{
  "id": "eating-disorder",
  "title": "Eating disorder",
  "lang": "en",
  "source_lang": "en",
  "summary": "A group of serious psychiatric conditions defined by disturbed eating, weight- and shape-related concerns, and significant impacts on physical health and daily functioning.",
  "category": "health",
  "subcategory": "diseases",
  "type": "concept",
  "aliases": [
    "Feeding and eating disorder",
    "Feeding or eating disorder",
    "饮食失调",
    "进食障碍"
  ],
  "generated_at": "2026-10-09",
  "model": "pro/claude-haiku-5-5",
  "url": "https://aiwiki.page/en/eating-disorder/",
  "translations": {
    "zh-Hans": {
      "url": "https://aiwiki.page/zh/eating-disorder/",
      "json": "https://aiwiki.page/zh/eating-disorder.json"
    }
  },
  "sections": [
    {
      "heading": "",
      "text": "An eating disorder is a group of psychiatric conditions in which persistent disturbances of eating or eating-related behaviour, together with strong concern about body weight or shape, damage physical health or psychosocial functioning. The major recognised forms are anorexia nervosa, bulimia nervosa and binge eating disorder, alongside less common or newly recognised conditions such as avoidant/restrictive food intake disorder. Although they are classified as mental disorders and are closely tied to psychology, they have measurable metabolic, cardiovascular and neurological consequences, and they carry one of the highest mortality rates among psychiatric illnesses. The entry explains how the conditions are defined and classified, what is known about their causes and risk factors, how they affect the body, and how they are treated and studied.\n\nClinical definitions are set mainly by the American Psychiatric Association's DSM-5-TR and the World Health Organization's ICD-11, which largely agree on the core features but differ in some details, such as how subjective binges are counted. Diagnosis therefore depends on specific criteria for behaviour, frequency and duration, as well as on medical assessment of weight, electrolytes and vital signs. The conditions are most often first seen in adolescence and young adulthood, though they occur across ages, sexes and backgrounds. Causes are understood as the product of genetic vulnerability, neurobiological factors, psychological traits and sociocultural pressures acting together, rather than of any single cause.\n\nTreatment in current evidence-based practice usually combines nutritional rehabilitation, medical monitoring and psychological therapy, with the specific therapy chosen according to age, diagnosis and clinical severity. This entry covers the classification of the disorders, their clinical features and complications, the factors that contribute to their development, the evidence on treatment and outcomes, and the open questions that remain in research and clinical practice."
    },
    {
      "heading": "Definition and scope",
      "text": "Eating disorders are a group of mental disorders defined by a persistent disturbance of eating or of eating-related behaviour. The disturbance alters how food is consumed or absorbed and causes marked distress or serious impairment. The DSM-5-TR wording makes clinically significant harm to physical health or psychosocial functioning part of the definition, and the condition is recognised only when that harm is present (The DSM-5-TR describes feeding and eating disorders as a persistent disturbance of eating or eating-related behaviour that changes food intake or absorption and significantly impairs physical health or psychosocial functioning.). Eating behaviour that is unusual but does not produce this harm, such as a restrictive personal preference, falls outside the definition.\n\nDieting is the main point of confusion. Both involve changes in eating, but the two differ in purpose and course. Dieting is usually a chosen, time-limited goal, while eating disorders are described as occupying most of a person's thinking and continuing until treated (Dieting is a choice that does not take over a person's mind and has a definite end point. An eating disorder is not a choice, takes over most of a person's brain space, and lasts indefinitely until treated.). Dieting is nonetheless a recognised risk factor. In one Australian cohort of schoolgirls, moderate dieters were about five times as likely, and severe dieters about eighteen times as likely, to develop bulimic syndrome as non-dieters (Moderate dieters in an Australian school-girl cohort were five times more likely, and severe dieters 18 times more likely, to develop an eating disorder than their non-dieting peers.). Researchers still debate whether dieting causes disorder or marks a wider pattern of overeating (Stice concluded that dieting is better understood as a marker of chronic overeating, with thin-ideal internalisation and body dissatisfaction better supported as risk factors.).\n\nAcross diagnoses, the shared cognitive core is disturbance of body image. The DSM criteria treat it as central: for anorexia nervosa, this appears as an intense fear of gaining weight and a distorted experience of body weight or shape, and for bulimia nervosa as self-evaluation that is unduly shaped by body weight and figure (Body-image disturbance is a core cognitive criterion in anorexia nervosa and bulimia nervosa, and has been proposed as a severity specifier for binge-eating disorder.). Researchers distinguish several strands. Overvaluation means self-worth rests excessively on shape, weight or the ability to control them (Overvaluation refers to individuals' self-evaluation depending excessively on their weight or shape, or on their ability to control them.). This differs from dissatisfaction, which is common among people without eating disorders (Overvaluation should be distinguished from body dissatisfaction, which is common in people without eating disorders and is less closely tied to self-esteem.). Preoccupation, meaning frequent and intrusive thoughts about the body, is a third strand. Preoccupation with shape and weight, and with food, is graded: anorexia and bulimia show more of it than binge-eating disorder, which shows more than healthy-weight comparison groups (Preoccupation with shape/weight and with food/eating showed a graded pattern of statistically significant differences: AN and BN had higher preoccupation than BED, which was higher than HW.).\n\nThe boundary with obesity is contested. For much of the twentieth century, eating disorders and obesity were treated as separate problems, handled by mental health professionals on one side and by medicine and nutrition on the other (Obesity has traditionally belonged to the biological sciences, medicine and nutrition, while eating disorders are handled by psychiatry and psychology.). Current clinical usage keeps them apart as diagnoses: obesity is a health condition, not an eating disorder, and each can occur without the other (Obesity is a health condition and not an eating disorder. People can have obesity without having an eating disorder and vice versa.). The overlap is nonetheless substantial. Most people with obesity have no eating disorder, but eating disorders are more common among people with obesity (Most people with obesity do not have an eating disorder, but eating disorders are more common in people living with obesity, and there is significant overlap between the two.). Binge-eating disorder shows the closest link, since its risk rises as obesity becomes more severe (The majority of people with obesity do not have binge-eating disorder, but the risk of it rises with the degree of obesity.). Shared genetic influences also exist. One example is a variant of the BDNF gene, where one allele raises susceptibility to obesity and another raises susceptibility to eating disorders (One example of shared genetic risk is the BDNF gene, where the valine allele of the Val66Met polymorphism predisposes to obesity and the methionine allele predisposes to eating disorders.). Weight change can also result from endocrine, gastrointestinal, malignant or infectious illness and from some medications, and these causes must be excluded before an eating disorder is diagnosed.\n\nEating disorders are classed as mental disorders because the diagnosis rests on a pattern of cognition and behaviour: restriction, binge and purge cycles, and self-evaluation that is organised around weight and shape. Sources describe them as behavioural conditions in which disturbed eating is linked to distressing emotions and thoughts, and which can affect physical, psychological and social functioning (Eating disorders are behavioral conditions characterised by severe disturbance in eating behaviours associated with distressing emotions and thoughts. This type of disorder can affect physical, psychological, and social function.). The physical harm is often severe, including bone thinning, heart damage, low blood pressure and multi-organ failure in extreme cases (Malnutrition can cause bone thinning, heart damage, low blood pressure and multi-organ failure that can prove deadly.). These are, however, largely consequences of the disordered behaviour and do not by themselves define the disorder. The classification also reflects history: the separation of eating disorders from obesity owes much to a long-standing view of them as culture-bound conditions tied to Western emphasis on weight and appearance, a view that some authors now regard as too narrow (Eating disorders have been regarded as Western culture-bound syndromes, but research and treatment would be better served by appreciating the psychosocial components of obesity and the biological and genetic components of eating disorders.)."
