Eating disorders constitute a range of illnesses characterised by abnormal eating and specific psychopathology. Eating disorders in children and adolescents pose unique issues. They often present atypically, they can defy our usual systems of classification and there is less evidence to guide our treatment.¹ In addition the threshold for intervention should be lower than in adults.²

Classification

The main eating disorders include anorexia nervosa (AN) and bulimia nervosa (BN), as well as a third group of patients who do not fully meet the formal criteria for AN or BN and so receive an atypical or ‘eating disorder not otherwise specified’ (EDNOS) diagnosis.³ In fact, EDNOS accounts for 40-60% of cases across all ages.^4,5 Children also present with a range of feeding disorders, including food avoidance emotional disorder, selective eating, pervasive refusal syndrome and functional dysphagia. Despite abnormal eating and weight loss, these disorders do not share the body image and weight concerns of the traditional eating disorder patients and so will not be discussed here.

The majority of studies employ the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) criteria for diagnosing AN and BN.⁶ The 10th revision of the International Classification of Diseases (ICD-10) requires a generally similar weight for AN, ie. at least 15% below that expected or a BMI of 17.5 or less.⁷ However, a set lower BMI limit is not as useful a criterion in children who generally have lower fat stores and where BMI norms are age and gender-specific.⁸ It is recommended that BMI centile reference charts be used in young people (calculated as BMI/% median BMI for age and gender).^9,10

These criteria pose some obvious difficulties. Limitations in cognitive development in younger children may prevent them from identifying or articulating ‘a fear of fatness’ or considering the value of body weight and appearance in the determination of self-worth. Amenorrhoea is clearly inapplicable in a group where many are premenarcheal and in males. 

An international workgroup of experts on the diagnosis and treatment of child and adolescent eating disorders hopes to address some of these difficulties by proposing certain improvements in the upcoming DSM-5, including: lower and more developmentally sensitive thresholds of symptom severity (eg. lower frequency of purging behaviours, significant deviations from growth curves as indicators of clinical severity) be used as diagnostic boundaries for children and adolescents; behavioural indicators of psychological features of eating disorders be considered even in the absence of direct self-report of such symptoms; multiple informants (eg. parents) be used to ascertain symptom profiles and multiple physical systems should be evaluated for the clinical management of eating disturbance; but no single physical sequela (eg. amenorrhoea) be required for diagnosis.⁸

Epidemiology

Epidemiological studies suggest that individuals with eating disorders are presenting at increasingly earlier ages.^1,11 The estimated overall prevalence for AN is 1%,¹² with a reported prevalence rate of 0.5% in adolescent females.¹³ BN occurs in approximately 1-2% of the adolescent population while clinically significant bulimic behaviours occur in an additional 2-3%.⁸ EDNOS prevalence in adolescent females ranges from 3-5%.¹³

It is well known that eating disorders are more common in females. Males generally comprise 10-15% of cases, however in prepubertal children the male-to-female ratio is often higher.^14,15 AN can develop from about eight years of age, reaching a peak around 15-18.¹⁶ BN is generally detected in a slightly older population than AN, with binge eating and purging behaviours usually beginning during middle adolescence. More recently patients have been reporting binges and purges far younger than 14 years.^8,12

Dieting behaviours in children and adolescents are widespread and impact on the prevalence of eating disorders.¹⁷ In EPICA, a study of eating problems in 3,031 Irish secondary school students, 26.7% of students felt that they should be on a diet, while 19.6% of girls and 10.8% of boys were on a diet.¹⁸

With an increase in overweight and obesity, dieting behaviours are also on the rise. This is concerning as dieting is considered the most important predictor of new-onset eating disorders.¹³ Obesity is now the most prevalent chronic childhood disease. Some studies are indicating that the number of children who are significantly overweight has trebled over the past decade.¹⁹

Aetiology

Eating disorders have traditionally been regarded as disorders with a sociocultural explanation. In recent years the emphasis has shifted towards neurobiological factors, with eating disorders now conceptualised as multifactorial illnesses with a biological basis, modified by emotional and sociocultural factors.^20,21

