Seminar
Eating disorders
Janet Treasure, Angélica M Claudino, Nancy Zucker
This Seminar adds to the previous Lancet Seminar about eating disorders, published in 2003, with an emphasis on
the biological contributions to illness ont and maintenance. The diagnostic criteria are in the process of review, and
the probable four new categories are: anorexia nervosa, bulimia nervosa, binge eating disorder, and eating disorder
not otherwi specified. The categories will also be broader than they were previously, which will aff ect the
population prevalence; the prent lifetime prevalence of all eating disorders is about 5%. Eating disorders can be
associated with profound and protracted physical and psychosocial morbidity. The causal factors underpinning eating
disorders have been clarifi ed by understanding about the central control of appetite. Cultural, social, and interpersonal
elements can trigger ont, and changes in neural network s can sustain the illness. Overall, apart from studies
reporting pharmacological treatments for binge eating disorder, advances in treatment for adults have been scarce,
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other than interest in new forms of treatment delivery.
Introduction
This Seminar adds to the previous Lancet Seminar about eating disorders, which was published in 2003.1 We provide a conci review of eating disorders in young people, focusing on factors of particular relevance to the clinician such as diagnosis, epidemiology, pathogenesis, treatment, and prognosis. In this Seminar we draw attention to biological factors that could contribute to new interve
ntions. Eating disorders also occur in prepubertal children, but studies in this age group are scarce and there is no connsus about either diagnosis or treatment. Classifi cation and diagnosis
Diagnosis is challenging becau diagnostic symptoms and associated behaviours substantially overlap across the range of eating disorders. For example, extreme dietary restraint, binge eating, and overvalued ideas about weight and shape can be prent in all forms of eating disorder. Additionally, the subjective interpretation and justifi cation behind diagnostic behaviours is often not clear or is limited by developmental constraints (as in childhood anorexia nervosa), further complicating diagnosis.
In the diagnostic and statistical manual of mental disorders fourth edition (DSM-IV),2 three broad categories are delineated: anorexia nervosa, bulimia nervosa, and eating disorder not otherwi specifi ed. The international classification of dias tenth revision (ICD-10) has three categories: anorexia nervosa, bulimia nervosa, and atypical eating disorder.3 Briefly, anorexia nervosa is characterid by extremely low bodyweight and a fear of its increa; bulimia nervosa compris repeated binge eating, followed by behaviours to counteract it. The category of eating disorder not otherwi specifi ed encompass variants of the disorders, but with subthreshold symptoms (eg, menstruation still prent despite clinically signifi cant weight loss, purging without objective binging).
The panel shows some key symptoms of eating disorders in general (more detailed information about the clinical features of each disorder is available in the previous Seminar1). The weight criteria ud for diagnosis need to be adjusted for age,4 height, x, and the developmental weight trajectory of the individual.
More than 50% of cas in the community fall into the
category termed eating disorder not otherwi specifi ed
(or atypical).5 Proposals to reduce the specifi city of some
of the diagnostic criteria in anorexia nervosa and bulimia
nervosa have been made, which would reduce the
proportion of cas that fall within the not-otherwi-
nellie mckayspecifi ed category.6 Subgroups within obesity with
mental or behavioural components, such as binge eating
disorder and night eating syndrome, can be delineated.7
Binge eating disorder is a subcategory of eating
disorder not otherwi specified, and is defi ned as不过如此是什么意思
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frequent binge eating distinguished from bulimia
nervosa by the abnce of recurrent inappropriate
compensatory behaviours. Hence binge eating disorder
is often associated with obesity. Transition from vere
restriction into binge eating behaviour is common;8
however, the rever process (a shift from binge eating
into restriction) is less usual. The criteria for diagnosis
of binge eating disorder in DSM-IV appendix B include
associated behavioural and aff ective features,2 and the
Lancet 2010; 375: 583–93
Published Online
November 19, 2009
DOI:10.1016/S0140-
6736(09)61748-7
Section of Eating Disorders,
Institute of Psychiatry, King’s
College London, London, UK
(Prof J Treasure FRCPsych);
Eating Disorders Programme,
Department of Psychiatry,
Federal University of São Paulo
(UNIFESP), São Paulo, Brazil
(A M Claudino PhD);
Department
of Psychiatry and Behavioral
Sciences, Duke University
Medical Center, Durham, NC,
USA (N Zucker PhD); and
Department of Psychology and
Neuroscience, Duke University,
Durham, NC, USA (N Zucker)
Correspondence to:
Prof Janet Treasure, Box P059,
Section of Eating Disorders,
Institute of Psychiatry, King’s
College London, De Crespigny
Park, Denmark Hill, London
SE5 8AF, UK
Search strategy and lection criteria
We arched the Cochrane Library, Medline, and Emba up
to March, 2009. We ud the arch terms: “anorexia
nervosa”, “bulimia nervosa”, “binge eating disorder”, and梦幻女郎
“eating disorders” in combination with the terms
“treatment”, “biology”, “outcome”, “epidemiology”,
“comorbidity”, “personality”, “osteoporosis”, “medical”,
“neuropsychology”, “neuroimaging”, “psychotherapy”, and “pharmacotherapy”. We manually arched the main eating
disorder specialist journals and reference lists of articles
identifi ed by this arch strategy. Several review articles or
books are included becau they provide comprehensive
overviews that are beyond the scope of this Seminar. We
largely lected publications in the past 6 years, but did not
exclude commonly referenced and highly regarded older
publications, or more recent ones published during the
review process and that we considered of relevance to the
scope of the Seminar. Whenever possible we have cited
systematic reviews on a topic.
