6.1.7 Eating disorders

Anorexia nervosa

Diagnosis

• ICD-11 anorexia nervosa (International Classification of Diseases, 11th revision) has three parts: significantly low body weight, a persistent pattern of behaviour that prevents weight restoration, and weight or shape dominating self-evaluation.

• The third part can instead be met when the person sees their low weight as normal or even excessive.

• Fear of weight gain is typical but not required, and people may show it through behaviour rather than say it.

• The adult body mass index (BMI) guideline is below 18.5, interpreted alongside weight history, developmental stage and the rest of the syndrome.

• Amenorrhoea is not required by ICD-11.

• Rapid weight loss, such as over 20% within six months, can replace the low-weight requirement in ICD-11 if the other features are present. Children need age-appropriate assessment.

• Binge eating and purging at a significantly low weight (adult BMI under 18.5) with fear of weight gain is anorexia nervosa. Bulimia nervosa requires that weight is not significantly low.

• Normal or high current weight does not exclude ICD-11 anorexia when rapid weight loss meets the alternative requirement and the other diagnostic features are present.

• ICD-11 describes excessive exercise as more common in males with anorexia nervosa and laxative misuse as more common in females.

Epidemiology

• Lifetime prevalence is about 0.5 to 1% in women, with lower recognised rates in men.

• Onset is usually in mid to late adolescence, with a mean age of about 16 to 17 and peak incidence at 15 to 19 years.

• Anorexia nervosa occurs across all socioeconomic groups with no excess in lower social classes; the older view linked it with higher social class.

Aetiology

• Heritability in twin and family studies is roughly 28 to 74%, with non-shared environment explaining much of the rest.

• The genetic architecture is polygenic and overlaps with anxiety, obsessive-compulsive disorder (OCD) and metabolic traits.

• Anxiety, perfectionism and rigid coping often precede onset. Restriction relieves anxiety and weight loss brings a sense of control, which reinforces the illness.

• Starvation itself worsens rigidity, mood and concentration, so nutritional and psychological treatment proceed together.

• Thinness ideals and dieting contribute but are not sufficient causes, and families are not to blame.

Comorbidity and differential diagnosis

• OCD, anxious and obsessional traits and anxiety disorders beginning in childhood are the most specific associations, and they usually start before the eating disorder.

• Depression is common but usually secondary, and some symptoms lift with nutrition. Severe independent depression or suicide risk is still treated without waiting for weight gain.

Physical features

• Starvation causes bradycardia, hypotension, hypothermia, muscle wasting, dry skin, lanugo and menstrual disturbance; children may show impaired growth and delayed puberty.

• Vomiting causes parotid swelling, dental erosion and Russell's sign.

• Bone loss starts early, and weight restoration may not fully reverse it.

• Starvation depletes hepatic glutathione, so the toxic paracetamol metabolite NAPQI is not neutralised and paracetamol liver injury follows more readily.

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Cardiac complications

• Bradycardia and hypotension are adaptive: heart rate and blood pressure fall together as the body conserves energy.

• Resting bradycardia comes from raised vagal tone and reduced metabolic demand. Anorexia nervosa does not cause raised blood pressure, widened pulse pressure, a shortened QT or cardiac enlargement.

• Sinus bradycardia and QT prolongation are the commonest cardiac abnormalities; torsades de pointes and ventricular fibrillation are rarer downstream complications.

• Corrected QT (QTc) prolongation happens because starvation and its electrolyte losses delay cardiac repolarisation.

• Low potassium and low magnesium lengthen the QT, whereas high potassium or high calcium shorten it.

• Hypokalaemia, typically from purging, is the electrolyte disturbance most likely to cause sudden cardiac death, by lengthening the QT (QU) interval and causing torsades and ventricular fibrillation.

• Cardiomyopathy with congestive cardiac failure and pulmonary oedema can occur in severe illness, because the atrophied myocardium has little reserve and decompensates when refeeding loads it.

• In that setting a heart rate in the normal range is a relative tachycardia.

• Takotsubo cardiomyopathy can complicate severe illness: a sympathetic catecholamine surge stuns the myocardium, possibly with multivessel spasm and microvascular dysfunction, without an occluded coronary artery.

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Blood results

In starvation the stress and counter-regulatory hormones rise while the reproductive, thyroid and growth axes are suppressed.

Vomiting loses gastric hydrochloric acid, and secondary hyperaldosteronism keeps the alkalosis going.

Refeeding syndrome

• Total body phosphate, potassium and magnesium fall in starvation even when serum levels look normal.

• When carbohydrate returns, an insulin surge moves phosphate, then potassium and magnesium, into cells. Low serum phosphate is the first and defining sign, so phosphate is the result to follow.

• Severe depletion causes arrhythmia, heart failure, respiratory weakness, seizures and death, and fluid shifts add risk.

• Give thiamine before or with feeding, replace deficient electrolytes, and check phosphate, potassium, magnesium, glucose and fluid balance, often daily at first in high-risk patients.

• Clinicians avoid both unsafe rapid feeding and prolonged underfeeding.

Medical risk assessment

• MEED (CR233, 2022) replaced MARSIPAN and covers all ages and eating disorders.

• MEED grades physical risk by numerical cut-offs, and one red value outranks several amber findings.

• The SUSS test (sit up, squat, stand) is a bedside test of proximal muscle power: the person fails if they cannot rise from lying or squatting without using their arms.

• SUSS detects starvation-related wasting that testing single muscle groups can miss, and it stays informative when recorded weight has been falsified. It is not a stand-alone admission rule.

• Severe hypokalaemia is the blood red flag needing urgent medical transfer, because of immediate arrhythmia risk, unlike the expected adaptive changes of starvation.

