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study of infantile psychosis. II. Social and behavioural outcome. Br J Psychiatryy 1967; 113: 1183–99. 8 DeMyer M K, Barton S, Norton J A. A comparison of adaptive, verbal and motor profiles of psychotic and non psychotic subnormal children. J Autism Child Schizophrr 1972; 2: 359–77. 9 WHO. ICD-10: classification of mental and behavioural disorders. Geneva: WHO, 1992. 10 American Psychiatric Association. Diagnostic and statistical manual of mental disorders. 4th ed. Washington: American Psychiatric Association, 1994. 11 Le Couteur A, ed. National autism plan for children. London: National Autism Society, 2003. 12 Wing L, Gould J. Severe impairments of social interaction and associated abnormalities in children: epidemiology and classification. J Autism Dev Disord d 1979; 9: 11–29. 13 Wing L. The autistic spectrum: a guide for parents and professionals. London: Constable, 1996. 14 Lord C, Risi S, Lambrecht L et al. The Autism Diagnostic Observation Schedule – Generic: a standard measure of social and communication deficits associated with the spectrum of autism. J Autism Dev Disord d 2000; 30: 205–23. 15 Baird G, Charman T, Baron-Cohen S. A screening instrument for autism at 18 months of age: a six-year follow-up study. J Am Acad Child Adolesc Psychiatryy 2000; 39: 694–702. 16 Scott F, Baron-Cohen S, Bolton P. Brief report: prevalence of autism spectrum conditions in children aged 5 to 11 years in Cambridgeshire, UK. Autism 2002; 6: 231–7. 17 Bertrand J, Mars A, Boyle C et al. Prevalence of autism in a United States population: the Brick Township investigations. Pediatrics 2001; 108: 1155–61. 18 Chakrabarti S, Fombonne E. Pervasive developmental disorders in pre-school children. JAMA 2001; 285: 3093–9. 19 Baron-Cohen S. Autism: a specific disorder of ‘mind blindness’. Int Rev Psychiatryy 1990; 2: 79–88. 20 McBride P A, Anderson G M, Hertzig M E et al. Effects of diagnosis, race and puberty on platelet serotonin levels in autism and mental retardation. J Am Acad Child Adolesc Psychiatryy 1998; 37: 767–76. 21 Lord C, Bailey A. Autism spectrum disorders. In: Rutter M, Taylor E, eds. Child and adolescent psychiatry. 4th ed. Oxford: Blackwell, 2002: 636–63. 22 Lord C, Magill-Evans J. Peer interactions of autistic children and adolescents. Dev Psychopathol 1995; 7: 611–26. 23 Cox A, Klein K, Charman T et al. Autism spectrum disorders at 20 and 42 months of age: stability of clinical and ADI-R diagnosis. J Child Psychol Psychiatryy 1999; 40: 719–32. 24 Stone W L, Lee E B, Ashford L et al. Can autism be diagnosed accurately in children under 3 years? J Child Psychol Psychiatryy 1999; 40: 219–26. 25 Dawson G, Osterling J. Early intervention in autism: effectiveness and common elements of current approaches. In: Guralnick M, ed. Effectiveness and early intervention: second generation research. Baltimore: Brookes, 1997: 307–26. 26 Jordan R, Jones G, Murray D. Educational interventions for children with autism: a literature review of recent and current research. (Research Report 77). London: Department of Education and Employment, 1998. 27 Handleman J S, Harris S. Preschool education programs for children with autism. Austin: Pro-Ed, 2000. 28 Howlin P, Charman A. Presentation to NIASA Working Group, 2001.

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Eating disorders J Treasure

Definitions • Anorexia nervosa is characterized by refusal to maintain weight at or above a minimally normal weight (85% of expected weight for age and height, or body mass index (BMI) 17.5 kg/m2), or failure to exhibit the expected weight gain during growth. There is often associated intense fear of gaining weight, preoccupation with weight, denial of the current low weight and its adverse impact on health, and amenorrhoea. • Bulimia nervosa shares some features with anorexia nervosa (e.g. intense preoccupation with weight and shape), but is characterized by regular episodes of uncontrolled eating (> 1000 kcal) associated with various methods of counteracting weight gain (vomiting and laxative abuse are most common). • Various subtypes of eating disorders are defined within the spectrum of eating problems (Figure 1).

