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Eating disorders: essential information
Paul Robinson provides an overview of the three main conditions
The eating disorders anorexia nervosa, bulimia nervosa, and binge eating disorder have become major health problems, particularly among young women, since the 1950s.1 The full disorders affect 12% with atypical and less severe eating disorders much more common. Their standardised mortality ratio is among the highest for any psychiatric condition.2 The common factor among all eating disorders is dissatisfaction with body shape and consequent dietary restriction. The differences reside in the degree to which dieting is effective and the lengths to which sufferers will go to achieve weight control. (See Box 2 for diagnostic criteria.)
Anorexia nervosa is present when weight loss is severe (BMI <17.5) and when amenorrhoea due to weight loss induced hypothalamic hypogonadism appears. Bulimia nervosa is present when episodes of massive overeating occur (usually in response to dietary restriction), and is associated with inappropriate compensatory behaviours (see Box 3) aimed at minimising the effects of overeating on weight. Both conditions require an abnormally intense hatred of fat, a feeling that one is fat, and a dislike of one's own body. The first two predominate in anorexia nervosa, and the third in bulimia nervosa. The diagnosis of binge eating disorder has been applied to people, usually obese, who engage in binges (bulimic episodes) without the behaviours listed in Box 3. The three conditions overlap and underweight patients who overeat and vomit have anorexia and bulimia nervosa, and patients who overeat go through periods in which they may not engage in vomiting, etc and times when they do, and so pass from one category to another.

A common factor among all eating disorders is dissatisfaction with body shape (MARTIN HASWELL)
Epidemiology3,4
The group at highest risk are young females between the ages of 15 and 30, with anorexia nervosa striking a somewhat younger age group and bulimia nervosa a rather older group. The sex incidence is one male to between 10 and 20 females. Anorexia nervosa is overrepresented in social classes one and two (professional and managerial) but bulimia nervosa appears to be distributed through all classes equally. Bulimia nervosa has had a prevalence in young women of 0.5-1.1% and anorexia nervosa 0.1-0.7%. Estimates of the prevalence of all clinically significant eating disorders, including those that just fail to meet full criteria (eating disorders not otherwise specified, EDNOS) are that 8.7% of females in the general population are affected.
Aetiology
There appears to be a genetic element,5 although the nature of what is inherited remains to be clarified. Early experiences, particularly family over-protectiveness,6 may be important in some cases, as may the opposite: various types of abuse and neglect.7 Engaging in training or careers with a strong emphasis on thinness, including ballet, modelling, and being a racing jockey, can predispose to eating disorder symptoms and, in an otherwise predisposed individual, a full blown eating disorder. The most powerful factor is female sex, with a male to female ratio of at least 1 to 10. This is usually attributed to the greater social pressure exerted via the media and peer pressure on women to be thin, although other factors, such as women's changing role in society,8 play an important part.
Clinical features of eating disorders
Eating disorders can present to a doctor with symptoms referable to almost any system. A case description, which should be read with reference to Box 4, is shown in Box 1.
Box 1 - Case description
An 18 year old woman collapses in the street and is brought to A & E by ambulance. She is found to be emaciated, and has scars of cuts on her left arm. She also has enlarged parotid glands and blood tests show a high paracetamol level and hypokalaemic alkalosis. In A & E she develops a ventricular arrhythmia which responds to a potassium infusion and she is treated for paracetamol poisoning. After a few days on a medical ward she recovers enough to give a history of weight loss, bingeing, and vomiting for several years. She refuses to eat and her weight declines to a body mass index of 12.5. She develops severe muscle weakness, a raised creatine kinase level, and thrombocytopaenic purpura. A muscle biopsy shows type 2 fibre atrophy and a bone marrow biopsy is hypocellular. Nasogastric feeding is instituted, and she is offered small meals. She recovers some strength, but manages to get hold of a large amount of bread and chocolate on which she binges, and develops abdominal swelling and severe vomiting. Abdominal x ray confirms gastric dilatation and she is treated conservatively with nasogastric suction and intravenous fluids. She is disoriented and has paranoid ideas about staff on the ward. She gradually recovers and, with constant psychiatric nursing care, agrees to take fluids and then food by mouth.