Biological factors

A number of studies have found an increased rate of AN and BN and their variants among the relatives of those with eating disorders. In a controlled family study of 1,831 relatives of 504 probands, the relative risk for AN was 11.3 if female relatives had AN and 12.3 if female relatives had BN. The relative risks for BN were 4.2 and 4.4 for female relatives of those with AN and BN, respectively.²² Quantitative genetics have identified preliminary candidate genes for AN on chromosomes 1 and 13, while BN has been linked to chromosome 10.²⁰ Both the serotonin (5-HT) 2A receptor gene and the brain-derived neurotrophic factor (BDNF) gene have also been implicated in the aetiology of AN.^16,20

Obstetric complications may contribute to an impairment in neurodevelopment, which could be implicated in the pathogenesis of eating disorders.⁶ Puberty has also long been recognised as a critical period for the onset of eating disorders, particularly in girls.¹ Puberty is associated with a greater increase in fat mass in girls than in boys. While boys also experience weight gain during puberty, much of it is accounted for by an increase in muscle bulk.²³

Recent studies have found that genetic influences on disordered eating increased linearly with increasing pubertal development.²⁴ Studies using both functional neuroimaging and neuropsychological testing in subjects with AN have found abnormalities in visuospatial functioning, specifically visuospatial memory, and in cognitive flexibility, as well as weak central coherence. These correlate with a reduction in blood flow (using SPECT) in the medial temporal region.²¹ Taken together, these findings, along with the characteristic features of AN, suggest abnormal function in the frontal, parietal and temporal regions, as well as in subcortical structures such as the amygdala, the basal ganglia and the nucleus accumbens. Such widely disseminated abnormalities seem exceedingly unlikely. Instead it is hypothesised that there is a disconnection between the structures, leading to the very specific features of AN.²⁵ It has been proposed that some form of dysfunction in the insula may play a central role, given that it serves as an integration cortex for convergence of various neural networks.²⁶

Additional biological risk factors for BN include childhood or parental obesity, critical comments from family members about weight, parental substance misuse and early menarche.^6,16,23 In a small proportion of acute-onset cases of AN, it has also been suggested that the disorder may be triggered by infection, a phenomenon known as paediatric autoimmune neuropsychiatric disorder associated with streptococcus (PANDAS), similar to obsessive-compulsive disorder and tic disorders.²⁷

Psychological factors

Psychological factors associated with eating disorders include temperament, low self-esteem, the processing of negative emotional experiences (particularly trauma and threat), family factors, and the aforementioned specific cognitive profiles.^16,28

Correlational research suggests that AN and BN are both characterised by perfectionism, obsessive-compulsiveness, narcissism, sociotropy (concern with acceptance and approval from others) and autonomy (an orientation towards independence, control and achievement), whereas impulsivity and sensation-seeking are more typical of disorders characterised by bingeing.²⁹ Poor self-esteem and feelings of ineffectiveness are extremely common.⁹

In the past, family dysfunction had frequently been implicated in the pathogenesis of eating disorders. Specifically, AN has been said to emerge in enmeshed families with rigid styles of interaction and difficulty managing conflict.³⁰ These theories are now seen as overly simplistic and in recent years there has been a shift away from an emphasis on a family aetiology of the eating disorder towards an understanding of the evolution of the family dynamics that may function as maintenance mechanisms in the context of the eating disorder.^31,32 In the family context, parental weight concern (and eating behaviour) is also thought to play a contributory role in the development of eating pathology.

Sociocultural factors

Pressure to be thin is a major source of body image disturbance and eating disordered behaviour. The slim physique portrayed in the media promotes weight control behaviours, particularly dieting.¹⁶ The effect of media portrayal of body image on a population has been most clearly documented in a study of Fijian adolescents, where a significant increase in eating pathology was observed following the introduction of television.³³ In groups where thinness is deemed to be particularly important, eg. in ballet dancers and models, high rates of AN have been reported.⁶

In the Eating Problems in Irish Children and Adolescence (EPICA) study, 68.3% of adolescents surveyed felt that the media portrayal of body weight and shape was too thin, while 71.4% of adolescents felt adversely affected by this media portrayal with those with the highest concern having the highest eating psychopathology.¹⁸ Related to media and peer pressure is weight-related teasing of children and adolescents who do not conform to the thin ideal. Weight teasing, in turn, is predictive of future disordered eating behaviour.³⁴

Clinical features and comorbidity

AN, BN and related eating disorders have at their core a morbid fear of weight gain and body dissatisfaction.¹⁰ While in girls this is usually manifest as a drive for thinness, in boys there is often a wish to increase upper body mass and muscle.