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criteria have been extensively ud in rearch in the past 15 years. Support is growing for recognition of binge eating disorder as a specifi c entity9 on the basis of taxometric analys,10 family aggregation studies,11 treatment respon rearch,12 and studies of clinical cour.13
Furthermore, interest is growing in a transdiagnostic approach to eating disorders, both within14 and outside the category of eating disorders, with proposals for links to the obssive compulsive and autistic spectrum of disorders15 and anxiety and mood disorders.16,17 Several articles prent the arguments for diagnostic change in DSM-V.7,18Psychiatric comorbidity
Comorbidity is the rule rather than the exception for patients with eating disorders.19,20 Developmental dis o rders (eg, tho of the autistic spectrum and attention-defi cit hyper a ctivity disorder) have been reported to aff ect about a fi fth of patients with anorexia nervosa.21,22 Moreover, a small propor t ion of adults with attention-defi cit hyperactivity disorder have additional symptoms of eating disorders.23 Obssive compulsive traits24,25 or disorder,26 and anxiety disorders27,28 and some borderline traits,25 have been repor-ted both before and after the ont of eating disorders, and are also diagnod in family members.29,30 Bulimia nervosa and binge eating disorder are associated with aff ective disorders31,32 and with alcohol33 or substance34 misu. Epidemiology
Eating disorders and related behaviours are common in young people. Investigators of a study of a large sample
Panel: Common symptoms in eating disorders Behaviours
Restrictive behaviour
泰语我爱你怎么说• Cutting back on amount of food eaten
• Strict rules about eating (eg, time of day, specifi c macronutrient content)
• Prolonged fasting (greater than 8 waking hours)
• Ritualid behaviour associated with the purcha, preparation, and consumption of food
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• Little variety in foods (eg, extreme vegan diets, avoidance of fat, etc)
• Avoidance of social eating
• Secret eating
• Social competitiveness around eating
Binge eating
• Eating an amount of food in a discrete time that is considered excessive in view of the situational context
(objective)
• Eating an amount of food that is not excessive in view of the context but is considered large by the individual
becau of associated feelings of loss of control over
eating (subjective)
Associated features of binge eating
• Eating more rapidly than normal
• Eating until uncomfortably full
• Eating large amounts when not hungry
• Eating alone becau of embarrassment
• Feeling disgusted, depresd, or very guilty becau of eating
Purgative behaviour
• Self-induced vomiting; spitting
• Misu of laxatives, diuretics, diet pills, etc
Excessive exerci
• Inten, highly driven exercising of a compulsive nature • The drive to exerci is associated with impaired social or physical function, or both
Drinking
• Limited drinking (<0·5 L per day)
• Excess drinking (>1·5 L per day)
(Continues in next column)(Continued from previous column)
Body checking
• Repeated weighing
• Pinching or measuring the size of body parts
(eg, circumference of wrist)
• Repeatedly checking the protrusion of specifi c bones • Checking that specifi c clothes fi t
• Mirror gazing
• Comparison with others’ bodies
Body avoidance
• Avoidance of behaviours above (eg, refusal to weigh, avoidance of mirrors, wearing bulky clothes) Psychopathology
Body image disturbance
• Weight and shape concerns (eg, preoccupation with weight, shape, or both)
• Overvaluation of shape and weight in determination of lf-worth
• Minimisation or denial of symptom verity
• Disturbance in the way body is experienced
• Inten fear of weight gain, even though underweight Physical symptoms
• Weight loss or failure of growth with associated features of starvation—eg, amenorrhoea
• Abnce of at least three concutive menstrual cycles (women)
• Reduced libido
• Reduction in waking erections (men)
• Reduced beard growth in men
• Sensitivity to cold
• Weakness, fatigue, etc
This panel outlines the most common symptoms of eating disorder. A range of symptoms caud by starvation are also prent in anorexia nervosa, which are not all detailed here. All the symptoms are not usually volunteered by the patient and often have to be gently elicited or are noted by informants.