• Marked QTc prolongation is an acute cardiac red flag that warrants transfer from a psychiatric to a medical setting, whereas a low BMI reflects chronic severity.

• An acceptable BMI or normal first blood results do not establish safety, and rapid weight loss matters at any weight.

• Clinicians ask about suicide, self-harm and substances, and assess decision-specific capacity: a person may understand the facts yet be unable to weigh the risks because of the illness.

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Treatment

Psychological treatment

• For adults, focal psychodynamic therapy is the next option when first-line therapy is unacceptable, contraindicated or ineffective.

• Family therapy is first line only for young people; adults' families are involved with consent.

• Reaching a healthy body weight or BMI for age is a main treatment goal in the National Institute for Health and Care Excellence (NICE) guidance.

Medication

• No medication, antidepressants included, works as the sole treatment. NICE advises against drug-only treatment, and any drug is at most an adjunct to psychological treatment and nutrition.

• Olanzapine is the one drug with placebo-controlled evidence of a modest rise in weight or BMI, with less consistent psychological benefit; prescribers weigh QT risk, metabolic effects and bone health.

• Mirtazapine is avoided because it strongly stimulates appetite and causes weight gain.

• Antidepressants may treat comorbidity but not the core syndrome.

• NICE does not support routine oestrogen for low bone mineral density in children and young people.

Course and outcome

• About half recover fully over two to three decades, and about a fifth remain chronically ill.

• Mortality is about 5% per decade, with a standardised mortality ratio around 5 to 6 (5.86 in the Arcelus 2011 meta-analysis); about one in five deaths is suicide.

• Comorbid alcohol use disorder is the strongest predictor of premature death, especially from natural causes.

• Poorer outcome goes with adult onset, self-induced vomiting or binge-purge behaviour, longer untreated illness, lower minimum weight and poor engagement.

• Better outcome goes with early (adolescent) onset, rapid presentation and close family involvement.

• Relapse is common in the first one to two years after weight restoration, especially at transitions.

Bulimia nervosa

Definition and boundaries

Bulimia nervosa is recurrent binges with loss of control, followed by regular compensatory behaviour, with shape and weight driving self-evaluation, in someone who is not significantly underweight.

• Compensatory behaviour in ICD-11 is any repeated inappropriate behaviour aimed at preventing weight gain, so self-induced vomiting is not required.

• Purging compensation includes vomiting, laxatives and diuretics; non-purging compensation includes strenuous exercise and fasting.

• Deliberate insulin omission in diabetes also counts as compensation.

• A binge in ICD-11 involves eating notably more or differently than usual with loss of control; the amount need not be objectively large.

• Binge eating disorder is told apart by the absence of regular compensatory behaviour.

• Anorexia nervosa is told apart by significantly low weight; where its criteria are met, binge-purge behaviour is classified within anorexia.

Epidemiology and course

• Community surveys place bulimia nervosa at about 0.5 to 1% of the general adult population, with lower recognised rates in men.

• Onset usually follows adolescent dieting, and people present in their late teens or early twenties.

• About half reach full remission within 5 to 10 years, while others relapse or stay symptomatic.

• The standardised mortality ratio is 1.93, against 5.86 for anorexia nervosa (2011 meta-analysis).

Maintaining factors

• Fairburn's cognitive behavioural model links overvaluation of weight and shape to restraint, bingeing and renewed compensation, with brief relief reinforcing the cycle.

• Cholecystokinin is a gut satiety hormone whose release after meals is blunted in bulimia nervosa, which makes it a theoretical treatment target.

Physical complications

Repeated vomiting causes complications at a normal weight, so a normal weight does not mean medical safety.

Signs of repeated vomiting

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Blood tests and ECG

• Hypokalaemia is the characteristic blood abnormality of purging, because vomiting loses potassium and chloride.

• Electrolyte disturbance can cause seizures and arrhythmia, and QT-prolonging drugs add to the arrhythmia risk.

• Hypokalaemia shows on the ECG as ST depression, flattened or inverted T waves and prominent U waves.

• Raised serum amylase of salivary origin marks recent self-induced vomiting; liver enzymes and bilirubin are not raised by vomiting itself.

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• Rebound oedema can follow when long-term purging stops, because aldosterone stays active; warn patients beforehand so fear of weight gain does not restart purging.

Ipecac

• Ipecacuanha (ipecac) syrup is the emetic classically misused to self-induce vomiting.

• Repeated ipecac use causes a toxic cardiomyopathy, because its alkaloid emetine is cleared slowly and accumulates in muscle.

Pregnancy

• Bulimia nervosa in pregnancy raises the risk of fetal loss and other adverse obstetric outcomes.

• Pregnancy warrants specialist review but does not automatically require admission.

Treatment

NICE (NG69) makes psychological treatment the first line for adults, and most care is outpatient.

1. Bulimia-focused guided self-help with brief clinician support comes first.

2. Individual eating-disorder-focused cognitive behavioural therapy (CBT-ED), usually up to about 20 sessions, follows if guided self-help is unsuitable or ineffective after about four weeks.

• CBT-ED is the best-evidenced psychological treatment and is given individually rather than in a group.

• CBT-ED establishes regular meals and snacks, reduces restraint and challenges the overvaluation of weight and shape.

• Family therapy is for young people, and interpersonal therapy is not a current first-line option.

• Medication must never be the sole treatment, because psychological treatment is the core of care.

• Fluoxetine at 60 mg daily is licensed as an adjunct to psychotherapy and reduces bingeing and purging even without depression.

• Clinicians correct electrolyte abnormalities and arrange dental care alongside therapy.