions over 4-5 months. Key components include self-monitoring, establishing regular eating, cognitive restructuring of shape and weight concerns, and relapse prevention. Response rates are approximately 40-60% for remission, with 70-80% showing significant improvement."

Q5: What would make you admit a patient with Bulimia Nervosa?

"Indications for inpatient admission include: severe hypokalaemia below 2.5 mmol/L requiring IV replacement and cardiac monitoring; cardiac arrhythmias or prolonged QTc greater than 500ms; haemodynamic instability from severe dehydration; haematemesis raising concern for Mallory-Weiss tear or oesophageal rupture; acute suicidal risk requiring psychiatric admission; or failure of outpatient treatment where specialist eating disorders inpatient care may be considered."

Common Mistakes That Fail Candidates

❌ Prescribing fluoxetine 20mg (Must be 60mg for BN) ❌ Prescribing bupropion (Contraindicated - seizure risk) ❌ Recommending psychological therapy alone when severe hypokalaemia present (Medical stabilisation first) ❌ Forgetting to check ECG in patient with electrolyte disturbance ❌ Missing suicidal ideation assessment (All ED patients need risk assessment) ❌ Recommending FBT for adults (FBT is first-line for adolescents, CBT-BN for adults)

---

13. Counselling Points for Patients

Key Messages

1. "Bulimia is an illness, not a choice."

   • "This is a recognised medical condition with biological and psychological components. You are not weak, vain, or to blame."

2. "Recovery is possible."

   • "With treatment, about half of people with Bulimia recover fully. Most others improve significantly. You can get better."

3. "Regular eating is the foundation."

   • "Eating three meals and two to three snacks at regular times, even when you don't feel hungry, reduces the urge to binge. Your body needs to learn that food is coming regularly."

4. "Purging doesn't work like you think."

   • "Vomiting only removes about half the calories from a binge. Laxatives work after calories are already absorbed. These behaviours damage your body without really preventing weight gain."

5. "Breaking the secrecy helps."

   • "Shame keeps the illness going. Telling someone you trust - a friend, family member, or professional - is often the first step to recovery."

6. "Setbacks are part of recovery, not failure."

   • "Recovery isn't a straight line. If you slip back, learn from it and get back on track. One episode doesn't undo your progress."

Dental Advice for Patients

• "Do not brush your teeth immediately after vomiting - the acid softens the enamel and brushing will wear it away faster."
• "Instead, rinse your mouth with water or a bicarbonate mouthwash to neutralise the acid."
• "Wait at least 30-60 minutes before brushing."
• "See a dentist regularly - they can help protect your teeth even if the behaviours continue."

---

14. Patient Information (Layperson Summary)

What is Bulimia Nervosa?

Bulimia Nervosa is an eating disorder where a person repeatedly eats large amounts of food in a short time (binge eating) and then tries to prevent weight gain by making themselves sick, using laxatives, exercising excessively, or fasting. Unlike anorexia, people with bulimia are usually a normal weight, which means the condition often stays hidden.

What causes it?

Bulimia is caused by a combination of factors:

• Genetics: It can run in families
• Brain chemistry: Differences in brain chemicals that control mood and appetite
• Psychological factors: Low self-esteem, perfectionism, difficulty coping with emotions
• Life experiences: Dieting, pressure about weight, stressful events, trauma
• Society and culture: Pressure to be thin from media and social media

What are the warning signs?

• Eating large amounts of food, often in secret
• Going to the bathroom immediately after meals
• Sore throat, damaged teeth, swollen cheeks
• Feeling guilty or ashamed about eating
• Being very concerned about weight and shape
• Mood swings, irritability
• Weakness, tiredness, heart palpitations

Is it dangerous?

Yes, bulimia can cause serious health problems:

• Low potassium levels that can cause heart problems
• Damage to teeth and throat
• Dehydration and kidney problems
• Depression and risk of suicide
• In rare cases, it can be life-threatening

How is it treated?

Treatment usually involves:

• Talking therapy (CBT): The most effective treatment, helping you change thoughts and behaviours
• Medication (fluoxetine): A high dose of this antidepressant can reduce the urge to binge
• Nutritional support: Learning to eat regularly without restricting
• Medical monitoring: Blood tests to check your body is healthy

Will I get better?

Yes. With proper treatment:

• About half of people recover completely
• Most others improve significantly
• The earlier you get help, the better the outcome

Where to get help?

• Talk to your GP - they can refer you to specialist services
• Contact eating disorder charities: Beat (UK), NEDA (US)
• If you're in crisis, call emergency services or attend A&E

---

15. Quality Markers and Audit Standards

---

16. Key Guidelines

---

17. Historical Context

• 1979: Gerald Russell first formally described Bulimia Nervosa as "an ominous variant of anorexia nervosa" in a landmark paper, distinguishing it from anorexia based on normal weight and specific binge-purge behaviours. [3]
• 1980: Bulimia included in DSM-III as a distinct diagnosis.
• 1987: DSM-III-R renamed the condition "Bulimia Nervosa" and refined criteria.
• 1980s-1990s: Development of CBT for Bulimia Nervosa by Christopher Fairburn in Oxford.
• 1987: First FDA approval of fluoxetine 60mg for Bulimia Nervosa following RCTs. [8]
• 1994: DSM-IV introduced severity specifiers based on purging frequency.
• 2013: DSM-5 reduced frequency threshold from twice weekly to once weekly.
• 2017: NICE NG69 published comprehensive UK guidelines.