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of American children aged 9–14 years reported that 7·1% of boys and 13·4% of girls displayed disor
dered eating behaviours.35 The pivotal eff ect on health has led to the inclusion of eating disorders among the priority mental illness for children and adolescents identifi ed by WHO.36 Eating disorders have been reported worldwide both in developed regions and emerging economies such as Brazil and China.37,38 The lifetime prevalence of eating disorders in adults is about 0·6% for anorexia nervosa, 1% for bulimia nervosa, and 3% for binge eating disorder.19,20 Women are more aff ected than are men, and the x diff erences in lifetime prevalence in adults could be less substantial than that quoted in standard texts: 0·9% for anorexia nervosa, 1·5% for bulimia nervosa, and 3·5% for binge eating disorder in women; and 0·3%, 0·5%, and 2·0%, respectively, in men.20 Many people with eating disorders, who were detected in community studies in the USA, do not ek treatment.20 Pathogenesis
A comprehensive review published in 2004 summarid the risk factors for eating disorders,39 and a position paper from the Academy of Eating Disorders outlined the evidence supporting the dias as biologically-bad forms of vere mental illness.40In this ction we draw attention to some prent areas of emphasis.
Genetic factors
The most potent risk factor is female gender. How much this association can be attributed to biological rather than social factors is uncertain. Sexual divergence is less pronounced in binge eating disorder23 and in prepubertal anorexia nervosa.41 Twin and family studies suggest that anorexia nervosa, bulimia nervosa, and binge eating disorder are complex genetic dias, and for each disorder the estimated heritability ranges between 50% and 83%.11,42,43 Linkage studies have identified loci for anorexia and bulimia nervosa and for associated behavioural traits such as compulsivity.44–46 About a third of genetic risk for eating disorders and depression,47 anxiety disorders,48 and addictive disorders49 is shared. All the above studies are limited becau of low power; however, international collaborations are working at pooling cas and using newer forms of analysis such as genome-wide associations.
Biological factors
Although many of the biological findings in eating disorders can be best understood as results of starvation and disturbed eating behaviours, some are causally linked as risk or maintaining factors. The brain is particularly vulnerable to the conquences of poor nutrition since it us around 20% of the caloric intake and is especially dependent on gluco. Therefore, poor nutrition has a general effect on brain function in addition to the specifi c effect on the appetite system. Most eating disorder
s emerge during adolescence—a vulnerable period of brain reorganisation—and malnutrition during this crucial period can negatively aff ect illness trajectories.
Starvation shrinks the brain and is associated with many behavioural and psychosocial disturbances such as rigidity, emotional dysregulation, and social diffi culties.50 Many symptoms resolve with weight gain and when brain mass is restored.51 Concentrations of brain-derived neurotrophic factor, a regulator of brain plasticity, in blood are reduced in acute anorexia nervosa,52 and genetic studies suggest a trait-related disturbance in this system.53
The characterisation of the central control of appetite54,55 could improve our understanding of eating disorders. A simplified heuristic is to consider three components. First is the homoeostatic system that is centred mainly in the brain stem and hypothalamus, which integrates peripheral metabolic markers with information from the gastrointestinal tract to aff ect subjective states of hunger, satiety, and autonomic nervous activity. Second is the drive system, with distributed neural circuitry within the mesolimbic cortex and striatum that has aff erent inputs from n organs and neural structures that are implicated in learning and memory. This system registers the reward value associated with food and is involved in the motivation to ek food and eat. Third is the lf-regulation system, within which a form of so-called top-down control contextualis appetite within lif
e goals, values, and meaning.