    },
    {
      "heading": "Classification in DSM-5-TR and ICD-11",
      "text": "DSM-5-TR categories\n\nDSM-5-TR is the 2022 text revision of the 2013 DSM-5 classification published by the American Psychiatric Association. Its feeding and eating disorder chapter lists anorexia nervosa (AN), bulimia nervosa (BN), binge eating disorder (BED), other specified feeding or eating disorder (OSFED), pica, rumination disorder, avoidant/restrictive food intake disorder (ARFID) and unspecified feeding or eating disorder (UFED). Pica, rumination disorder and ARFID were earlier grouped under conditions first diagnosed in infancy, childhood or adolescence. Placing these disorders in their own chapter is meant to make the diagnoses applicable across the lifespan.\n\nChanges from DSM-IV to DSM-5\n\nDSM-IV recognised only AN, BN and a residual category, eating disorder not otherwise specified (EDNOS). In DSM-IV, binge-eating disorder was described in an appendix of criteria sets for further study and could only be diagnosed as EDNOS. DSM-5 made it a formal diagnosis. The AN criteria were also revised. The requirement that the patient show refusal to maintain body weight was dropped, because the word \"refusal\" implies intention on the part of the patient and can be difficult to assess. The amenorrhoea requirement was removed as well, so that low weight alone can be sufficient for diagnosis. The effect was to widen the AN category. In one reclassification study, OSFED/UFED diagnoses fell from 46% to 29%, while AN diagnoses rose from 35% to 47%.\n\nOSFED and UFED\n\nThe residual category is now split. OSFED covers five named examples (atypical anorexia nervosa, subthreshold bulimia nervosa, subthreshold binge eating disorder, purging disorder and night eating syndrome), along with other clinically significant presentations that do not meet full criteria for another disorder. UFED is used when full criteria are not met or insufficient information is known. Even so, a large proportion of cases remain in the ill-defined category of other specified feeding and eating disorders. Attempts to subdivide this group have been limited. A cluster analysis of a treatment-seeking sample failed to identify clusters based on symptoms of restraint, binge eating, purging and over-evaluation of shape and weight. The authors concluded that further investigation of this highly heterogeneous group is required. The share of residual diagnoses also depends on setting. In a residential treatment study, clinicians assigned a residual diagnosis to 12.0% of patients under DSM-5, compared with 28.7% under DSM-IV.\n\nICD-11\n\nThe ICD-11 classification keeps the core diagnoses and treats the eating disorders in broadly similar terms. The DSM-5 and ICD-11 have similar criteria for bulimia nervosa and binge-eating disorder, but the ICD-11 criteria are broader. The most cited difference is the inclusion of subjective binges. ICD-11 includes subjective binges in the definitions of bulimia nervosa and binge-eating disorder, which DSM-5 does not. DSM-5 instead requires the amount eaten to be objectively large. Other differences concern duration, specifiers and thresholds. DSM-5 requires at least three months of binge eating for both BN and BED, while the proposed ICD-11 criteria allow one month for BN and treat three months as the norm for BED, with exceptions for very frequent episodes. Diagnostic specifiers are required for BED in DSM-5, but they are not essential in the provisional ICD-11. ICD-11 also does not specify OSFED groups comparable to those of DSM-5. Its residual category, Other Feeding or Eating Disorder (OFED), is closer to the DSM-5 UFED than to OSFED.\n\nThese differences have measurable effects. In an Australian community sample, the estimated prevalence of BED was 0.20% under DSM-5 criteria and 1.4% under ICD-11 criteria. In a high-BMI treatment sample, fewer individuals received a subthreshold other or unspecified diagnosis with ICD-11 than with DSM-5 (5% vs. 21%). Across a larger clinical sample, the two systems gave the same full-threshold diagnosis for over 90% of patients, while sub-threshold and feeding disorders showed a discrepancy of 25%."
    },
    {
      "heading": "Anorexia nervosa",
      "text": "Diagnostic criteria\n\nAnorexia nervosa is defined by restricting food and energy intake relative to requirements, which produces a body weight below the expected range for a person's age, sex, developmental trajectory and physical health. The DSM-5 criteria resemble those of DSM-IV in their behavioural and psychological features, which cover restriction leading to low body weight, an intense fear of gaining weight or becoming fat, and a disturbance of body image. Unlike earlier versions, the DSM-5 criteria do not specify a particular degree of weight loss, but give guidance for grading severity.\n\nThe DSM-5-TR revision moved the criteria towards observable behaviour. The term \"refusal\" was removed to avoid implying intentional noncompliance, which can be difficult to assess and may be stigmatizing. The requirement for amenorrhoea was also dropped, so the diagnosis no longer depends on menstrual status. The ICD-11 definition follows a similar logic, emphasising behaviours that interfere with weight gain rather than an inferred intent to refuse food.\n\nSubtypes\n\nDSM-5-TR recognises two subtypes. In the restricting type, weight loss is accomplished primarily through dieting, fasting, and/or excessive exercise, and there are no recurrent binge-eating or purging episodes in the preceding three months. The binge-eating/purging type requires recurrent episodes of binge eating or purging behaviour in the same period, where purging includes self-induced vomiting and the misuse of laxatives, diuretics or enemas.\n\nThe two subtypes differ in medical risk mainly through the purging component. Fluid loss due to purging is a frequent occurrence, and changes in body fluid homeostasis may lead to life-threatening electrolyte abnormalities. The boundary between subtypes is itself debated. DSM-5-TR does not give a specific threshold of binge and/or purge episodes separating the two subtypes, and cutoffs used in research are rarely reported and highly heterogeneous. A study of 731 adolescents and adults using machine learning reported that one binge eating and/or purging episode in the past month adequately distinguishes subtypes. Some researchers also see restrictive and binge-purge presentations as possibly lying along a shared clinical spectrum.\n\nOnset, sex distribution and clinical presentation\n\nThe disorder usually begins in adolescence or early adulthood, and most patients are female. In the 731-person clinical sample mentioned above, participants were 94% female with a mean age of 20, although such samples come from treatment settings and do not establish population rates. Clinically, patients often minimise the seriousness of their weight loss and may resist treatment, a feature that complicates assessment and engagement. Adolescents with the disorder are also more likely to have other negative health outcomes including mental health disorders, substance use, self-harm, and continued challenges with body weight.\n\nMedical complications\n\nCardiac involvement is common. Studies of cardiac haemodynamics continue to find near-universal bradycardia, as well as decreased heart rate variability, in patients with AN. Sinus bradycardia is the most common arrhythmia in patients with AN, and it reflects increased vagal tone in the setting of malnutrition. Bradycardia reverses with weight restoration, and permanent pacemaker placement is considered unwarranted. Hypotension and myocardial atrophy also occur. In an echocardiographic study of 124 severely malnourished adults, subclinical myocardial impairment was common.\n\nEndocrine and skeletal effects are closely linked. Estrogen deficiency and the resulting amenorrhoea contribute to bone loss, but other factors also play a part. Estrogen replacement trials failed to improve bone density, which pointed to additional causes. Reduced density is especially marked at the lumbar spine, and the deleterious effects on bone mineral density are not completely reversible despite weight restoration. Growth and pubertal development can also be affected, as growth retardation, pubertal delay, and reduction in peak bone mass are common complications.\n\nRefeeding risk\n\nNutritional rehabilitation carries its own dangers. The biggest risk factor for refeeding syndrome is a low BMI, and the risk rises as BMI falls. The core mechanism involves a shift of phosphate from the extracellular space into cells during refeeding, which produces the characteristic refeeding hypophosphatemia, the most common complication of nutritional restoration in AN. Other consequences include acute thiamine deficiency that can result in Wernicke's encephalopathy and Korsakoff syndrome. In one cohort of 281 severely malnourished adults with a BMI below 15, 38% developed hypoglycaemia, 35% developed hypophosphatemia, and 33% developed oedema during refeeding. Severe cases can be fatal, which is why cardiovascular collapse and even death have been linked to rapid high-calorie intake.\n\nMortality\n\nAnorexia nervosa carries substantial mortality. The aggregate mortality is 5.6% per decade of illness, with suicide accounting for half of the deaths and cardiac arrest accounting for a majority of the remainder. Fuller discussion of mortality belongs to the prognosis section."
    },
    {
      "heading": "Bulimia nervosa",
      "text": "Core features and diagnostic thresholds\n\nBulimia nervosa is built around a cycle of binge eating and compensation. A binge is an episode of eating an amount clearly larger than most people would eat in similar circumstances, accompanied by a sense of lack of control overeating during the episode. The compensatory part of the cycle aims to offset the food eaten and can take the form of self-induced vomiting; misuse of laxatives, diuretics, or other medications; fasting; or excessive exercise.\n\nFrequency and duration are central to the diagnosis. Under DSM-5-TR, the binge eating and inappropriate compensatory behaviours both occur, on average, at least once a week for 3 months. The DSM-5 lowered the frequency threshold to this level, and the number of times a person binges and purges per week is no longer a central criterion in the way it had been. Within the diagnosis, severity is graded by how many compensatory episodes occur in a typical week: mild, an average of 1–3 episodes; moderate, 4–7; severe, 8–13, and an extreme category applies at 14 or more episodes per week. Two further criteria distinguish the disorder. Self-evaluation is unduly influenced by body shape and weight, and the disturbance does not occur exclusively during episodes of Anorexia Nervosa.\n\nBody weight and presentation\n\nBulimia nervosa differs from anorexia nervosa mainly in body weight. Anorexia is defined by a low weight, whereas people with bulimia usually sit in the normal range or above it. Most people with bulimia nervosa are young and of normal weight, or even overweight, making detection and diagnosis difficult. Body weight can also swing noticeably, with fluctuations in weight, both up and down, which is one reason clinicians rely on the reported pattern of behaviour rather than on weight alone.\n\nPhysical effects\n\nThe most serious medical consequences arise from purging. Purging behaviors can lead to electrolyte imbalances, such as hypokalemia (low potassium levels), hyponatremia (low sodium levels), and hypochloremia (low chloride levels). These disturbances can cause fatigue, weakness, muscle cramps, heart arrhythmias, and seizures. Electrolyte and metabolic problems are regarded as the most common causes of morbidity and mortality in patients with bulimia nervosa, and low potassium is treated urgently to prevent electrocardiographic changes and arrhythmias such as torsades de pointes. Vomiting can also remove stomach acid and produce metabolic alkalosis, or elevated serum bicarbonate levels, while chronic dehydration from purging can lead to pseudo-Bartter syndrome. In some cases a hospital stay may be needed to treat electrolyte problems.\n\nDental damage is among the most frequent findings. Stomach contents are acidic, so repeated vomiting can lead to dental erosion as early as six months after the onset of the behavior. The enamel loss is progressive, and dental erosion is permanent once it develops. Vomiting can also cause enlarged parotid/submandibular glands and cuts and calluses across the top of finger joints from inducing vomiting.\n\nGastrointestinal complaints are common. Gastroesophageal reflux disease is frequently reported, and Mallory-Weiss syndrome describes tears in the esophageal lining, which can be marked by blood in the vomit. Symptoms such as fatigue, bloating and constipation are typically milder. Rarer complications are more serious; gastric rupture is uncommon but is the most severe of them. Most complications resolve with cessation of purging, although some, particularly dental and oesophageal damage, may persist, especially in untreated cases."