In AN, patients refuse to maintain body weight at a minimally normal weight for age and height. Weight loss is achieved by restriction of calorific foods, exercise and occasionally vomiting or purging.⁹ Children often restrict fluid as well as food. Older adolescents, on the other hand, may fluid load to falsify weights or to fill themselves up to prevent hunger.¹⁰ Note that because children should be growing, failure to gain weight can be regarded as equivalent to weight loss in adults.¹⁶ Clinical features often found in young people with AN include depression, obsessive-compulsive disorder or traits, social anxiety, and difficulties with change, ritualised behaviours and perfectionism.¹⁰

In BN a persistent preoccupation with eating is present, with craving and consequent binges (often with a subjective feeling of loss of control). Weight is maintained within a normal range by compensatory vomiting or purging.⁹ BN requires a degree of psychological maturation that AN does not, including capacity for self-evaluation, often manifest as shame or guilt. It may follow on from AN, or develop secondary to repeated dieting behaviour. Common associations include depression, self-harm, substance misuse and other risk-taking behaviours.

Those with eating disorders suffer a number of abnormal cognitions, the central one that is characteristic of eating but not feeding disorders of earlier childhood being the over-evaluation of the self in terms of weight and shape. All other personal qualities and attributes are relegated below the belief that self-worth is dependent on what the weighing scales say or the ability to restrict food intake in the face of hunger.⁹

The physical changes in AN are predominantly related to the effects of starvation and dehydration, while in BN they reflect chronic purging.^15,35 Eating disorders have the potential to affect all organ systems in the growing body. Medical complications include immediate threats such as cardiac arrhythmias and metabolic derangements. Long-term problems such as growth impairment and low bone mineral density may result.³ Other systems commonly affected include the gastrointestinal (impaired motility), haematological (leucopaenia, anaemia, thrombocytopaenia), renal, endocrine and neurological systems.¹⁰ Specific effects of starvation on the mind include low mood/depression, irritability, intense preoccupation with thoughts of food, reduced concentration, decrease in self-initiated activity and social introversion.³⁶

Though not classified as an eating disorder, the comorbidity associated with childhood obesity deserves mentioning. With the metabolic complications well recognised, psychological complications faced by overweight and obese youth are now gaining increased recognition. Though precise rates are uncertain, mental health associations in obesity include body dissatisfaction, symptoms of depression, loss-of-control eating, unhealthy and extreme weight control behaviours, impaired social relationships, obesity stigma and decreased health-related quality of life.³⁷

Treatment

The evidence base for treatment of children and adolescents with eating disorders is limited.^9,28 There is no one treatment of choice and typically combinations of treatment are needed.³⁸ A co-ordinated multidisciplinary approach is required and should include attention to nutrition, medical and psychological issues.¹

 Most patients should be managed on an outpatient basis.³⁸ The Treatment Outcome for Child and adolescent Anorexia Nervosa (TOuCAN) trial, a multi-centre randomised controlled trial of treatments available for adolescents in the UK, concluded that first-line inpatient treatment does not provide advantages over outpatient management. Specialist outpatient treatment proved to be the most cost-effective.^39,40 Admission to hospital is advised for medically compromised patients, where outpatient treatment has failed, where the diagnosis is unclear and a period of observation may be of value, when families seem to be struggling to cope, or where there is significant risk of suicide or self-harm.^10,15

Medical management

Medical management involves both the acute management of the medically compromised patient, as well as long-term monitoring of the patient’s physical state. Given the potentially irreversible effects of AN on physical growth and development, it is argued that the threshold for medical intervention in young people should be lower than in adults.² Close liaison with paediatric services is recommended.^10,38

It is important to consider other reasons for weight loss. These include medical diagnoses such as inflammatory bowel disease, malignancies, hyperthyroidism, diabetes and chronic infections. Psychiatric disorders such as depression (with loss of appetite) and psychotic illnesses (occasionally presenting with food avoidance) should also be excluded.⁴¹

The extent of malnutrition should be assessed. Weight, height and BMI should be calculated and compared with BMI centile reference charts. Temperature, pulse and blood pressure should be recorded and an ECG carried out if the patient is emaciated.⁹ Bloods and an ECG can help in assessing both the immediate medical risk and the risk of re-feeding (see below), but normal blood parameters are not necessarily a cause for reassurance if other signs of malnutrition are present.¹⁰ Address fluid and electrolyte balance where vomiting is frequent or there is frequent use of laxatives.¹⁵