Abnormal changes in all three of the systems have a role in the risk and maintenance of eating disorders. A hypothesis suggests that the disorders could result from pervasive deficits in lf-regulatory systems.56 Furthermore, eating disorder behaviours aff ect the drive system, as shown by models of binge eating in laboratory rodents for which scientists have replicated the conditions implicated in the increa of binge eating—ie, food restriction, gastric drainage (an analogue of vomiting), stress, and intermittent access to highly palatable food—and produced animals with an addiction to food. The investigators noted that not only did the animals binge eat, but they also showed withdrawal eff ects. Moreover, they had a propensity to relap after a time, and cross-tolerance to alcohol and cocaine.57,58 Under p inning the behavioural changes are alterations in the chemical transmitters (dopamine and opioids). Finally, the respon to changes in food intake of the putative homoeostatic system could contribute—eg, anorexia nervosa is often linked to premorbid and familial leanness,59 whereas the rever is the ca for bulimia nervosa and binge eating disorder.60
Brain monoamine function in eating disorders has been studied in the acute state (which can be confounded by illness eff ects) and after recovery with specifi c ligands and positron emission tomog
raphy. The fi ndings for anorexia nervosa have been synthesid into an explanatory model.61 5HT2A receptors are reduced and
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5HT1A receptors are incread in both the acute and recovered state, and dopamine receptors (DA2) within the striatum are incread after recovery.62 Less rearch has been done into binge eating disorders and bulimia nervosa, but anomalies in the dopamine system could heighten food reward.63
Abnormalities in both illness-related (food and body shape) and non-illness-related information processing are detected in eating disorders. An attentional bias is evident towards food and body shape64 associated with incread activation in distributed neural networks connected with lf-regulation and hedonic motivation.61,65 General problems include diffi culties in decision making,66 abnormal striatal activation by reward,67,68 reduced fl exibility69 associated with decread activation in the striatum and associated areas,70 a bias towards focusing on detail at the expen of eing the general picture (weak central coherence),71 problems in social cognition,72 and dysfunctional emotional regulation.73 The functional anomalies can maintain eating disorder beha
viours. For example, an eye for detail and infl exibility can allow an individual to understand the laws of thermodynamics in relation to energy intake and expenditure and succeed in weight loss, whereas impaired social and emotional regulation could isolate the individual. Environmental context
The environment shapes the developmental cour of the individual beginning at the time of conception. For example, mothers of people who later develop an eating disorder might be more expod to stress during pregnancy.74 Birth-related perinatal complications (eg, cephalohaematoma) and premature delivery increa the risk of development of an eating disorder.75 Epigenetic mechanisms or damage to the brain from hypoxia can also mediate the eff ects.
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 lf-esteem.76 Criticism, teasing, and bullying focud on food, weight, and shape issues specifi cally increa the risk of developing an eating disorder.77 The tension between the stigmatisation of fatness, idealisationspecialist
of thinness, and easy access to highly palatable foods, perhaps eaten in cret, could lead to weight
control behaviours that can have a destabilising effect on the biology of appetite control. In addition to food-related and weight-related harmful experiences, general adversity (neglect and physical and xual abu) also increas the risk of developing an eating disorder.
Interactions between the environment and
individual biology
The postpubertal years are a crucial time of vulnerability. Developmental changes of puberty (the hormonal fl uxes and synaptic pruning and myelination within the brain), stressful events, and challenges (eg, changes in social affiliation and ranking) could trigger eating disorder behaviours. The conquent nutritional defi cits can induce factors that maintain the illness. The factors have been grouped into four broad domains: the medical
eff ect on the body and brain, the interpersonal eff ect, the exaggeration of avoidant coping, and obssive compulsive traits.78
Treatment
Medical complications
Although eating disorders can begin in adulthood, the highest incidence is between 10 and 19 years of age,79 potentially disrupting optimum growth and development. Most pathophysiological complications are reversible with improved nutritional status or remittance of abnormal eating and purging behaviours. However, some physical conquences can be life-threatening, such as electrolyte imbalances (eg, hypokalaemia) due to excessive vomiting or laxative and diuretic misu. Additionally, nutritional deficiencies increa the risk of cardiac arrhythmias and intercurrent infection. Comprehensive reviews80,81 and the previous Seminar1 discuss the physical abnormalities of eating disorders in great depth.
Many practice guidelines discuss how to measure and asss medical risk.82–84 Children and adolescents have
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less nutritional rerve than do adults, so their risk can rapidly escalate. Body-mass index (BMI) is not a uful index of nutritional compromi for men, children, tall and muscular individuals, and tho with water retention. Other comorbid medical disorders also increa vulnerability and might need regular monitoring, such as diabetes mellitus, which can increa risk at any level of BMI. Apart from the caveats, standard forms prent a means of giving both personalid and normative feedback on medical risk. (Examples include the Maudsley BMI chart and the Risk Asssment in Eating Disorders). Table 1 shows an abridged t of markers of nutritional and cardiovascular decompensation that signal the need for incread or urgent care. The markers should be considered in the context of the complete clinical picture, experti of the treating team, and local availability of eating disorder units. Signs of incread medical risk suggest the need for immediate specialist consultation or inpatient treatment, or both, especially in people with a recent, acute ont.