A full history reveals that she was a victim of a sexual assault by a stranger at the age of 10, and that symptoms of depression, anorexia nervosa, and bulimia nervosa coincided with the onset of puberty at 14. She had been amenorrhoeic for three years, and a bone mineral density scan showed moderately severe osteoporosis. Further treatment consists of individual and family therapy, attendance at a day service, and fluoxetine medication.
The key diagnostic features of each of the three conditions are given in Box 2. Patients may conceal the true nature of their illness by convincing doctors to engage in fruitless and expensive investigations. Thus, patients with eating disorders may be investigated for malabsorption, pituitary disease, gastric problems, and food allergies. The last can be particularly unhelpful, because patients diagnosed as allergic to, say, grains, will then be able to avoid them with a medical blessing and lose weight. Treatment of infertility due to anorexia nervosa with assisted conception also raises ethical objections, in view of the problems faced by the children of women with active eating disorders.
Box 2 - Diagnostic criteria for eating disorders
Anorexia nervosa (ICD 10)16
- Self imposed weight loss due to dieting, vomiting, or other means leading to <85% expected weight or a body mass index of <17.5. In younger patients, lack of expected growth.
- Abnormal attitudes to food and weight. Preoccupation with desire to be thinner. Feeling fat even though underweight.
- Endocrine disturbance. Loss of menstrual periods in females. Loss of libido, sexual interest, and erectile function in males. Primary amenorrhoea and delayed puberty in prepubertal children.
Bulimia nervosa (ICD 10)
- Persistent craving with episodes of overeating.
- Counteracting the "fattening" effects of food by self induced vomiting, purgative abuse, starvation, appetite suppressants, thyroid preparations, diuretics or, in diabetics, neglect of insulin.
- Morbid dread of fatness. Self imposed weight threshold below a healthy weight. Often a previous overt or cryptic episode of anorexia nervosa.
Binge eating disorder (DSM IV)17
- Recurrent episodes of binge eating involving
a) eating, within a discrete time period (eg <2 hours) an abnormally large amount of food
b) a sense of lack of control over eating.
- Marked distress about binge eating.
- Binge eating on at least two days per week for six months.
- Not associated with regular use of inappropriate compensatory behaviours.
Box 3 - Inappropriate compensatory behaviours used after eating in anorexia and bulimia nervosa
| Behaviour |
Comments |
| Severe dietary restriction (including prolonged starvation) |
In restricting type anorexia nervosa |
| Excessive exercise |
|
| Self induced vomiting |
Most common behaviour |
| Laxative abuse |
Uncertain whether it leads to reduced nutrient absorption |
| Abuse of enemas |
|
| Diuretic abuse |
Seen in medical personnel |
| Anorectic drug abuse (including amphetamines) |
Prescribed or "street" |
| Thyroid hormone abuse |
Seen in medical personnel |
| Neglect of insulin in diabetics |
Extremely difficult to manage |
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Prognosis and management
The keys to management are medical and psychosocial assessment, engagement in therapy, medical and psychiatric monitoring, support, and specific therapy for the eating disorder.
Assessment includes attention to information needed to make a diagnosis (Box 2), definition of any complications present (Box 4), a history from the patient and family to allow a formulation of the possible predisposing, precipitating, and perpetuating causes of the disorder, and a mental and physical examination to supplement historical information and allow diagnoses to be postulated.