    },
    {
      "heading": "Binge eating disorder and related conditions",
      "text": "Under DSM-5-TR, binge eating disorder requires binge episodes that occur on average at least once a week for three months, a sense of lacking control while eating, and at least three of five associated features, such as eating much faster than usual, eating until uncomfortably full, or eating alone out of embarrassment. A binge is defined as eating, within a discrete period, a quantity clearly larger than most people would eat in similar circumstances. Marked distress about the binge eating is also required. The diagnosis is not made when binges occur only during an episode of anorexia nervosa or bulimia nervosa, and the binge eating is not associated with recurrent inappropriate compensatory behavior such as purging. That absence of regular compensation is the main feature separating the disorder from bulimia nervosa, whose diagnostic criteria also include compensatory behaviour. Weight or appearance is not part of the diagnostic criteria for binge eating disorder. Its strong association with obesity, particularly among people seeking weight-loss treatment, is therefore a clinical pattern rather than a diagnostic requirement.\n\nThe frequency threshold was lowered in DSM-5. The research criteria in DSM-IV-TR required bingeing on at least two days a week for six months, whereas the DSM-5 diagnostic criterion is that binge eating must occur an average of once per week, for a minimum of three months. Severity is graded by frequency: 1–3 binge-eating episodes per week is mild, 4–7 is moderate, 8–13 is severe, and 14 or more is extreme, with the level potentially raised for other symptoms or functional disability.\n\nOther specified feeding or eating disorder (OSFED) applies when symptoms that are clinically significant predominate but the full criteria for no single disorder are met, and the clinician records the specific reason. In atypical anorexia nervosa, all of the criteria for anorexia nervosa are met except that, despite significant weight loss, the individual's weight is within or above the normal range. Medical risk is not reduced by this distinction: people with atypical anorexia have been found to experience similar symptoms of medical instability to those with anorexia nervosa, and rapid weight loss at any body size can cause serious complications. Subthreshold bulimia nervosa and binge eating disorder are defined by lower frequency or shorter duration than the full criteria require. Purging disorder involves recurrent purging behavior to influence weight or shape in the absence of binge eating. Night eating syndrome involves eating after awakening from sleep, or excessive food consumption after the evening meal, and the behaviour is not better explained by environmental influences or social norms. OSFED is heterogeneous, and it can include individuals with a range of eating disorder presentations (OSFED-other). The category is large in practice: more than 50% of eating disorder patients are diagnosed with OSFED or the unspecified category (UFED), which is used when full criteria are not met but the reason remains unspecified, or the clinician lacks adequate information for a more definitive diagnosis.\n\nAvoidant/restrictive food intake disorder (ARFID) is defined by an eating disturbance that leads to persistent failure to meet nutritional or energy needs, which may appear as significant weight loss, nutritional deficiency, dependence on tube feeding or supplements, or marked psychosocial interference. Its three recognised presentations are lack of interest in eating, avoidance based on the sensory features of food, and concern about the aversive consequences of eating. In the sensory presentation, people may eat few foods and may exclude entire food groups. In the fear presentation, common fears include vomiting, choking, abdominal pain, allergic reactions, and illness. Unlike anorexia nervosa, these eating problems are not driven by body image concerns, but rather by persistent low appetite, sensory sensitivity, and/or fear of aversive consequences of eating. Onset patterns also differ: avoidance due to fear of aversive consequences can arise at any age, whereas avoidance linked to lack of interest or to sensory characteristics most commonly develops in early childhood and is generally stable into adulthood. ARFID occurs more commonly in children than in adults, and there is often a long delay between onset and clinical presentation.\n\nPica and rumination disorder are placed in the same chapter as the eating disorders but are often less closely tied to body image. Pica is the persistent eating of non-food substances, such as chalk, hair, or soil, for at least one month, when this is inappropriate for the person's developmental stage and not part of a culturally normative practice. Rumination disorder involves repeated regurgitation of food after eating, with the food brought back into the mouth without nausea, involuntary retching, or disgust, and then re-chewed and either spat out or swallowed again. These conditions overlap with eating disorders where distress, food avoidance or weight loss coexist with them, which is why clinicians must check for them during differential assessment."
    },
    {
      "heading": "Epidemiology and course",
      "text": "Estimates of how many people have an eating disorder depend heavily on the diagnostic system, the age group sampled and the survey method. A systematic review of studies published between 2000 and 2018 reported a weighted mean lifetime prevalence of 8.4% in women and 2.2% in men, and a point prevalence of 5.7% in women and 2.2% in men. Its authors also found that point prevalence rose over the period, from 3.5% for 2000–2006 to 7.8% for 2013–2018. Part of that rise may reflect changes in study design, so it should not be read as a simple increase in cases. Regional comparisons are less secure: the same review gave point prevalence means of 4.6% for the Americas, 2.2% for Europe and 3.5% for Asia, but these rest on a small and uneven set of studies.\n\nEating disorders are most common in women and girls. In a review of young people, between 5.5% and 17.9% of young women had met criteria for a DSM-5 eating disorder by early adulthood, compared with 0.6% to 2.4% of young men. The diagnosis-specific lifetime ranges for women were 0.8% to 6.3% for anorexia nervosa, 0.8% to 2.6% for bulimia nervosa, 0.6% to 6.1% for binge-eating disorder and 0.6% to 11.5% for other specified feeding or eating disorders. The last of these is the broadest category, and its large share explains much of the variation between studies. Criteria matter in other ways too. Broader DSM-5 definitions of binge-eating disorder and related presentations raise totals compared with DSM-IV, while studies using DSM-5 criteria remain relatively scarce, and some reviews argue that prevalence is therefore underestimated.\n\nAnorexia nervosa typically begins in adolescence, whereas bulimia nervosa and binge-eating disorder more often emerge in later adolescence or young adulthood. Diagnoses are not fixed. Many people move between categories over time, for example from anorexia nervosa with restriction to a binge-purging presentation, or from bulimia nervosa to binge-eating disorder, and some move from a partial syndrome into a full diagnosis. Cohort studies of young people also show that symptoms can remain stable for years, and that persistent symptoms are associated with poorer mental health.\n\nCourse is variable and often prolonged. In a study of inpatient family-based treatment with a mean follow-up of about four and a half years, around a third of patients remained below a healthy body weight and roughly a third were classed as fully recovered. Studies of childhood-onset anorexia nervosa with follow-up of five to eight years have reported that about a quarter of children had a poor outcome. Relapse and chronicity are more likely among adolescents who had longer inpatient stays or co-occurring psychiatric conditions. Full recovery, partial recovery and persistent illness are therefore all common patterns, and long follow-up periods show that improvement after acute treatment does not always last.\n\nMortality is the most serious outcome. A 2011 meta-analysis of 36 studies, covering more than 200,000 person-years, estimated a weighted mortality rate of 5.1 deaths per 1,000 person-years for anorexia nervosa, compared with 1.7 for bulimia nervosa and 3.3 for eating disorders not otherwise specified. Its standardised mortality ratio for anorexia nervosa was 5.86, and about one in five people with anorexia nervosa who died had died by suicide. A later systematic review and meta-analysis gave a pooled standardised mortality ratio of 5.06, with suicide and cardiac causes accounting for about 21% and 19% of deaths respectively, and similar ratios for male and female patients. Large clinical cohorts have found that patients with anorexia nervosa die earlier than those with other eating disorders, and that chronicity, later age at onset, living without a partner and irregular discharge from inpatient treatment predict shorter survival. The relationship between body mass index and mortality remains disputed, with some meta-analyses finding no significant association. Cardiac complications, electrolyte disturbance and suicide are the main routes to premature death, and the medical aspects are discussed in medical and cardiovascular sections of this entry."
