Eating disorders - summary of an article by Treasure, Claudino & Zucker

Eating disorders
Treasure, Claudino & Zucker
The Lancet


Classification and diagnosis

Diagnostic symptoms and associated behaviours substantially overlap across the range of eating disorders. The subjective interpretation and justification behind diagnostic behaviours is often not clear or is limited by developmental constraints.

In the DSM-IV, three broad categories of eating disorders are delineated. These are: Anorexia nervosa, Bulimia nervosa, Eating disorder not otherwise specified. Binge eating disorder is a subcategory of this.

Support is growing for recognition of binge eating disorder as a specific entity.

Interest is growing in a transdiagnostic approach to eating disorders.

Psychiatric comorbidity

Comorbidity is common for people with eating disorders.

Epidemiology

Eating disorders and related behaviours are common in young people. Eating disorders have been reported worldwide. Women are more affected than men.

Pathogenesis

Genetic factors

The most potent risk factor is female gender. How much this association can be attributed to biological factors is uncertain.

Eating disorders are complex genetic diseases.

Biological factors

Although many of the biological findings in eating disorders can best be understood as results of starvation and disturbed eating behaviours, some are causally linked as risk for maintaining factors.

Poor nutrition has a general effect on brain function in addition to the specific effect on the appetite system. Most eating disorders emerge during adolescence. This is a vulnerable period for being reogranisation. Malnutrition during this period can negatively affect illness trajectories.

Starvation shrinks the brain and is associated with many behavioural and psychosocial disturbances, such as rigidity, emotional dysregulation, and social difficulties. Many symptoms resolve with weight gain and when brain mass is restored.

The characterisation of the central control of appetite could improve our understanding of eating disorders. This contains: 1) The homeostatic system is centred mainly in the brain stem and hypothalamus, which integrates peripheral metabolic markers with information form the gastrointestinal tract to affect subjective states of hunger, satiety, and autonomic nervous activity. 2) The drive system, with distributed neural circuitry within the mesolimbic cortex and striatum that has afferent inputs from sense organs and neural structures that are implicated in learning and memory. This registers the reward value associated with food and is involved in the motivation to seek food and eat. 3) Self-regulation system. A form of top-down control contextualises appetite within life goals, values, and meaning

Abnormal changes in all three of these systems have a role in the risk and maintenance of eating disorders.

These disorders might result from pervasive deficits in self-regulatory systems. Eating disorder affect the drive system. Underpinning behavioural changes are alterations in the chemical transmitters. The response to changes in food intake of the putative homeostatic system could contribute.

Abnormalities in both illness-related and non-illness-related information processing are detected in eating disorders. An attentional bias is evident toward food and body shape, associated with increased activation in distributed neural networks connected with self-regulation and hedonic motivation. Funcitonal anomalies can maintain eating disorder behaviours.

Environmental context

The environment shapes the developmental course of the individual beginning at the time of conception. Epigenetic mechanisms or damage to the brain from hypoxia can mediate these effects.

In some developed countries, the excess value placed on thinness encourages extreme dieting and weight control practices. Negative comparisons between an individual’s body shape and that of the ideal contributes to poor self-esteem. Negative reactions like criticism increase the risk of developing an eating disorder. General adversity also increases the risk of developing an eating disorder.

Interactions between the environment and individual biology

Developmental changes of puberty, stressful events and challenges could trigger eating disorder behaviours. The consequent nutritional deficits can induce factors that maintain the illness. This consists of four domains: the medical effect on the body and brain, the interpersonal effect, the exaggeration of avoidant coping, and obsessive compulsive traits

Treatment

Medical complications

The highest incidence of eating disorders is between 10 and 19 years of age, potentially disrupting optimum growth and development. Most pathophysiological complications are reversible with improved nutritional status or remittance of abnormal eating and purging behaviours.

Some physical consequences can be life-threatening. Nutritional deficiencies increase the risk of cardiac arrhythmias and intercurrent infection.

The deficits in anorexia nervosa gradually evolve and are general rather than specific.

Long-term effects on physical health

Some medical consequences of eating disorders can be irreversible or have later repercussion on health. Especially those affecting the skeleton, the reproductive system, and the brain.

Pathways of care

High levels of health-care use are common across all forms of eating disorders.

Evidence-based treatments

Anorexia nervosa

Two factors contributing to difficulties in trials of treatment for anorexia nervosa are clinician-instigated protocol withdrawal because of failure to stabilise risk and patient withdrawal and difficulties in recruitment because of poor acceptability of treatments

Treatment guidelines rely on expert recommendations. These emphasise the importance of a multidisciplinary approach.

Psychotherapy can be delivered individually or with the family. The involvement of families in treatment depends on age of the patient, living arrangements, the patient’s level of risk and dependence and the ethos of the treatment team.

Bulimia nervosa

The evidence base for the CBT model of bulimia nervosa and its use in first-line treatment is strong.

Evidence for long-term effects after medication is scare.

Binge eating disorder

CBT, interpersonal therapy, and dialectical behavioural therapy have positive results.

Prognosis

Recovery from anorexia nervosa becomes much less likely the longer the illness has persisted.

The chance of recovery becomes higher in bulimia nervosa, the longer the illness persisted.

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