In the longer term, paediatric knowledge and skills are needed to manage the impact of eating disorders on growth and development. The effect of prolonged malnutrition on bone density predisposes patients to osteoporosis and increased fracture risk.⁴² The most effective treatment for and prevention of decreased bone density is achieving a healthy weight. A diet rich in calcium is important, with no evidence for the role of bisphosphonates, oestrogen supplementation, calcium supplements or vitamin D supplements.^2,10 In patients who are vomiting regularly, attention to the adverse dental effects of vomiting and specific preventative guidance on oral hygiene is recommended.³⁸

Nutrition

The implementation or restoration of healthy eating patterns is one of the main goals of treatment for eating disorders. Regularising eating patterns should be distinguished from refeeding, ie. ensuring adequate nutrition and hydration. This is only indicated when there is evidence of nutritional deficiency such as electrolyte deficiency, dehydration, circulatory failure or growth delay.¹⁶

Key elements of a nutritional plan include structured mealtimes and close monitoring of intake and weight.¹⁰ It is important to involve parents or carers in any dietary education or meal planning.¹⁵ The dietitian is an invaluable member of the clinical team and can help in planning an intake acceptable to the young person, increasing the intake gradually as food becomes less ‘scary’, recommending substitutions as necessary, emphasising the essential nutrients and advising regarding supplements such as high-calorie drinks.¹⁶

Weight restoration should utilise the least invasive procedures possible.⁹ A weight gain of around 0.5-1kg per week is generally recommended for inpatients and 0.5kg per week for outpatients.⁴³ Some recommend that a target weight range be defined, with a minimum objective a weight which enables resumption of a normal menstrual cycle (where applicable).^5,28 Others recommend using ovarian ultrasonography to help determine a healthy weight.¹⁶ After an initial safe weight has been achieved, the young person’s food intake should be adjusted to ensure that growth is in keeping with normal weight and height trajectories.⁹

When treating a malnourished patient, care should be taken to avoid the refeeding syndrome, a rare potentially life-threatening disturbance of fluid and electrolyte balance which can follow sudden increases in nutritional intake in those who have been in a state of starvation.⁹ It remains unclear exactly what a safe initial rate of calorific provision prevents refeeding syndrome, especially in younger children. Recommended rates of refeeding vary from 10 to 60 kcal/kg/day up to nearer 70-100 kcal/kg/day. Convention has been to start slowly and then build up cautiously, however more aggressive approaches may be safe and delay in feeding needs to be balanced with the less recognised syndrome of ‘underfeeding’, with subsequent ongoing complications and poorer outcome.^10,44 Recent publications suggest that the composition of macronutrients, in particular avoiding a high proportion of calories from carbohydrates, appears to be more important than the absolute number of calories.⁴⁵ Serum electrolytes (including phosphate, glucose, potassium and magnesium) and vital signs should be monitored closely.^2,9 In patients with BN, calorie restriction contributes to the maintenance of binge eating and a key objective in planning dietary programmes is to break the vicious cycle of dieting and binge eating.^5,46

Psychological interventions

The formation of a therapeutic alliance with the parents and their child is a vital part of treatment.^5,16 Family members, including siblings, should normally be included in the treatment of children and adolescents with both AN and BN. Interventions may include psychoeducation on the nature, course and treatment of eating disorders, advice on behavioural management and facilitating communication.³⁸

Given the effects of starvation on the brain, the most severe weight loss should be reversed in emaciated patients before full-scale psychotherapy is initiated.²⁸ Family therapy has the greatest evidence base and family interventions that directly address the eating disorder should be offered to all children and adolescents with AN.³⁸ These interventions aim to mobilise family resources, whether delivered as ‘conjoint’ family therapy, separated family therapy (in which parents and the child are seen separately), parental counselling or multifamily group therapy.^9,46

Individual therapies to be considered in AN include cognitive behaviour therapy, cognitive analytic therapy and interpersonal psychotherapy. Psychodynamic psychotherapy may be indicated when psychopathology is so deeply entrenched that a more in-depth approach is required.¹⁶ Psychological treatment should focus both on eating behaviour and attitudes to weight and shape, and on wider psychosocial issues.³⁸ A common view is that young people with eating disorders are struggling with dilemmas of adolescence and turn to an intense focus on weight and shape as an avoidance strategy. Hence, individual therapy aims at improving self-efficacy, self-esteem and self-mastery such that the symptoms of anorexia are no longer needed to master the challenges of adolescence.⁹ Underlying cognitive deficits in patients with AN should not be ignored. Cognitive remediation is a relatively new form of therapy, focused on correcting cognitive deficits rather than the eating disorder symptoms.⁶