    },
    {
      "heading": "Causes and risk factors",
      "text": "Genetic and familial influences\n\nEating disorders cluster in families, and twin research has been the main tool for separating inherited effects from shared household environment. Pooled twin data put concordance at about 44% for identical pairs, compared with an average of 12.5% for fraternal pairs. Heritability estimates depend on study design: twin studies and family studies have produced heritability estimates of 48%–74% for anorexia nervosa.\n\nMolecular genetic work has been slower to yield results. An early genome-wide association study of 3,495 AN cases and 10,982 controls found one significant locus. Larger later analyses have identified more loci, and one review of the field counts nine genome-wide significant loci, while cautioning that it is still unclear which associated variants are causal. Genetic overlap also extends beyond eating disorders. In one analysis, anorexia nervosa showed significant genetic correlations with neuroticism (rg=0.39), schizophrenia (rg=0.29), and a meta-analysis across psychiatric phenotypes, and a previous study reported a correlation of 0.53 with obsessive-compulsive disorder. Twin data also reveal shared liability between eating disorders and substance use, with the strongest link between bulimia nervosa symptoms and problem alcohol use.\n\nPersonality and temperament\n\nPersonality traits are among the better-supported individual vulnerabilities. Negative emotionality, perfectionism and negative urgency have been identified as candidate traits, and longitudinal studies have consistently shown that these can predict the later development of an eating disorder. Perfectionism is particularly well studied: it is associated with body dissatisfaction and drive for thinness in people with and without a diagnosis, and higher scores on self-oriented and socially prescribed perfectionism are linked with greater body dissatisfaction and more concern about weight and shape. Proposed mechanisms include dichotomous thinking, self-criticism, rumination, and avoidance, which may sustain the disorder once it has begun. Harm avoidance and obsessional traits have also been reported at elevated levels in people with anorexia nervosa, and some appear to persist after weight is restored. This makes them candidate vulnerability markers, although whether they precede illness or partly reflect starvation remains an open question.\n\nEnvironmental and developmental factors\n\nEnvironmental risk is more heterogeneous and harder to quantify. Early adversity, including abuse, bullying and family conflict, has been linked to later eating pathology in several studies, and dieting is one of the most consistent precursors, particularly when combined with body dissatisfaction. Sociocultural environment and thin-ideal internalization are thought to affect body dissatisfaction and eating pathology directly, and also to interact with other established risks such as negative affect and dieting. Weight-related teasing by peers or family members is another recognised risk factor. Developmental transitions, such as puberty, leaving home, starting university, or entering a demanding job or sport, may coincide with onset because they increase stress, change routines, or intensify attention to appearance.\n\nSociocultural influences\n\nSociocultural pressure is among the most discussed influences. Researchers have argued that thin-ideal internalization is a causal risk factor for body dissatisfaction and eating pathology. Internalization operates unevenly, however: only a minority of individuals are susceptible to thin-ideal messages, and even fewer go on to develop an eating disorder, which suggests that individual susceptibility moderates the effect of sociocultural influences. Media exposure, appearance-based social comparison and, more recently, social media have been examined as channels for these messages. Commentators have argued that the introduction of Facebook and Instagram has increased exposure to retouched images and thin ideals. Sports and occupations that reward leanness, such as ballet, distance running, gymnastics, modelling, and weight-class sports, also carry elevated risk, particularly where weight is judged or enforced.\n\nTaken together, the evidence points to interacting rather than single causes. Genetic liability and temperament may shape who is most affected by thinness norms, while dieting, teasing and life transitions may determine timing. Most research has examined biological and psychosocial factors separately, and integrated models remain an active area of work."
    },
    {
      "heading": "Biological and neurobiological mechanisms",
      "text": "Hormonal changes\n\nStarvation and low body weight alter several endocrine systems at once. In anorexia nervosa, the hypothalamus and pituitary communicate less effectively across the gonadal, adrenal, thyroid and growth hormone axes, and these changes are often described as a coordinated, energy-conserving response to chronic undernutrition rather than a simple malfunction. In the gonadal axis, reduced pulsatile release of gonadotropin-releasing hormone from the hypothalamus lowers luteinizing hormone and follicle-stimulating hormone, and with them oestrogen in women and testosterone in men. This \"hypothalamic hypogonadism\" underlies the amenorrhoea common in affected women, and in early endocrine studies, gonadotropin excretion was undetectable in most of the patients examined. Low oestrogen also has consequences for bone, which are covered in the medical complications section.\n\nThe stress axis shows a different pattern. Cortisol is typically raised, and some patients show a loss or reversal of its normal daily rhythm; corticotropin-releasing hormone also appears to be increased. Thyroid findings often resemble the pattern seen in non-thyroidal illness: triiodothyronine (T3) is low, while thyroxine and thyroid-stimulating hormone are low to normal. Growth hormone secretion is often elevated while insulin-like growth factor 1 is low, which has been described as a state of growth hormone resistance. Appetite-related signals are also disturbed, including leptin and the gut-derived peptides ghrelin and peptide YY. Many of these abnormalities improve with nutritional rehabilitation, which restores gonadotropin secretion, although the stress-axis changes are less consistently reversible and their mechanisms remain incompletely understood.\n\nNeurotransmitter systems\n\nEarly work focused on serotonin and dopamine, and the field has since been shaped by receptor-binding and imaging studies. In anorexia nervosa, reduced serotonin 5-HT2A receptor binding has been reported both during illness and after recovery, which has been taken to suggest possible trait-level alterations; in bulimia nervosa, studies have reported increased 5-HT1A receptor binding and reduced serotonin transporter binding during illness. Such trait-level findings are relevant to the question of whether the changes are causes or consequences of the disorder, but they have not established a single mechanism.\n\nDopaminergic reward circuitry has also been studied with taste-reward paradigms. Some work suggests that this circuitry responds unusually strongly in anorexia nervosa but weakly in bulimia nervosa and obesity, although the replication base is limited. In binge eating, reviews have found that most neuroimaging, genetic and pharmacological studies report an altered dopamine state, yet the direction of the change differs between studies, so the picture remains unresolved. Animal models add useful but indirect evidence: in the activity-based anorexia model, which combines food restriction with excessive wheel running, changes in mesolimbic dopamine and serotonin have been observed. Neuroimaging, therefore, shows that reward and monoamine systems are involved, but it does not yet show which change drives the eating behaviour, and its findings vary with the diagnosis, the state of illness and the method used.\n\nBrain structure and cognition\n\nStructural imaging has consistently found reduced grey and white matter volumes and enlarged cerebrospinal fluid spaces in underweight patients. A 2020s meta-analysis of acute anorexia nervosa reported grey matter reductions of about 4.8% and white matter reductions of about 2.5%, with larger reductions in adolescents, and the most affected areas included the cingulate gyrus, precentral gyrus and precuneus. Volume deficits tend to improve with weight restoration, but a meta-analysis found they can still be measurable more than a year after recovery. Early studies of weight-recovered women reported persistent grey matter deficits, which were interpreted as possibly partly irreversible, whereas a later voxel-based study of long-term recovered women found grey matter volumes similar to controls. Animal work using refeeding after starvation has shown almost complete reversal of volume and astrocyte loss, which suggests that starvation itself can account for a substantial part of the change.\n\nCognitive findings follow a similar logic. Reduced brain volume has been associated with impairments in learning and visuospatial memory, and with greater preoccupation with thinness. The central unresolved question is whether these traits predate the illness or result from starvation. Cross-sectional comparisons cannot separate the two, so longitudinal studies that follow patients through weight restoration are needed to distinguish starvation effects from disorder-specific traits.\n\nMetabolic and gut-related mechanisms\n\nStarvation shifts energy balance toward conservation: intake falls far below expenditure, and the endocrine changes described above help reduce energy use and protect lean tissue. This adaptive state is one reason why the brain and body changes are closely tied to nutritional status. The gut-brain axis links the digestive tract to the hypothalamus through hormonal and neural signals. Gut-derived hormones such as ghrelin, which promotes hunger, and peptide YY, which promotes satiety, are central to this signalling, and their altered regulation in anorexia nervosa is thought to contribute to the persistent difficulty with hunger and fullness cues. Research on the gut microbiota and its possible role in eating disorders is at an early stage, and current evidence does not allow firm conclusions about its causal contribution. Overall, the biological findings point to a dynamic interaction between starvation, hormonal regulation, reward processing and brain structure, in which the direction of cause and effect is still being clarified."