Box 4 Some of the ways in which eating disorders can present to doctors1
| System |
Symptom/condition |
Mechanism |
| Psychiatric |
Depression |
Low weight Bulimia Co-existing depressive illness |
| |
Obsessive-compulsive disorder Deliberate self harm Psychosis |
Low weight, obsessional traits Depression, personality disorder Refeeding, stimulant abuse, Co-existing psychotic illness |
| Alimentary |
Dental erosion Parotid enlargement Haematemesis |
Gastric acid, carbonated drinks, bingeing on sweet foods Vomiting, bingeing, chewing and spitting food Pharyngeal damage, oesophagitis Mallory Weiss |
| |
Prolonged gastric fullness |
Delayed gastric emptying Distorted interoception |
| |
Abdominal pain Diarrhoea/constipation Prolapse |
Gastric dilatation/perforation Laxative abuse Laxative, enema abuse |
Paediatric Endocrine |
Failure to grow in weight, height or both Amenorrhoea Infertility |
Anorexia nervosa in child OR in mother Hypothalamic hypogonadism Hypothalamic hypogonadism Polycystic ovaries in bulimia nervosa |
| |
Problems with pregnancy, low birth weight |
Malnutrition |
| Rheumatology |
Osteoporosis |
Low oestrogen, malnutrition, ?high cortisol |
| Cardiology |
Low blood pressure Arrhythmias |
Cardiac wasting, dehydration Hypokalaemia, low phosphate in refeeding |
| Haematology |
Pancytopaenia, purpura |
Low weight, bone marrow depression |
| A & E |
Overdose, deliberate self harm Collapse |
Depression, personality disorder Cachexia, GI bleed, acute abdomen |
| Infectious diseases |
TB |
Depressed immunity |
| Neurology |
Delirium Myopathy Neuropathy Pressure palsy (eg ulnar, peroneal) |
Refeeding, Wernicke's encephalopathy Nutritional myopathy (type 2 fibre degeneration) Unknown Wasting, pressure on vulnerable nerves |
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| 1Mnemonists might like PAPER CHAIN as a help in remembering this list |
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Engagement in treatment is a very important area that has given rise to the technique of motivational enhancement9 in which the level of motivation is assessed and patients are moved as far up the scale in the direction of higher motivation as is possible.
Medical monitoring requires the use of reproducible ways of measuring physical state so that care can be shared between primary and secondary care, the patient, and family. Three physical tests that are sensitive to muscle and cardiovascular function are the sit-up, stand up, and postural dizziness tests (Box 5). In addition, serum potassium, especially if vomiting or laxative abuse is present, blood count, creatine kinase (for myopathy) and liver function tests can be monitored if BMI <13. Consider admission (psychiatric or medical) if physical measures are deteriorating. Note that weight or BMI alone may be completely unreliable in a patient who may drink up to 4 litres of water before weighing. Psychiatric monitoring should form part of follow up so that depression is identified and treated, either through improvement of the eating disorder or using antidepressant medication. Fluoxetine has been studied most in bulimia nervosa10 and may be the drug of choice for depression in this disorder. Osteoporosis appears to respond to weight gain, but no other treatment (including hormone replacement) has been shown to reverse the disease, in the absence of weight restoration.11
| Box 5 Medical monitoring in anorexia nervosa |
| Name |
Address |
Hospital Number |
| DOB |
Phone |
| GP |
Hospital Contact |
| Date |
BMI |
Squata |
Sit-upb |
Stand upc |
Other symptoms, signs |
Tests (K, Na, creatine kinase, etc) |
a) ability to rise from squatting (0 unable to rise even with help from hands, 1 can only rise with help from hands, 2 some difficulty, 3 no difficulty)
b) ability to sit up from lying flat (no pillow, firm surface; scale as for (a))
c) dizziness on standing up from a lying posture (0 no symptoms, 1 transient, 2 persistent, 3 unable to stand because of dizziness) |
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Support to the patient and the family in the form of individual sessions and support groups can be provided by statuary or voluntary bodies (for example, the Eating Disorders Association, Norwich).
A few specific therapies have been subjected to controlled studies, including family therapy in anorexia nervosa12 and cognitive behavioural therapy and interpersonal therapy13 in bulimia nervosa. The value of inpatient care for anorexia nervosa has not been established, although it is unavoidable if weight loss or other complications are life-threatening. The Mental Health Act (1983)14 can be used to admit a patient with an eating disorder to hospital and, under the act, feeding is regarded as treatment, so can be given against the patient's will, in the rare circumstances in which this is necessary to save life.
Prognosis for normal weight bulimia nervosa appears to be favourable, with the majority improving after 10 years, although treatment accelerates recovery. For anorexia nervosa the outlook is less optimistic, with a mortality of 5-20%,15 and recovery in about one third of patients. With earlier detection and more specific treatment, these rather gloomy figures should improve.