Externalisation is a helpful and often used technique in young people, whereby a clear distinction is made between the child and the illness. This involves explaining to the child and parents that just as a child with a chest infection does not choose to have a cough, a fever and pain when breathing, so the child with AN does not choose to see herself/himself as fat and to become terrified of weight gain. Instead, just as the chest infection is conceptualised as a distinct entity so is ‘the anorexia’.⁴⁶ Together the child, family and clinician can work to eliminate this unhelpful illness.

Adolescents with BN may be treated with cognitive behaviour therapy for BN (CBT-BN), a specifically adapted form of CBT, adapted as needed to suit their age, circumstances and level of development, and including the family as appropriate.³⁸ The focus is on changing the specific eating attitudes and behaviour that maintain the eating disorder.² Interpersonal psychotherapy should be considered as an alternative to CBT, bearing in mind that it can take longer to achieve results comparable with CBT.³⁸ Self-help approaches, including those delivered through the internet, such as the BYTE project for bulimia, are growing.⁹

There has been considerable recent interest in the importance of motivational interventions for engagement and treatment of all eating disorders, based on the transtheoretical model of change. Motivational interviewing is a potentially useful technique that aims to make people more prepared to contemplate change, and it is commonly incorporated into CBT programmes.⁴⁶ Group work is also commonly used for the management of eating disorders. These include groups for children, teenagers and parents and can take the form of discussions, psychoeducation, art, drama, dance, body awareness and social skills training.¹⁶

Pharmacotherapy

Psychotropic drugs are not recommended as the primary treatment for child and adolescent eating disorders.⁴⁷ There is little empirical support for the use of psychopharmacological interventions targeted at AN specifically. Nonetheless, for those with high levels of anxiety, obsessionality or mood disorder, the use of either selective serotonin reuptake inhibitor (SSRI) antidepressants or atypical antipsychotics or both may be clinically useful.⁹ Caution should, however, be exercised in its use for comorbid conditions, as these may resolve with weight gain alone.³⁸ A number of studies have confirmed the effectiveness of SSRIs (particularly fluoxetine) in adult BN, resulting in a decrease in the frequency of binge eating and purging.^9,47 Adolescents with BN may be offered a trial of fluoxetine; the effective dose may be higher than for depression.¹⁵

Prognosis

Eating disorders have the highest mortality rate of any psychiatric disorder.⁴⁸ Crude mortalities are estimated at around 4% for AN, 3.9% for BN and 5.2% for EDNOS.⁴⁹

The outcome is variable. The course of AN is protracted and rates of recovery usually increase with a longer duration of follow-up.^46,50 Approximately half of patients recover, in 30% the symptoms persist and in 10-20% the disorder becomes chronic.²⁸ Good prognostic factors include early age of onset (before 18 years) and a short duration of illness before treatment.⁵ A poor outcome has, however, been reported in those developing AN under the age of 11.⁵¹ A poorer outcome has also been associated with bulimic features such as vomiting and purging, excessive weight loss, poor childhood social adjustment and poor parental relationships.¹⁵

There are few long-term outcome studies on BN in children and adolescents. As with AN, the number of symptom-free patients increases with a prolonged follow-up, and around half of patients become completely free of eating disorder symptoms.⁵² A longer duration of disorder at presentation, substance misuse, low self-esteem, unstable family relationships and higher rates of bingeing and purging have been associated with a poor outcome.^46,53,54

Conclusion

Eating disorders are complex multifactorial disorders that remain a serious cause of morbidity and mortality in children and adolescents. These disorders impact on psychological maturation, cognitive development and social, personality and emotional development, including self-concept and identity formation. It can result in delay or regression in some or all of these areas.¹⁰ Childhood and adolescence are also critical periods of neural development and physical growth. The malnutrition and related medical complications resulting from eating disorders may have more severe and potentially more protracted consequences during youth than during other age periods.⁸ Early identification and intervention is therefore crucial to prevent long-term sequelae.

Declaration of interest: none.

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