    },
    {
      "heading": "Medical complications and physical assessment",
      "text": "Cardiovascular complications\n\nCardiovascular complications have been described in up to 80% of adults with anorexia nervosa, and they also significantly affect children and adolescents. Sinus bradycardia (below 60 bpm) is the most common heart rhythm found in underweight young people with eating disorders. Clinicians often read it as an energy-conserving adjustment to malnutrition, and it is generally well tolerated and resolves with refeeding. Pacing is seldom needed, even when the slow rate is marked (see 6-4).\n\nRhythm disturbances of both fast and slow types can arise from low potassium, magnesium or calcium, from malnutrition, and from autonomic dysfunction, with starvation-related myocardial fibrosis and fat infiltration possibly contributing Arrhythmias, including both tachy- and bradyarrhythmias, occur secondarily to electrolyte imbalances (especially low potassium, magnesium, and calcium), malnutrition, and autonomic dysfunction. Severe hypokalaemia is particularly hazardous because it can result in a prolonged corrected QT interval on electrocardiography, subsequent torsades de pointes, and other life-threatening cardiac arrhythmias. Fatal arrhythmias are also linked to electrolyte abnormalities Fatal arrhythmias may be triggered by electrolyte abnormalities.\n\nEndocrine, bone and fertility effects\n\nMissed periods are the most visible endocrine change. Researchers generally treat them as a functional, energy-protective shift away from reproduction during prolonged undernutrition Although reproduction, an energetically costly process, is necessary for the survival of a species, it is not necessary for the survival of an individual. Reduced fat tissue lowers leptin, which suppresses the hypothalamic-pituitary-gonadal axis, reducing oestrogen and testosterone, increasing bone resorption and slowing bone formation Decreased leptin secretion by a diminished adipose tissue inhibits the hypothalamic–pituitary–gonadal axis (HPG). This leads to low levels of oestrogen and testosterone, increased bone resorption, and decreased bone formation.\n\nLow bone mineral density is a major long-term problem. In AN, low weight, hypothalamic amenorrhoea, and longer illness duration are established risk factors for low BMD. A meta-analysis of women with eating disorders found that low BMI, low fat mass, low lean mass and being amenorrhoeic were significantly associated with lower total body and spine BMD. The consequences can extend well beyond the illness, since reduced density can bring chronic pain, loss of height and increased risk of fractures. Deficits are more common when the disorder begins at a younger age, and they may be irreversible reduced bone mineral density is more common in those who developed their eating disorder at a younger age and may be an irreversible complication of anorexia nervosa.\n\nHormonal treatment has been tested with mixed results. Randomized and/or prospective studies demonstrated no overall benefit in BMD in individuals receiving oral estrogen versus placebo. By contrast, transdermal estrogen showed possible benefit in a randomized, placebo-controlled study in adolescent girls. Fertility, by comparison, often normalizes with recovery.\n\nGastrointestinal, dental and renal effects\n\nPurging has the most direct effects on the mouth and gut. Acid exposure from vomiting is the most frequent cause of dental harm: enamel erosion is the most common oral manifestation of people who engage in self-induced vomiting. Dentin hypersensitivity is the second most common oral symptom in patients with bulimia, following dental erosion. Repeated vomiting can also produce oesophageal tears and reflux Gastrointestinal complaints are common and include gastroesophageal reflux disease.. Laxative misuse can damage the gut's nerve plexus, so that severe constipation on withdrawal of laxatives may follow.\n\nKidney involvement is common in purging patients. Electrolyte abnormalities including hyponatremia, hypokalemia, and metabolic alkalosis are common in eating disorders and vary depending on whether patients engage in purging behaviors. Persistent potassium loss can cause lasting damage: chronic hypokalemia due to purging in patients with anorexia nervosa-binge purge subtype or bulimia nervosa can lead to hypokalemic nephropathy and chronic kidney disease. One secondary summary reports that this nephropathy occurs in up to 14.2% of patients with AN-R, 42.4% of patients with AN-BP, and 26.2% of patients with bulimia nervosa. Vomiting and diuretic misuse also trigger the loss of intravascular fluid, which causes increased production of aldosterone and development of Pseudo-Bartter syndrome. When purging stops, fluid shifts back, which can cause edema and rapid weight gain in patients who cease purging behavior.\n\nRefeeding risk and assessment of medical instability\n\nRefeeding syndrome has been considered one of the most serious complications related to anorexia nervosa, one which can occur, and possibly prove fatal, with oral as well as enteral and parenteral feeding. Its features include sodium and water retention (leading to oedema and possible cardiac failure), hypophosphatemia due to intracellular disturbances, and depletion of potassium, magnesium and thiamine, which can lead to Wernicke's syndrome or cardiomyopathy. The risk is greatest early, since it occurs during the first days of refeeding. For more on this, see refeeding syndrome.\n\nAssessment of medical instability combines regular electrocardiograms with echocardiography, which should be performed in selected patients. Vital signs, including temperature, blood pressure and heart rate, are central, as an emergency presentation may show hypothermia, hypotension, and bradycardia. Electrolytes, electrolyte levels in particular, must be tracked during refeeding, which is managed by gradual refeeding and careful monitoring of electrolytes to avoid refeeding syndrome (RFS) as well as ensure adequate fluid intake. Commonly cited admission thresholds include a daytime heart rate below about 50 beats per minute, systolic blood pressure under about 90 mmHg, body temperature below about 35.6 °C and serum potassium below 3.0 mmol/L. These figures differ between guidelines and are weighed together with weight, orthostatic change and the patient's ability to eat."
    },
    {
      "heading": "Diagnosis and assessment tools",
      "text": "Diagnosis rests mainly on a clinical interview, supplemented by self-report questionnaires, anthropometric measurement and an examination of physical status. Because the same clinical picture can arise from several sources, the assessment has to exclude medical and other psychiatric explanations before an eating disorder is recorded.\n\nInterviews and questionnaires\n\nThe most widely used clinician-administered instrument is the Eating Disorder Examination (EDE), which relies on retrospective self-report. Its interview is validated in several languages, and studies of retrospective administration report acceptable reliability for most subscales and items, although some items, such as those about specific eating episodes, perform less well. Results suggest that the instrument remains reliable even when administered retrospectively.\n\nThe self-report counterpart, the EDE-Questionnaire (EDE-Q), has a less settled structure than its authors originally proposed. A 2022 systematic review of 60 factor-analytic studies found that the originally proposed four-factor solution received little empirical support, and that items assessing shape and weight concerns frequently coalesce in factor solutions. Brief versions have produced more consistent results. Mode of administration also matters: in one comparison of interview and online self-assessment, diagnoses derived from questionnaire responses alone differed from clinician-derived diagnoses, with the online version agreeing more closely, and diagnostic accuracy rose to nearly 90% once objective weight data were added.\n\nDifferential diagnosis\n\nWeight loss and restriction can arise from several other sources, and each must be considered. Endocrine disorders such as hyperthyroidism, gastrointestinal diseases (including coeliac disease and inflammatory bowel disease), diabetes, and malignancy can all produce weight loss and appetite change. Depressive disorders, psychotic illnesses, body dysmorphic disorder and obsessive-compulsive disorder may involve food avoidance or body-related preoccupations. Misuse of stimulants, laxatives or diuretics can produce a presentation that resembles bulimia nervosa or anorexia nervosa. Clinicians therefore usually check electrolytes, thyroid function and drug history, and ask about the patient's own explanation of the weight change, before settling on a diagnosis.\n\nGroups that are harder to identify\n\nDiagnostic criteria were built largely on young women, and this has affected who is recognised. In DSM-IV-TR, the criteria for anorexia nervosa required an absence of three consecutive menstrual cycles, which excluded males and some other patients from diagnosis. ICD-11 removed the amenorrhoea criterion and no longer treats fear of weight gain as an essential feature.\n\nMen are a clear example of underrecognition. Men are often described as having persistent stereotypes that eating disorders primarily affect females, and due to the stigma that EDs only affect women, fewer men are willing to openly discuss their disordered eating or body image issues. Muscularity-oriented concerns, which are not central to most diagnostic descriptions, are common in men.\n\nOlder adults face a related problem. Estimates for older women range from 2.1 and 7.7%, and the same source notes that these figures are likely to underestimate true rates, particularly for men. Symptoms are sometimes attributed to ageing or to medical illness; one review noted that a medical explanation of symptoms is more likely to be considered and investigated than body shape and eating issues.\n\nWeight-based criteria create a further difficulty for people in larger bodies. Because anorexia nervosa is defined partly by low weight, a person whose weight remains in the normal or higher range may be missed despite significant restriction and fear of weight gain. Bulimia nervosa is also frequently under-identified in people whose weight does not change noticeably. Cultural factors add variation: symptoms, idioms of distress and expectations about food and the body differ across communities, and clinicians may interpret them through their own cultural frame.\n\nDSM-5-TR, ICD-11 and their consequences\n\nThe two systems agree closely on the core diagnoses. In one comparison of ICD-11 and DSM-5 diagnoses, agreement was high for anorexia nervosa (98.9%), BN (97.2%) and BED (100%), and lower for other feeding and eating disorders (OFED; 75.2%). The main source of disagreement is the handling of subjective binges. In the same study, one-hundred and twenty-one patients received an ICD-11 diagnosis of BN or BED because of subjective binges.\n\nOther differences matter for prevalence. The DSM-5 requires the amount eaten during a binge to be objectively large, and also requires specifiers for BED, whereas ICD-11 does not make those specifiers essential. In an Australian community sample, the estimated prevalence of BED was significantly lower when applying DSM-5 criteria, which the authors attributed largely to the binge-eating specifiers.\n\nThese differences have practical effects. A patient diagnosed under one system may not meet the threshold under the other, which can affect eligibility for care, insurance coverage and reimbursement, and the timing of early treatment. In research, studies that use different criteria produce prevalence estimates and treatment samples that cannot easily be compared, which complicates both meta-analysis and the interpretation of trial results."