The defi cits in anorexia nervosa gradually evolve and are general rather than specifi c. Therefore they should be rectifi ed slowly, orally, and with food supplemented with multivitamin and multimineral preparations. In the fi rst pha (3–7 days), a soft diet of about 5–10 kcal/kg per day with thiamine and vitamin B co-strong in small portions throughout the day, and foods with high phos
phorus content (eg, milk-bad products) accords with guidelines from the UK National Institute for Health and Clinical Excellence (NICE) describing refeeding of verely undernourished patients, and reduces the risk of refeeding syndrome.85 On special units with skilled nursing, feeding by tube is rarely necessary. At moderate levels of risk the aim is to produce a weight gain between 250 g and 450 g per week in outpatients, and around 1 kg in tho treated in hospital.83
Some weight change strategies—such as vomiting or misu of diuretics, laxatives, or caff einated and carbonated drinks—can result in underhydration or overhydration and electrolyte imbalance. Acute renal failure can occur in vere cas. Oral replacement is usually the fi rst line of management, but the full clinical diagnosis and level of risk (table 1) decide the appropriate tting and method of replacement. Persistent hypokalaemia can be linked to low calcium and magnesium (which also need rectification), or to sustained purging behaviours. Proton-pump inhibitors to inhibit gastric acid cretion reduce metabolic alkalosis and help to conrve potassium.86 They can also prevent oesophageal and tooth damage.
Long-term effects on physical health
Some medical conquences of eating disorders can be irreversible or have later repercussions on
health, especially tho aff ecting the skeleton, the reproductive system, and the brain. Dental problems, growth retardation, and osteoporosis are some of the long-term
problems. Bone loss in lumbar spine, radius, and
proximal femur can be detected within a year of illness
and progress to produce fractures, kyphoscoliosis, and
chronic pain. Weight gain alone improves bone density,
especially if it is sufficient to restore mens. Several
treatments have been investigated, including
antiresorptive agents, oestrogens, insulin growth factor,
and calcium supplementation, but none can be
recommended on the basis of prent evidence.87
The fertility and maternity rate of women with anorexia
nervosa is reduced; a Swedish study88 suggested that the
rate of fertility was 70% of that in the general population.
Infant birthweight is lower in mothers with anorexia
nervosa89 but higher in tho with bulimia nervosa.90 The
miscarriage rate for women with bulimia nervosa is
higher than for healthy women—tho with bulimia
nervosa were twice as likely to have two or more
miscarriages compared with the general population.89
Perinatal problems can be incread,91 and feeding
diffi culties reducing infant growth have been reported.92
Infertile and pregnant women should be screened for
tlc
eating disorders and off ered treatment to optimi the
wellbeing of their off spring.82
Pathways of care
High levels of health-care u are common across all
forms of eating disorders.93 The management of bulimia
nervosa and binge eating disorder can be complicated by
medical (eg, diabetes and obesity) and psychiatric
(eg, aff ective disorders and addictions) comorbidity, but
acute medical risk is less of a problem than it is for
anorexia nervosa, and care is typically delivered on an
outpatient basis in adult rvices.
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NICE guidelines recommended that people with
anorexia nervosa should first be off ered outpatient
treatment82 and that inpatient care be ud for tho who
do not respond or who prent with high risk and little
psychosocial resources. Whether inpatient admissions
should be short to alleviate acute risk or prolonged to
attain full weight restoration (thought to reduce relap)
is controversial.94 Models of day treatment provide an
intermediate rvice model.95
Practice recommendations emphasi the importance
of specialid care for the treatment of eating disorders,
but such care is not often accessible. Hence, new forms
of rvice delivery (eg, e-mailing, text-messaging) with
u of treatment directed via mobile phones, the
internet, or telemedicine (eg, cognitive behavioural
therapy [CBT] delivered by a therapist via the internet)
are being assd.96–99 A systematic review98 of lf-help
interventions (computerid or manual) modelled after
empirically validated approaches concluded that with
professional oversight (guided lf-help) the interven-
tions could have benefi t in bulimia nervosa and binge
eating disorder, although some uncertainty still
remains.98,100,101
For more about the Maudsley
BMI chart and the Risk
Asssment in Eating Disorders
e www.iop.kcl.ac.uk/
sites/edu/?id=73