---

18. References

1. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5). Arlington, VA: American Psychiatric Publishing; 2013.

2. Treasure J, Claudino AM, Zucker N. Eating disorders. Lancet. 2010;375(9714):583-593. doi:10.1016/S0140-6736(09)61748-7. PMID: 19931176

3. Russell G. Bulimia nervosa: an ominous variant of anorexia nervosa. Psychol Med. 1979;9(3):429-448. doi:10.1017/S0033291700031974. PMID: 482466

4. Mehler PS, Rylander M. Bulimia Nervosa - medical complications. J Eat Disord. 2015;3:12. doi:10.1186/s40337-015-0044-4. PMID: 25914826

5. Brown CA, Mehler PS. Medical complications of self-induced vomiting. Eat Disord. 2013;21(4):287-294. doi:10.1080/10640266.2013.797317. PMID: 23767670

6. Arcelus J, Mitchell AJ, Wales J, Nielsen S. Mortality rates in patients with anorexia nervosa and other eating disorders. A meta-analysis of 36 studies. Arch Gen Psychiatry. 2011;68(7):724-731. doi:10.1001/archgenpsychiatry.2011.74. PMID: 21727255

7. National Institute for Health and Care Excellence. Eating disorders: recognition and treatment. NICE guideline [NG69]. 2017. https://www.nice.org.uk/guidance/ng69

8. Fluoxetine Bulimia Nervosa Collaborative Study Group. Fluoxetine in the treatment of bulimia nervosa. A multicenter, placebo-controlled, double-blind trial. Arch Gen Psychiatry. 1992;49(2):139-147. doi:10.1001/archpsyc.1992.01820020059008. PMID: 1550466

9. Romano SJ, Halmi KA, Sarkar NP, Koke SC, Lee JS. A placebo-controlled study of fluoxetine in continued treatment of bulimia nervosa after successful acute fluoxetine treatment. Am J Psychiatry. 2002;159(1):96-102. doi:10.1176/appi.ajp.159.1.96. PMID: 11772696

10. Smink FR, van Hoeken D, Hoek HW. Epidemiology of eating disorders: incidence, prevalence and mortality rates. Curr Psychiatry Rep. 2012;14(4):406-414. doi:10.1007/s11920-012-0282-y. PMID: 22644309

11. Steinhausen HC, Weber S. The outcome of bulimia nervosa: findings from one-quarter century of research. Am J Psychiatry. 2009;166(12):1331-1341. doi:10.1176/appi.ajp.2009.09040582. PMID: 19884225

12. Bulik CM, Sullivan PF, Tozzi F, Furberg H, Lichtenstein P, Pedersen NL. Prevalence, heritability, and prospective risk factors for anorexia nervosa. Arch Gen Psychiatry. 2006;63(3):305-312. doi:10.1001/archpsyc.63.3.305. PMID: 16520436

13. Kaye WH, Wierenga CE, Bailer UF, Simmons AN, Bischoff-Grethe A. Nothing tastes as good as skinny feels: the neurobiology of anorexia nervosa. Trends Neurosci. 2013;36(2):110-120. doi:10.1016/j.tins.2013.01.003. PMID: 23333342

14. Lo Russo L, Campisi G, Di Fede O, Di Liberto C, Panzarella V, Lo Muzio L. Oral manifestations of eating disorders: a critical review. Oral Dis. 2008;14(6):479-484. doi:10.1111/j.1601-0825.2007.01422.x. PMID: 18826380

15. Morgan JF, Reid F, Lacey JH. The SCOFF questionnaire: assessment of a new screening tool for eating disorders. BMJ. 1999;319(7223):1467-1468. doi:10.1136/bmj.319.7223.1467. PMID: 10582927

16. Fairburn CG, Cooper Z, Doll HA, O'Connor ME, Bohn K, Hawker DM, Wales JA, Palmer RL. Transdiagnostic cognitive-behavioral therapy for patients with eating disorders: a two-site trial with 60-week follow-up. Am J Psychiatry. 2009;166(3):311-319. doi:10.1176/appi.ajp.2008.08040608. PMID: 19074978

17. Walsh BT, Wilson GT, Loeb KL, et al. Medication and psychotherapy in the treatment of bulimia nervosa. Am J Psychiatry. 1997;154(4):523-531. doi:10.1176/ajp.154.4.523. PMID: 9090340

18. Le Grange D, Lock J, Agras WS, Bryson SW, Jo B. Randomized clinical trial of family-based treatment and cognitive-behavioral therapy for adolescent bulimia nervosa. J Am Acad Child Adolesc Psychiatry. 2015;54(11):886-894.e2. doi:10.1016/j.jaac.2015.08.008. PMID: 26506579

19. Hay P, Chinn D, Forbes D, et al. Royal Australian and New Zealand College of Psychiatrists clinical practice guidelines for the treatment of eating disorders. Aust N Z J Psychiatry. 2014;48(11):977-1008. doi:10.1177/0004867414555814. PMID: 25351912

20. Mitchell JE, Crow S. Medical complications of anorexia nervosa and bulimia nervosa. Curr Opin Psychiatry. 2006;19(4):438-443. doi:10.1097/01.yco.0000228768.79097.3e. PMID: 16721178

---

Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. It does not constitute medical advice. If you are struggling with an eating disorder, please seek help from a healthcare professional. In the UK, contact your GP or the eating disorders charity Beat (0808 801 0677). In crisis, attend A&E or call emergency services.