    },
    {
      "heading": "Psychological and family-based treatments",
      "text": "Psychological treatment is the core of care for most eating disorders once medical stability is secured, but the evidence differs by diagnosis, age and treatment setting. For adolescents with anorexia nervosa, family-based treatment (FBT) is the usual first-line option. Parents take on responsibility for supervising meals and weight restoration at home, with therapists coaching them, and the young person's autonomy over eating is returned in stages as weight and eating stabilise. Because the parental role is central, the approach depends on parents being able and willing to carry it out.\n\nThe trial evidence for adolescents is limited in size. One trial enrolled 121 participants aged 12 through 18 years and compared FBT with adolescent-focused individual therapy. There were no differences in full remission between treatments at the end of treatment. However, at both the 6- and 12-month follow-up, FBT was significantly superior. A later trial comparing parent-focused treatment (PFT), in which parents work with the family without conjoint sessions, with FBT found that remission was higher in PFT than in FBT at the end of treatment (43% versus 22%), but the difference was not statistically significant at 6- or 12-month follow-up. Observational data from a Finnish clinic reported that 32 patients (61.5%) had achieved full weight restoration at the end of treatment, and a review cited in that report estimated overall response to FBT at about 75% (range 60–85%), although reported remission rates vary widely across studies. Predictors of response include parental capacity: in one trial, among parents who reported low self-efficacy at baseline, adding an extra component to FBT was associated with higher remission rates than FBT alone.\n\nThe National Institute for Health and Care Excellence (NICE) recommends CBT for eating disorders in adolescents when family therapy is unacceptable, contraindicated, or ineffective. The recommendation rests largely on the adolescent version of enhanced cognitive-behaviour therapy (CBT-E), which is delivered one-to-one and does not necessitate the full involvement of the family. A non-randomised effectiveness trial found that CBT-E achieved a similar outcome to family-based treatment at 6- and 12-months. In that study, participants chose their treatment: FBT produced a faster rate of weight gain at the end of treatment, but there were no differences in the EDE Global Score or most secondary outcome measures at any time-point. Those who chose CBT-E tended to be older and less well, which complicates direct comparison.\n\nFor adults, CBT-E is the most extensively studied form of treatment. In a randomised trial of 143 adults against treatment as usual, the recovery rate at 20 weeks of CBT-E was significantly higher (57.7%) than of TAU (36.0%), but at 80 weeks, this difference was no longer significant. A trial comparing CBT-E with interpersonal psychotherapy (IPT) in adults with a range of diagnoses found that at post-treatment 65.5% of the CBT-E participants met criteria for remission compared with 33.3% of the IPT participants, and the gap narrowed but remained over follow-up. Exploratory analyses suggest that patients with a longer duration of disorder were less likely to benefit from either treatment, and that higher levels of over-evaluation of the importance of shape predicted a less good treatment outcome. Summarising the adult evidence, one review concluded that CBT should retain its status as the recommended treatment approach for bulimia nervosa (BN) and BED, and the front running treatment for anorexia nervosa (AN) in adults, with interpersonal psychotherapy (IPT) considered a strong empirically-supported alternative.\n\nOther psychotherapies have a smaller and more specialised evidence base, mostly for binge eating disorder. Guided self-help based on CBT-E, for example, produced a marked reduction in binge eating in one trial, where objective binges reduced from an average of 19 (SD 16) to 3 (SD 5) binges, and 40% (36/90) showed full recovery in the guided self-help CBT-E group, although at follow-up, after both groups received treatment, there was no longer a difference between the groups. Dialectical behaviour therapy (DBT) has been tested in guided self-help formats; a small waitlist-controlled pilot found that most improvements in the DBTgsh group were maintained, although binge eating abstinence rates decreased to 30%. A systematic review and meta-analysis reported that DBT improved emotion dysregulation, with the clearest effects in binge eating disorder and bulimia nervosa, but these findings are drawn from small, heterogeneous studies. For anorexia nervosa, supportive self-help adaptations of FBT have been piloted, with a feasibility trial recruiting 40 adolescents ages 12–18 years with DSM‐5 AN and their families, though such work remains preliminary.\n\nComparing outcomes across these treatments is difficult because trials use different primary outcomes, such as weight restoration, full or partial remission, or change in eating-disorder psychopathology, and they differ in duration, dropout and follow-up length. Most adolescent trials show that FBT and alternatives achieve broadly similar symptom improvement, with weight gain and remission more sensitive to the choice of treatment. Most adult trials show early advantages for focused psychotherapies that often narrow over longer follow-up. Across all treatments, a substantial proportion of patients do not fully respond, which is one reason why research on predictors and matching of patients to treatment continues."
    },
    {
      "heading": "Medical, nutritional and inpatient care",
      "text": "Refeeding and nutritional rehabilitation\n\nRestarting food intake in severely underweight patients carries a specific hazard. Clinicians describe refeeding syndrome as a cluster of low phosphate, cardiac events, neurological problems and sudden death that can follow the resumption of nutrition. A systematic review of adolescent refeeding found an average incidence of refeeding hypophosphatemia of 14%, with a range of 0–48%. Phosphate levels below about 0.32 mmol/L are linked to increased risk of severe complications.\n\nEarlier practice relied on low starting energy intakes. Consensus recommendations for adolescents began at roughly 1200 kcal/day and rose slowly, but critics noted that these approaches often contribute to initial weight loss and delayed or slow weight gain during re-alimentation. Later studies from specialist clinics have reported higher starting intakes of about 2000 kcal/day, combined with phosphate supplementation and close monitoring, without a rise in electrolyte abnormalities. Even so, the target rate of weight gain remains contested, with proposed inpatient targets ranging from 500 to 1,400 g per week.\n\nMonitoring protocols typically start before feeding begins. Guidance advises checking serum sodium, potassium, urea, creatinine, magnesium, phosphate, and albumin adjusted calcium levels before feeding, and then checking electrolytes daily for at least the first five days. Thiamine is usually given to at-risk patients, and one UK hospital guideline recommends very low calorie starts of about 5–10 kcal/kg/day for patients with severe anorexia nervosa or very low BMI, with reassessment at least every 12 hours.\n\nLevels of care\n\nThe American Psychiatric Association's 2006 guideline sets out a graded framework: outpatient, intensive outpatient, partial hospitalisation, residential treatment and inpatient hospitalisation, with placement determined by medical status, suicidality and weight as a percentage of expected weight. Weight level per se should never be used as the sole criterion for discharge from inpatient care.\n\nOutpatient care suits patients who are medically stable and do not require daily medical monitoring. Partial hospitalisation is a day programme in which patients commute to treatment while living at home. Residential programmes are for patients who are medically stable and do not require acute medical intervention, and who have not responded to, or who are too unwell for, lower levels of care. Stays in residential settings are often reported to average 30-90 days.\n\nEmergencies, hospitalisation and medication\n\nInpatient admission is reserved for medical or psychiatric instability. Hospital care is generally needed when patients require intravenous fluids, nasogastric tube feedings, or multiple daily laboratory tests, and when vital signs are unstable or depressed. Patients who are psychiatrically unstable, may show rapid worsening of their eating disorder symptoms and may be suicidal and unable to contract for safety also meet criteria for admission. Inpatient units usually provide 24-hour medical monitoring and care, with a focus on medical stabilization.\n\nThe evidence for medication is limited and uneven across diagnoses. For anorexia nervosa, there is limited evidence supporting benefits of medications. Second-generation antipsychotics, particularly olanzapine, show some benefit for weight gain but are not advised as a stand-alone treatment. In a meta-analysis, olanzapine, but not fluoxetine, outperformed placebo for weight gain. A retrospective service evaluation of adolescents in South Wales, however, concluded that olanzapine does not provide additional benefits for weight restoration or functioning. In bulimia nervosa, fluoxetine has exhibited some efficacy leading to regulatory approval in some countries, and in BED, lisdexamfetamine reduced weight and binging. Medication for co-occurring conditions such as depression or anxiety disorders is generally chosen according to those conditions rather than the eating disorder itself."
    },
    {
      "heading": "Prognosis, outcomes and long-term care",
      "text": "Long-term follow-up studies show that many people with anorexia nervosa recover, but a substantial minority remain ill or die. In a prospective study of 84 women followed about 21 years after first hospitalisation, roughly half had fully recovered, about one in ten still met full criteria, and around 16% had died of illness-related causes. The standardised mortality ratio in that cohort was 9.8 (51% fully recovered, 10% still meeting full criteria, 16% deceased from causes related to anorexia nervosa; standardized mortality rate 9.8). A 30-year follow-up of adolescent-onset cases reported a more favourable picture, with 64% achieving full eating disorder symptom recovery, defined as being free of all eating disorder criteria for six consecutive months, yet one in five had a chronic eating disorder. Recovery rates also vary by how studies define remission and recovery, which makes direct comparison difficult (inconsistent study definitions, short follow-up and diagnostic crossover).\n\nPredictors of outcome\n\nDuration of illness is one of the more consistent predictors. Longer duration of eating problems before presentation for treatment is associated with poorer outcome in most studies, and the probability of recovery falls as the illness lengthens. Age at onset is less straightforward. Some long-term studies link later onset with worse outcome, but a 30-year study of adolescent-onset cases found that later age at onset among adolescent-onset anorexia nervosa and premorbid perfectionism predicted better outcome, so the direction of the association depends on the population studied. Reviews of the literature describe the findings for many prognostic factors as considerably heterogeneous.\n\nClinical and psychosocial features also matter. Purging, physical symptoms and advanced age at clinical presentation have been associated with unfavourable courses, while family relationship difficulties and premorbid personality problems have been linked with poorer outcome in other cohorts (a relatively late age of onset, longer duration, previous psychiatric admissions, disturbed family relationships and premorbid personality difficulties). Findings on comorbidity are not uniform: one cohort reported that psychiatric comorbidity did not predict outcome, whereas another found that people with anorexia and comorbid depression were considerably less likely to recover at 22-year follow-up (six times less likely).\n\nRelapse, chronicity and continuing care\n\nRecovery is not necessarily permanent. Long-term cohorts show that patients can relapse, becoming symptomatic again despite previously achieving recovery status. A review of earlier studies reported relapse rates ranging from 9% to 52%, tending to rise as follow-up lengthened (reported relapse rates ranged between 9 and 52%, and tended to increase with increasing duration of follow-up). Those with a poor outcome often do not seek further help, and the authors of one 21-year study recommended regular monitoring and offering treatment whenever possible (only a few patients with poor outcome sought any form of treatment). Reviews of recent evidence describe a similar pattern, with low rates of remission and high risk of mortality, despite evidence-based treatments, especially for AN.\n\nQuality of life, employment and social functioning\n\nEven where symptoms improve, psychosocial functioning may lag. In one 22-year study, eating behaviour and general psychopathology improved but did not reach the level of healthy controls. Research on very long-term outcomes has found that mental health, psychosexual, and socioeconomic status are affected up to 30 years after AN onset, particularly among those with autism. Older work linked early onset and employment in professional or skilled occupations with better prognosis, though those findings come from very small samples. For women, reproductive outcomes after weight restoration appear more favourable: a meta-analysis of long-term follow-up studies found that appropriate treatment of AN leads to the normalization of reproductive function, although the pooled childbirth odds were not statistically different from the general population.\n\nTransition from adolescent to adult care\n\nBecause onset is typically in adolescence, many patients move between services. Transition typically occurs at 18 years of age, when important biological, psychosocial, and vocational changes take place. Reviews argue that smooth and effective transitions are paramount for ensuring service continuity, as well as reducing the risk of ED relapse and premature death. Patient and carer accounts, however, describe a difficult process: qualitative research reports difficulties in accessing care, lack of information, high levels of fear and a sense of cultural change between settings. Proposed improvements include recovery-oriented personal therapies with a focus on long-term goals, as well as tailored and flexible intensive day treatment that allows the pursuit of educational and vocational goals."