Useful websites
- http://www.bbc.co.uk/health/womens/hevbod_eatingdisorders.shtml
Characteristically informative BBC site on eating disorders.
- http://www.rcpsych.ac.uk/public/help/anor/anor_frame.htm
Royal College of Psychiatrists' leaflet on eating disorders.
- http://www.mentalhealth.org.uk/eat.htm
The Mental Health Foundation's leaflet for sufferers
- http://www.gurney.org.uk/eda
The Eating Disorders Association site
- http://www.mentalhealth.com
US psychiatry site with a large amount of information on mental health problems, with a US slant.
- http://www.something-fishy.org/
Large site covering every aspect of eating disorders, mainly for sufferers. Includes a chilling memorial page to victims of eating disorders.
Dr P H Robinson, consultant psychiatrist, Eating Disorders Service, Royal Free Hospital
Email: paulhrobinson@hotmail.com
studentBMJ 2000;08:175-216 June ISSN 0966-6494
- Robinson PH. Recognition and treatment of eating disorders in primary and secondary care. Aliment Pharmacol Ther 2000;Apr 14: 367-77.
- Harris EC, Barraclough B. Excess mortality of mental disorder. Br J Psychiatry 1998;173:11-53.
- Gotestam KG, Agras WS. General population-based epidemiological study of eating disorders in Norway. Int J Eat Disord 1995;18:119-26.
- Rooney B, McClelland L, Crisp AH, Sedgwick PM. The incidence and prevalence of anorexia nervosa in three suburban health districts in south west London, UK. Int J Eat Disord 1995;152:299-307.
- Gorwood P, Bouvard M, Mouren-Siméoni MC, Kipman A, Adès J. Genetics and anorexia nervosa: a review of candidate genes. Psychiatr Genet 1998;8:1-12.
- Shoebridge P, Gowers SG. Parental high concern and adolescent-onset eating disorders. Br J Psychiatry 2000;176:32-137.
- Welch SN, Fairburn CG. Childhood sexual and physical abuse as risk factors for the development of bulimia nervosa: a community-based case control study. Child Abuse Negl 1996;20:633-42.
- Katzman MA, Lee S. Beyond body image: the integration of feminist and transcultural theories in the understanding of self starvation. Int J Eat Disord 1997;22:385-94.
- Treasure JL, Katzman M, Schmidt U, Troop N, Todd G, de Silva P. Engagement and outcome in the treatment of bulimia nervosa: first phase of a sequential design comparing motivation enhancement therapy and cognitive behavioural therapy. Behav Res Ther 1999;37:405-18.
- Goldstein DJ, Wilson MG, Thomson VL, Potvin JH, Rampey AH Jr. Long term Fluoxetine treatment of bulimia nervosa. Br J Psychiatry 1995;166:660-666.
- Grinspoon S, Herzog D, Klibanski A. Mechanisms and treatment options for bone loss in anorexia nervosa. Psychopharmacol Bull 1997;128:399-404.
- Eisler I, Dare C, Russell GF, Szmukler G, le Grange D, Dodge E. Family and individual therapy in anorexia nervosa. A 5-year follow-up. Arch Gen Psychiatry 1997;54:1025-30.
- Fairburn CG, Jones R, Peveler RC, Carr SJ, Solomon RA, O'Connor ME, Burton J, Hope RA. Three psychological treatments for bulimia nervosa. A comparative trial. Arch Gen Psychiatry 1991;48:463-469.
- Mental Health Act Commission (UK). Guidance on the treatment of anorexia nervosa under the Mental Health Act, 1983. Mental Health Act Commission, Nottingham, 1997.
- Ratnasuriya RH, Eisler I, Szmukler GI, Russell GF. Anorexia nervosa: outcome and prognostic factors after 20 years. Br J Psychiatry 1991;158:495-502.
- World Health Organization. The ICD-10 Classification of Mental and Behavioural Disorders, 1993.
- American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders: DSM-IV, 4th edn. American Psychiatric Press, 1994.
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