Eating disorders: anorexia nervosa, bulimia nervosa, atypical and other eating disorders. Epidemiology, etiology, clinical features, course, and treatment

01Definition and overview

Eating disorders are persistent disturbances of eating or eating-related behaviour that damage physical health or psychosocial functioning. In anorexia nervosa, bulimia nervosa and binge eating disorder, self-worth is judged largely by shape, weight and their control; in avoidant-restrictive food intake disorder, it is not. ICD-11 gathers them as feeding or eating disorders (6B80–6B8Z).

Binges in ICD-11 are episodes of eating more than usual, or differently, with a loss of control; in DSM-5 they are an amount clearly larger than most people would eat in a similar time. For bulimia, ICD-11 gives as a guide binges at least weekly over a month, while DSM-5 requires binges and compensation at least weekly for three months.

The weight thresholds for anorexia nervosa differ between systems:

Amenorrhoea is no longer required. Other specified eating disorders include atypical anorexia nervosa (all the features after major weight loss, but a weight still in or above the normal range), purging disorder and night eating syndrome. In type 1 diabetes, deliberately omitting insulin to lose weight is a dangerous compensatory behaviour that can occur in any of them.

02Etiology and pathophysiology

Eating disorders arise from genes, temperament and environment acting together, usually in adolescence, and starvation itself then holds them in place.

The genetic findings support a view of anorexia nervosa as a metabolic as well as psychiatric disorder: some people seem able to sustain starvation, and feel less anxious when they restrict.

Starvation produces many of the psychological features: preoccupation with food, rituals around eating, low mood, irritability, poor concentration, rigid thinking and social withdrawal, as healthy men showed when semi-starved in the Minnesota experiment of the 1940s. These lift with refeeding, which is why weight restoration comes before most psychological change. Hormones adapt: the hypothalamic-pituitary-gonadal axis shuts down, cortisol rises, T3 falls, and the brain shrinks reversibly.

The transdiagnostic cognitive model links the disorders:

1. 1

   Overvalued shape and weight

   Self-worth comes to depend on controlling shape, weight and eating.
2. 2

   Strict dieting

   Rigid rules about what, when and how much to eat; in anorexia nervosa, restriction succeeds, and starvation then reinforces the preoccupation.
3. 3

   Binges

   In bulimia, breaking a rule and hunger trigger a binge, made likelier by stress and low mood.
4. 4

   Compensation

   Vomiting, laxatives or fasting relieve the fear of weight gain, then lead to more dieting, which sets up the next binge.

03Clinical features

Anorexia nervosa

It typically begins in mid-adolescence, around 15 to 19 years, though onset before puberty and in adulthood occurs. The person eats little, often low-energy foods, cuts food into small pieces, eats slowly, avoids eating with others and may cook for others. Exercise is often excessive and driven. Some also purge or binge (binge-purge type). They see themselves as fat or a body part as too large, and often deny that they are ill, which brings them to doctors through worried parents, a GP or a school. Depression, anxiety, OCD and self-harm are common.

Bulimia nervosa

It begins a little later, usually in late adolescence, often after dieting and sometimes after a period of anorexia. Binges are secret, often of high-energy foods, with a sense of loss of control and then shame; they are followed by vomiting, laxatives, diuretics, fasting or exercise. Weight is usually normal, so it is easily missed. Signs of vomiting include hypokalaemia, which can cause arrhythmia, swollen parotid glands, calluses on the back of the hand from the teeth (Russell's sign), oesophagitis and, rarely, oesophageal tears. Stomach acid causes dental erosion, first on the palatal surfaces of the upper front teeth. Depression, self-harm, and alcohol and drug misuse are common.

Binge eating disorder

The commonest eating disorder in adults, and the one most evenly spread between women and men: binges with loss of control and marked distress, eating rapidly, alone or until uncomfortably full, without regular compensation. It is often linked with obesity, type 2 diabetes and depression.

ARFID and other forms

ARFID usually begins in childhood and is commoner in boys and in autistic children. Its three main drivers are sensory sensitivity (texture, smell, colour), fear of an aversive consequence (after choking, vomiting or pain), and low interest in eating. It can cause weight loss, faltering growth, deficiencies and dependence on supplements or tube feeding. Atypical anorexia nervosa carries the same medical risks as anorexia nervosa, including bradycardia and refeeding syndrome, despite a normal BMI. Insulin omission in type 1 diabetes greatly raises the risk of ketoacidosis, retinopathy and early death.

04Diagnosis and management

Recognition and assessment

Most people with an eating disorder are never diagnosed. NICE advises thinking of one with low or high weight for age, rapid weight loss, worrying dieting, social withdrawal around food, menstrual disturbance, unexplained electrolyte imbalance or hypoglycaemia, atypical dental erosion, difficulty managing diabetes, and in those in weight-focused sport, dance or modelling. The SCOFF questions are a brief screen, but do not use a screening tool, BMI or duration alone to decide whether someone has an eating disorder or needs treatment.

Assessment covers eating, weight history and compensatory behaviours, mental state and risk of suicide, and a physical examination with weight, height, pulse, lying and standing blood pressure, temperature and the sit-up-squat-stand test. Tests include full blood count, urea and electrolytes, phosphate, magnesium, calcium, liver tests, glucose and an ECG. The differential includes hyperthyroidism, diabetes, coeliac and inflammatory bowel disease, malignancy, depression with loss of appetite, and psychosis with beliefs about food.