    },
    {
      "heading": "Prevention and public health",
      "text": "Universal, selective and indicated approaches\n\nPrevention work is usually sorted into three tiers: universal programmes offered to whole populations, selective programmes for groups judged to be at raised risk, and indicated programmes for people already showing early signs. Results have been mixed. In a 2007 meta-analysis, 51% of eating disorder prevention programs reduced eating disorder risk factors and 29% reduced current or future eating pathology. The same review linked larger effects to programmes that targeted selected rather than general groups, used interactive and multi-session formats, were limited to girls, served participants over 15, and were delivered by professionals .\n\nAmong universal approaches, media literacy has the strongest backing. Such programmes teach young people to read thin-ideal images critically. A systematic review of randomised trials found that media literacy had the most support for universal prevention. In one pooled analysis, media literacy sessions lowered shape and weight concern in both girls and boys .\n\nFor selective prevention, the best-supported approach is the dissonance-based model, in which participants write, speak about and act out arguments against the thin ideal. The aim is to reduce internalisation of that ideal and, in some individuals, the onset of disorder . A trial reported by Stice and colleagues in 2008 found that such a programme cut new cases of DSM-IV eating disorders by 60% over three years, compared with an assessment-only control . Cognitive behavioural programmes were also effective for selective prevention, with effects maintained at follow-up, and were supported for indicated prevention .\n\nEvidence limits and unintended harm\n\nA recurring gap lies between changing attitudes and preventing illness. Programmes reliably improve knowledge, but in pooled analyses they produce only small net changes in maladaptive attitudes and behaviours . Few trials have measured onset directly; one meta-analysis of that question pooled 15 trials . Most studies rely on self-reported risk factors and rarely report how many cases were prevented . A recent systematic review of school-based programmes found that they can reduce symptoms after the intervention, but the effects did not reliably hold across groups and over time .\n\nA long-standing concern is that psychoeducational material might inadvertently encourage symptoms. One meta-analysis found no support for this worry . Another found larger effects for programmes without psychoeducational content , so which components help, and which might backfire, remains unresolved.\n\nEarly detection\n\nEarly detection shortens the interval between symptom onset and treatment. A rapid review found that early intervention, particularly within the first three years of onset, may increase motivation and help-seeking and so reduce the duration of untreated illness . Primary care clinicians are often the first to encounter weight loss, restrictive dieting or purging in a patient, and screening during routine visits can bring cases forward. Schools may notice changes in eating at mealtimes, in athletic performance or in attendance, and families are frequently the first to raise concern. Each of these settings depends on staff or relatives recognising that eating behaviour has moved beyond ordinary dieting, which is why training and clear referral pathways matter as much as screening itself.\n\nPolicy and access\n\nPolicy responses centre on access to treatment, insurance coverage and workforce capacity. In the United States, the Mental Health Parity and Addiction Equity Act of 2008 requires that coverage for mental health conditions not be substantively less generous than coverage for medical and surgical care, which bears directly on eating disorder treatment; its practical effect has varied with implementation. Workforce concerns include the limited number of clinicians trained in specialist approaches such as family-based treatment and enhanced cognitive behavioural therapy, and the need to prepare general practitioners and school staff to recognise early symptoms. Broader policy debates about cultural messaging on body size, and about regulating idealised images in advertising, are active, but the evidence on their effects on eating disorder incidence is not yet firm."
    },
    {
      "heading": "Special populations",
      "text": "Males\n\nMen make up a substantial minority of people with eating disorders, and the proportion varies by diagnosis. Males account for approximately 20% of people with anorexia nervosa, 30% of people with bulimia nervosa, 43% of people with binge-eating disorder, 55-77% of people with other specified feeding or eating disorder and 67% of people with avoidant/restrictive food intake disorder. The true number of affected men is probably higher, because underdiagnosis, misdiagnosis, and stigma all hide cases.\n\nMen who seek help are also treated differently. Despite reporting the same symptoms as women, men are more likely to be misdiagnosed and are less likely to receive an eating disorder diagnosis. Part of the problem lies in the criteria and tools themselves. Amenorrhoea was historically treated as a hallmark of anorexia, so most 20th-century literature doesn't recognize anorexia among males because they didn't fit the criteria. Self-report screening instruments also remain oriented toward female presentations. One high-school study found overvaluation of weight and shape in about 5% of boys, compared with 24% of girls.\n\nMale presentations often differ in content. EDs in males span the full diagnostic spectrum and often present with muscularity‐oriented body dissatisfaction, compulsive exercise, and performance‐enhancing substance use that are poorly captured by traditional, thinness‐focused tools. Muscularity-focused concerns are linked to muscle dysmorphia and related presentations, which the existing diagnostic framework may handle poorly.\n\nSexual and gender minorities\n\nSexual and gender minority populations show consistently higher rates. In the United States, lifetime prevalence for anorexia nervosa (1.7%), bulimia nervosa (1.3%), and binge-eating disorder (2.2%) diagnoses are higher among sexual minority adults compared with cisgender heterosexual adults. Among transgender adults, provider-diagnosed eating disorders over a lifetime were reported by about 10% of transgender men and about 8% of transgender women. In a US survey of sexual and gender minority adolescents aged 13 to 17, roughly one in six reported at least one form of disordered eating. Compared to sexual minority adolescents, gender minority adolescents experience eating disorders at an even greater prevalence and severity.\n\nThe main explanatory framework is minority stress. Shame, concealment of one's sexual identity, and discrimination increase the risk of eating disorders in sexual minority men and women. Weight-related victimisation adds to this burden: in one study, over half of sexual and gender minority youth reported weight-based victimisation, which was associated with binge eating, dieting and other unhealthy weight-control behaviours. For transgender people, body dissatisfaction may be a central stressor, and gender dysphoria treatment has been shown to increase body satisfaction.\n\nOlder adults and people in larger bodies\n\nSymptoms in older adults often date back to adolescence, but later life brings specific triggers. Life transitions, including changes such as menopause, divorce, or grief, can worsen disordered eating in midlife and beyond. Weight-related experiences also persist into later life: a US national study found weight discrimination reported by 6% of adults aged 65 and older.\n\nPeople in larger bodies face a different problem, which is under-recognition. Individuals in bigger bodies are half as likely to receive an eating disorder diagnosis as those in smaller bodies, despite equally severe symptoms, according to one cited analysis. In weight-stigma samples, few participants reported a history of a diagnosed eating disorder despite high rates of current full‐ or subthreshold symptoms. Some patients avoid care because they regard themselves as not being \"sick enough\". Clinical practice has also been criticised: some eating disorders interventions have compounded weight stigma, including using BMI as part of diagnostic criteria. Weight stigma within treatment can therefore affect recovery, and some specialists worry that any clinical attempt at weight loss puts people, especially adolescents at higher weights, at risk for eating disorders. Binge-eating disorder is the diagnosis most closely associated with higher body weight, since BED is often associated with higher body weight and elevated weight-based stigma.\n\nAthletes and occupational groups\n\nSports and occupations that judge or reward leanness carry elevated risk. These include aesthetic sports such as gymnastics, figure skating and ballet, endurance disciplines such as distance running, and modelling. Weight-category sports, including wrestling, boxing and rowing, add pressure through repeated rapid weight loss. Restriction in athletes may be normalised as part of training, which can delay recognition, and energy deficiency in athletes can produce physical signs that overlap with those of eating disorders, complicating assessment.\n\nCultural variation\n\nCore features of eating disorders are recognised across societies, but their expression varies. Where thin ideals are promoted through mass media, fear of fatness and a drive for thinness tend to be prominent. In other settings, distress may appear more often as bodily complaints such as abdominal pain or fatigue, or it may be framed in terms of religion, family obligation or purity. Diagnostic criteria developed largely from Western clinical samples may therefore fit some presentations poorly, and this bears on how far cultural context is considered in diagnosis and treatment."