Epidemiology Anorexia nervosa has a long history and is present in diverse cultural settings. The content of the psychopathology of anorexia nervosa varies with time and place; for example, weight phobia is not always present in non-Western societies. Bulimia nervosa became more common in the second half of the 20th century and was recognized as a new syndrome in Western societies in 1979.1 The mean incidence of anorexia nervosa in females is 19/100,000/year (about tenfold more than the male incidence).2 The highest prevalence is 0.5% in female teenagers. The prevalence of bulimia nervosa is 1% in young women. Overall, 5–10% of young women have some form of eating problem.

Aetiology and risk factors Family, biological, social and cultural factors may have a role in the development and the maintenance of eating disorders. The evidence for such risk factors is collated in two recent systematic reviews.3,4 • The risk of eating disorders in first-degree relatives of affected individuals is increased tenfold, and twin studies suggest that this is because of inherited factors. Preliminary studies suggest that a region on chromosome 1 is linked with anorexia nervosa5 and on chromosome 10 with bulimia nervosa.6

J Treasure is Director of the Eating Disorder Unit and Professor of Psychiatry at Guy’s, King’s and St Thomas’ Medical School, London, UK.

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in a state of pre-contemplation). Techniques such as motivational interviewing can be used to explore mixed feelings about changes to move patients towards action. Individuals with bulimia nervosa generally want to stop bingeing, but may be reluctant to stop their weight-control strategies.

Spectrum of eating disorders Tendency to fatness

Treatment strategies: treatment for anorexia nervosa focuses on restoration of nutritional balance and psychotherapeutic techniques to overcome the factors that maintain the illness. A detailed discussion is beyond the scope of this contribution (see Further Reading). Cognitive behavioural treatment achieves full remission in 40% of patients with bulimia nervosa9 and is recommended by the UK National Institute for Clinical Excellence (NICE). Stabilization of at-risk patients Nutritional risk k – nutritional deficits in anorexia nervosa develop slowly and are general rather than specific. It is therefore preferable to rectify them slowly, orally, and with ordinary food supplemented with multi-vitamin/multi-mineral preparations. In the first phase (3–7 days), a soft diet of about 30–40 kcal/kg/day given in small portions throughout the day is recommended. Fluid and electrolyte balancee – weight-change strategies such as vomiting and diuretic or laxative abuse can result in severe dehydration (or over-hydration), acute renal failure and electrolyte imbalance. Oral replacement is preferable. Serum potassium levels may remain low even with potassium supplements if vomiting persists. It has been suggested that proton pump inhibitors to inhibit gastric acid secretion (e.g. lanzoprazole) may reduce metabolic alkalosis and help to conserve potassium. Medication – the risk of harm from, for example, QT prolongation must be weighed against the negligible evidence of benefit from antidepressants, antipsychotics and antihistamines in patients at low weight. Small doses of promethazine or some of the new antipsychotic agents can help the severe anxiety and overactivity associated with refeeding.

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• Other psychiatric disorders (e.g. depression, generalized anxiety disorder) are slightly over-represented in the families of individuals with eating disorders, and the risk of obsessive–compulsive personality disorder is increased threefold. The risk of developing an eating disorder is greater in those with obsessive–compulsive traits such as perfectionism and rigidity in childhood.7 • Prematurity is associated with a sixfold increased risk of later development of anorexia nervosa, particularly if the baby was small for gestational age. • Adversity during childhood (e.g. sexual or physical abuse) increases the risk of bulimic disorders.8 • The risk of bulimia nervosa is increased in those who had a robust appetite during childhood, were heavy, and were teased or criticized about eating or their weight.

Diagnosis and assessment Eating disorders are usually diagnosed from the history, particularly when informants contribute to the consultation. It is occasionally necessary to exclude other medical conditions (Figure 2); ESR and thyroid function tests exclude the most common. Albumin is seldom reduced, but haematological deficiencies and electrolyte disturbances are often seen. The most useful investigations for defining the acute medical risk are listed in Figure 3. Most body systems are affected by the negative energy balance (Figure 4). The markers of nutritional decompensation that signal a need for urgent care are shown in Figure 3. In-patient treatment should be considered for patients in the high-risk category. Use of the Mental Health Act may be considered for out-patients who remain at risk despite maximal support (including meeting with the family) but who decline admission to hospital.