Medical risk

MEED, the Royal College of Psychiatrists' 2022 guidance that replaced MARSIPAN, rates risk on many measures together, in red (high risk) and amber (alert). Adult thresholds for red include:

One red rating, or two or more amber ones, should probably be treated as high risk. In children and young people, weight is judged as a percentage of median BMI for age, with under 70 per cent high risk. These are guides; the trend and the whole picture matter more than any one number.

Where to treat

Most patients are treated as outpatients by a specialist eating disorder service. Admission is for high medical risk, failure to improve, or high suicide risk, to a medical ward for stabilisation when the danger is physical, ideally with eating disorder input, and to a specialist unit for longer weight restoration. No absolute BMI threshold decides admission. Anorexia nervosa can impair the ability to weigh information about food and weight, so capacity must be assessed for the decision at hand; when life is at risk and the patient refuses, mental health law allows treatment, including nasogastric feeding, as treatment of the mental disorder.

Refeeding syndrome

Refeeding syndrome occurs when food is reintroduced after starvation. Carbohydrate releases insulin, which drives phosphate, potassium and magnesium into cells and uses up thiamine, while sodium and water are retained. Blood phosphate can fall steeply, usually within 72 hours of starting to feed, sometimes later in the most malnourished, and with it cellular energy: muscle weakness, respiratory failure, heart failure, arrhythmias, oedema, confusion, seizures and death. It is commonest with a very low BMI, little intake for days, rapid recent weight loss, low electrolytes before feeding, and alcohol misuse.

1. 1

   Before feeding

   Check electrolytes, glucose and ECG, and start thiamine (with a multivitamin), continued for 7 to 10 days.
2. 2

   Start steadily

   In high-risk adults, MEED suggests about 20 kcal/kg a day, rising by 5 kcal/kg every two days; if not high risk, 30 to 35 kcal/kg a day. If phosphate falls, hold the intake steady rather than cutting it.
3. 3

   Monitor closely

   Phosphate, potassium and magnesium every 12 to 24 hours for the first five days in those at high risk, otherwise three times a week, and again at 7 to 10 days, since refeeding syndrome can come late; a low threshold for cardiac monitoring.
4. 4

   Supplement, do not stop

   Replace falling electrolytes while feeding continues, aiming for a weight gain of 0.5 to 1 kg a week.

Underfeeding is as dangerous: more deaths in anorexia nervosa have been reported from feeding too cautiously than from refeeding syndrome.

Psychological treatment

All include dietetic support, attention to physical health and, in anorexia, a focus on weight restoration. Advice for those who purge: laxatives and diuretics do not reduce the absorption of calories and should be tapered and stopped; excessive exercise should stop.

Drugs and bone health

Medication must never be the sole treatment for anorexia, bulimia or binge eating disorder. No drug restores weight in anorexia: olanzapine gives a small gain in some trials and is unlicensed, and ECG monitoring is needed with any drug that prolongs the QTc. In bulimia, fluoxetine at 60 mg a day reduces binges and vomiting, as an adjunct to therapy, and is licensed for this in the UK. In binge eating disorder, lisdexamfetamine is approved in the USA but not for this use in the UK or EU, and topiramate is sometimes used off-label, with a pregnancy prevention programme for women who could become pregnant. Low bone density is treated mainly by restoring weight; NICE suggests a bone density scan after two years of underweight in adults (one year in young people), bisphosphonates only for adult women with long-term low weight and low bone density, after discussing the risks in pregnancy, and no routine oestrogen for young people.

05Epidemiology

report anorexia nervosa in their lifetime, up to 2 per cent bulimia and up to 4 per cent binge eating disorder

up to 4per cent of European womenreport anorexia nervosa in their lifetime, up to 2 per cent bulimia and up to 4 per cent binge eating disorder

with an eating disorder is detected by health services

1 in 3peoplewith an eating disorder is detected by health services

the expected death rate in anorexia nervosa

5.9timesthe expected death rate in anorexia nervosa

in anorexia nervosa are suicides

1 in 5deathsin anorexia nervosa are suicides

Eating disorders affect about 0.3 to 0.7 per cent of European men, and women about ten times more often for anorexia; binge eating disorder is the most evenly split. Point prevalence worldwide rose from about 3.5 per cent in the early 2000s to 7.8 per cent by 2018, partly through wider definitions, and referrals and admissions rose further during the COVID-19 pandemic. Over 70 per cent have a comorbid disorder: anxiety in more than half, mood disorders in more than 40 per cent, self-harm in more than a fifth. Anorexia nervosa peaks in incidence in mid-adolescence; bulimia nervosa a little later.

06Prognosis

• Anorexia nervosa has a crude mortality of about 5 deaths per 1000 patients each year, a standardised mortality ratio of about 5.9, among the highest of any psychiatric disorder, from starvation, arrhythmia, infection and suicide. Bulimia nervosa and other eating disorders carry roughly twice the expected rate.
• In long-term follow-up of anorexia nervosa, about half recover fully, a third improve with residual symptoms, and a fifth remain chronically ill. Some cross over to bulimia.
• Poor outcomes follow a long illness before treatment, very low weight, binge-purge symptoms, onset in adulthood, comorbid personality disorder or substance misuse, and difficult family relationships. Onset in adolescence with early family therapy does best.
• Bulimia nervosa does better: most improve with treatment, though relapse is common.
• Lasting harm includes osteoporosis, infertility, dental damage and impaired growth.