Complications Refeeding syndromee – severe medical complications collectively termed ‘refeeding syndrome’ may occur, particularly in those with a BMI of less than 12 kg/m2, those who binge and purge, and those with concurrent physical conditions. Close monitor-

Differential diagnosis of eating disorders Weight loss Malabsorption (e.g. coeliac disease, inflammatory bowel disease), neoplasm, illicit drug use, infection (e.g. tuberculosis), autoimmune disease, endocrine disorders (e.g. hyperthyroidism) Amenorrhoea Pregnancy, primary ovarian failure, polycystic ovary syndrome, uterine problems, pituitary prolactinoma, other hypothalamic causes Psychiatric disorders Depression, obsessive–compulsive disorder, somatization, psychosis (rare)

Management Engagement is the most difficult aspect of management in eating disorders. Characteristically, patients with anorexia nervosa do not accept that anything is wrong. This can cause conflict (usually covert) within the medical encounter, reflecting that within the family. Issues of confidentiality often cause problems. Models of health behaviour change can help in structuring the therapeutic interaction (Figure 5). Most people with anorexia nervosa are not ready for active change and have positive beliefs about the symptoms and interpersonal effects of the condition (i.e. they are

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Measuring risk in patients with eating disorders Nutrition

Circulation

Musculoskeletal (squat test1)

Core temperature Investigations

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Examination • BMI • BMI centiles • Weight loss per week • Purpuric rash • Systolic blood pressure • Diastolic blood pressure • Postural decrease • Pulse rate • Oxygen saturation • Extremities • Unable to get up without using arms for balance • Unable to get up without using arms for leverage FBC, urea, electrolytes (including phosphate), liver function tests, albumin, creatinine kinase, glucose ECG

Moderate risk < 15 kg/m2 < 3 kg/m2 > 0.5 kg < 90 mm Hg < 60 mm Hg > 10 mm Hg < 50 < 90%

High risk < 13 kg/m2 < 2 kg/m2 > 1.0 kg + < 80 mm Hg < 50 mm Hg > 20 mm Hg < 40 < 85% Dark blue/cold

+ + < 35°C Concern if outside normal limits

Rate < 50

< 34.5°C Potassium < 2.5 mmol/litre Sodium < 130 mmol/litre Phosphate < 0.5 mmol/litre Rate < 40 Prolonged QT interval

In the squat test, the patient is asked to squat and then stand up without, if possible, using his or her arms

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ing is necessary, because various electrolyte disturbances (e.g. hypokalaemia, hypocalcaemia, hypomagnesaemia) and physical

complications may be seen during refeeding. Fatal consequences such as acute gastric dilatation and hypophosphataemia can develop rapidly. Acute gastric dilatation may occur with rapid internal refeeding or in patients who binge. Hypophosphataemia can develop with a high carbohydrate load; if severe, it can cause cardiac and respiratory failure, delirium and seizures. Longer-term medical complications – osteoporosis results from prolonged poor nutrition during the critical phase of development of peak bone mass. The most effective treatment is weight restoration, which can increase bone density by 10% per year. The role of hormone replacement therapy is uncertain; it can be harmful by causing premature closure of the epiphyses. Restoration of menstruation may be delayed, particularly when dietary abnormalities persist.

Physical effects of anorexia nervosa Large cerebral ventricles Hirsuties Mitral valve prolapse Liver abnormalities Osteoporosis

Follow-up: NICE guidelines recommend that patients admitted to hospital with anorexia nervosa continue with out-patient treatment for a minimum of 1 year. Regular medical reviews are essential for those with severe, enduring anorexia nervosa.

Collapsed vertebrae Shrunken uterus

Prognosis

Small, multi-follicular ovary

Prognostic factors in anorexia nervosa are listed in Figure 6. There is less certainty about the relevant factors in bulimia nervosa. In more than 50% of patients, anorexia nervosa has a protracted course of a median of 6 years, and one-third of patients never recover fully. About one-third of patients develop bulimic features. Bulimia nervosa has a relapsing and remitting course. Fewer than 10% of patients have a persistent eating disorder at 10-year follow-up.

Proximal myopathy Marrow suppression

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Matching interventions to the stage of change Pre-contemplation No wish to change

Contemplation In two minds about change

Determination Prepared to make changes

Readiness to change

Explore illness perception of others and probe gently for symptoms and signs that cause concern

What are the positives and negatives about anorexia nervosa?

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8 Johnson J G, Cohen P, Kasen S et al. Childhood adversities associated with risk for eating disorders or weight problems during adolescence or early adulthood. Am J Psychiatryy 2002; 159: 394–400. 9 Hay P J, Bacaltchuk J. Psychotherapy for bulimia nervosa and binging (Cochrane Review). Cochrane Database Syst Revv 2003; CD000562. FURTHER READING Birmingham C, Beumont P. Anorexia nervosa: a practical guide to medical management. Cambridge: Cambridge University Press. Crisp A H, Joughin N, Halek, C et al. Anorexia nervosa. The wish to change. Hove: Psychology Press, 1996. (A self-help book for those with anorexia nervosa.) www.nice.org.uk/pdf/cg009niceguidance.pdf (NICE eating disorder guidelines.) Treasure J. Anorexia nervosa. A survival guide for sufferers and those caring for someone with an eating disorder. Hove: Psychology Press, 1997. (A self-help book.) Treasure J, Schmidt U, Van Furth E. Handbook of eating disorders. 2nd ed. Chichester: Wiley, 2003. (A comprehensive textbook.)

Prognostic factors in anorexia nervosa • Severity, duration, degree of weight loss, hyperactivity • Co-morbidity – bulimia and purging, obsessive–compulsive symptoms, childhood difficulties • Response to treatment – poor weight gain, weight remains below normal • Age of onset – the younger, the better the prognosis

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Prevention General strategies such as fostering self-esteem and good communication skills in children help to establish psychological well-being. More specific approaches (e.g. moderating extreme personality traits) may also be beneficial. A Cochrane systematic review of prevention is available. ‹

Practice points

REFERENCES 1 Russell G. Bulimia nervosa: an ominous variant of anorexia nervosa. Psychol Med d 1979; 9: 429–48. 2 Pawluck D E, Gorey K M. Secular trends in the incidence of anorexia nervosa: integrative review of population-based studies. Int J Eat Disord d 1998; 23: 347–52. 3 Stice E. Risk and maintenance factors for eating pathology: a meta-analytic review. Psychol Bull 2002; 128: 825–48. 4 Jacobi C, Hayward C, Agras W S et al. Coming to terms with risk factors for eating disorders: application of risk terminology and suggestions for a general taxonomy. Psychol Bull 2003; in press. 5 Grice D E, Halmi K A, Fichter M M et al. Evidence for a susceptibility gene for anorexia nervosa on chromosome 1. Am J Hum Genett 2002; 70: 787–92. 6 Bulik C M, Devlin B, Bacanu S A et al. Significant linkage on chromosome 10p in families with bulimia nervosa. Am J Hum Genet 2003; 72: 200–7. 7 Anderluh M B, Tchanturia K, Rabe-Hesketh S et al. Childhood obsessive-compulsive personality traits in adult women with eating disorders: defining a broader eating disorder phenotype. Am J Psychiatryy 2003; 160: 242–7.

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Ensure that the environment provides alternative Reinforcement Plan and stage implementation

• About 10% of young women have an eating problem • Increased ESR should raise the suspicion of an alternative diagnosis • It is difficult to engage patients with anorexia nervosa because they have positive attitudes about the condition and do not want to change • Bulimia nervosa is treated using cognitive behavioural therapy (self-help adaptations are available) • Admission should be considered in patients with signs of myopathy, reduced core temperature, circulatory decompensation or abnormal biochemistry and haematology • Avoid mononutrient treatments – global deficits are the norm; whenever possible, give nutrient and mineral replacements orally • Stabilization of high-risk anorexia nervosa requires gradual introduction of food with standard doses of vitamin and mineral supplements • Close physical monitoring is essential to prevent refeeding syndrome

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