    },
    {
      "heading": "History of understanding",
      "text": "Self-starvation before the modern diagnosis\n\nDeliberate refusal of food has a long record, but it was not always read as an illness. Medieval and early modern accounts often framed extreme fasting within religious devotion, and the notion that a person could not survive long without eating was itself a precondition for treating prolonged abstinence as a psychological problem. Medical writing gradually took up individual cases: the English physician Richard Morton's 1689 account is sometimes cited as an early description of what would later be called anorexia nervosa, although it was not widely accepted by the profession until much later.\n\nThe naming of anorexia nervosa, 1868–1874\n\nThe modern concept emerged in the early 1870s. In 1868, William Gull referred to the condition as apepsia hysterica, then revised the label to anorexia hysterica and finally to anorexia nervosa. Gull preferred the more general word \"nervosa,\" because the disease also occurred in males and was probably central rather than peripheral. In 1873, the French physician Ernest-Charles Lasègue published his own paper on what he called hysterical anorexia. Historians still debate priority: Gull and Lasègue independently described anorexia nervosa around 1873, with no clear priority established. The two accounts also differed in emphasis. Gull reported mainly physical and behavioural features, whereas Lasègue paid more attention to his patients' psychological aspects. The discarded word \"hysterica\" reflected Victorian assumptions that the term applied to female behaviour.\n\nBulimia nervosa and the 1979 naming\n\nBulimia nervosa had a later and more abrupt origin. The British psychiatrist Gerald Russell began noticing patients in the early 1970s who did not fit the classic picture of anorexia, and his 1979 paper described the condition as a \"chronic phase of anorexia nervosa,\" in which patients overeat and then use compensatory mechanisms such as self-induced vomiting or laxatives. His report covered thirty patients who were troubled by urges to overeat and by a strong fear of becoming fat. The name, drawn from Greek words for ox-like hunger, highlighted the \"gross overeating\" that defined all of these patients. Russell's syndrome definition and the name that would last both came from that paper, even though other clinicians had observed similar states.\n\nBinge eating disorder: from obesity research to DSM-5\n\nBinge eating entered the psychiatric literature through obesity research rather than eating-disorder clinics. Albert Stunkard's work from the 1950s and 1959 described night eating and related patterns, and he observed three main behaviours: night eating, eating with no satiation, and binge eating. Sources differ on dates and labels; one account notes that proposed names included \"Stuffing Syndrome,\" \"Hyperorexia,\" and \"Dietary Chaos Syndrome.\" In the American system, binge eating was first treated as a feature of other diagnoses. In the DSM-IV, other clinically significant eating disorder symptoms were absorbed by residual categories, with binge eating disorder placed among criteria for further research. Binge eating disorder became a standalone diagnosis only in 2013, when the DSM-5 was published by the American Psychiatric Association.\n\nDSM-III onward\n\nThe American Psychiatric Association's classification shaped how these conditions were recognised. The DSM-III, released in 1980, listed anorexia nervosa and \"bulimia\" as mental disorders in a section called \"Eating Disorders.\" Bulimia was defined largely by binge eating, and the DSM-III-R (1987) renamed the diagnosis \"bulimia nervosa\" and altered the criteria to make them more specific. Early editions also placed eating disorders among disorders of childhood or adolescence, perhaps contributing to underdiagnosis of later-onset cases. The DSM-5 later revised the anorexia nervosa criteria, a change that falls outside the scope of this section.\n\nShifts in treatment models\n\nTreatment thinking moved through several phases. Early twentieth-century approaches were often shaped by a view of the psychological basis of eating disorders in which the individual's inner conflicts were central. Hilde Bruch's 1973 work emphasised the disturbed body perception and sense of self at the core of anorexia, a psychodynamic framing that remained influential into the following decade. From the late 1970s, family-systems models argued that the family itself was part of the maintaining context, and by the late 1980s this thinking had produced structured family-based treatment for adolescents. Cognitive and behavioural models gained ground in parallel: Christopher Fairburn's 1981 cognitive-behavioural approach to bulimia became a template for later enhanced cognitive-behavioural therapy. These shifts reflect changing ideas about causation and about who should take part in treatment, rather than a single linear progression."
    },
    {
      "heading": "Open questions and current research",
      "text": "Heterogeneity within the \"other specified\" category\n\nThe residual categories hold a large share of patients. One editorial notes that more than 50% of eating disorder patients are diagnosed as \"Other Specified Feeding or Eating Disorder (OSFED)\" or \"Unspecified Feeding and Eating Disorders\" (UFED). These groups combine very different presentations, including atypical anorexia nervosa, purging disorder, subthreshold bulimia nervosa, subthreshold binge eating disorder, and night eating syndrome. Early comparisons suggested that the subtypes differ in prognosis: in one analysis, purging disorder patients showed the best prognosis, whereas atypical AN and subthreshold BN patients did not differ from full-threshold disorders. A later cognitive-behavioural therapy study of 176 women found similar clinical and personality profiles between the diagnostic subtypes, with hardly any differences, and no significant differences in remission, adherence or dropout.\n\nSubdividing the category by dominant clinical feature has been tested directly. One analysis tried grouping cases by restraint versus binge-purging, but cluster analysis failed to identify clusters in a treatment-seeking sample based on symptoms of restraint, binge eating, purging and over-evaluation of shape and weight. Whether subtyping can improve diagnosis or match patients to treatment therefore remains unresolved.\n\nLimits of current treatment and the search for predictors\n\nExisting treatments help a minority to a limited degree. One review estimates that current treatments are only effective for 40–55% of people. The authors attribute part of this to the high heterogeneity of eating disorder symptoms and high rates of co-occurrence with other transdiagnostic symptoms, which are not currently addressed in standard treatments. A meta-analysis of 33 studies found that approximately half of patients across clinical samples showed early response to psychological therapy, and early improvement was moderately associated with later outcome. Early response is therefore a candidate predictor, but its use in changing treatment plans has not been established.\n\nOutcomes differ by diagnosis. For bulimia nervosa, a meta-analysis of case series reported full recovery at 45.0% and partial remission at 27.0%, with 23.0% experiencing a chronic course. For adults with anorexia nervosa, a meta-review concluded that no reliable evidence supports the clear superiority or inferiority of any treatment recommended by the NICE guidelines for standalone outpatient care.\n\nGenetic research and what it can explain\n\nTwin studies consistently point to substantial heritability. Anorexia nervosa has twin-based heritability estimates of 50-60%. The first large genome-wide association study combined the Anorexia Nervosa Genetics Initiative with the Psychiatric Genomics Consortium and identified eight significant loci among 16,992 cases of anorexia nervosa and 55,525 controls. Its authors found significant genetic correlations with psychiatric disorders, physical activity, and metabolic (including glycemic), lipid and anthropometric traits, and proposed a reconceptualization of anorexia nervosa as a metabo-psychiatric disorder.\n\nCommon variants explain much less than twin estimates suggest. A 2025 preprint with 24,223 cases reported a liability-scale SNP-based heritability was 13%, which is well below the twin figures. Larger analyses have since added loci. A 2023 study used conditional false discovery rate methods to identify 58 novel AN loci, and 38 unique loci shared between AN and major psychiatric disorders. Genetic correlation does not establish causation, and a later meta-analysis that used Mendelian randomisation reported shared and potentially causal relationships between AN and multiple psychiatric and metabolic traits, which remains to be confirmed.\n\nBiomarkers, neuroimaging and harmonisation\n\nNo biological marker is yet validated for diagnosing eating disorders or for predicting response to treatment. Neuroimaging studies have often used small, heterogeneous samples, and many findings may reflect the effects of starvation rather than stable traits, so what they reveal about causation is limited. Differences between DSM-5-TR and ICD-11, such as how binge episodes are defined, mean that prevalence estimates, trial cohorts and genetic samples are not always directly comparable. Harmonising the systems, or moving towards transdiagnostic models that cut across diagnoses, would make research findings easier to combine, although the consequences for clinical access remain to be determined."
    }
  ],
  "links": [
    "mental-disorder",
    "psychology",
    "metabolism",
    "cardiovascular-disease",
    "brain",
    "genetics",
    "neuroscience",
    "evidence-based-medicine",
    "medicine",
    "hormone",
    "electrolyte",
    "pharmacology",
    "depression",
    "anxiety-disorders",
    "health-promotion",
    "social-media",
    "randomized-controlled-trial",
    "culture"
  ],
  "sources": [
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    },
    {
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      "url": "https://www.psychologytoday.com/us/basics/eating-disorders"
    },
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      "url": "https://www.researchgate.net/publication/333377747_Prevalence_of_eating_disorders_over_the_2000-2018_period_a_systematic_literature_review"
    },
    {
      "title": "(PDF) An update on the prevalence of eating disorders in the general population: a systematic review and meta-analysis",
      "url": "https://www.researchgate.net/publication/350744153_An_update_on_the_prevalence_of_eating_disorders_in_the_general_population_a_systematic_review_and_meta-analysis"
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    {
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    },
    {
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      "url": "https://pmc.ncbi.nlm.nih.gov/articles/PMC12979973/"
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    {
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      "url": "https://onlinelibrary.wiley.com/doi/10.1002/eat.22501"
    },
    {
      "title": "From efficacy to effectiveness: child and adolescent eating disorder treatments in the real world (Part 2): 7-year follow-up",
      "url": "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8817149/"
    },
    {
      "title": "Genetic factors in anorexia nervosa",
      "url": "https://www.cambridge.org/core/journals/european-psychiatry/article/abs/genetic-factors-in-anorexia-nervosa/BA6BC298250AF65699FFBB387E38746D"
    },
    {
      "title": "Papers by katherine halmi",
      "url": "https://independent.academia.edu/halmikatherine"
    },
    {
      "title": "S-EPMC6139670 - Genetics of Anorexia Nervosa. - OmicsDI",
      "url": "https://www.omicsdi.org/dataset/biostudies-literature/S-EPMC6139670"
    },
    {
      "title": "Genome-Wide Association Study Reveals First Locus for Anorexia Nervosa and Metabolic Correlations",
      "url": "https://www.biorxiv.org/content/10.1101/088815.full.pdf"
    },
    {
      "title": "Understanding eating disorder susceptibility requires an integrated sociological, biological and genetic approach",
      "url": "https://www.acamh.org/research-digest/understanding-eating-disorder/"
    },
    {
      "title": "Risk and resilience in eating disorders: differentiating pathways among psychosocial predictors",
      "url": "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11110273/"
    },
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  ],
  "license": "https://creativecommons.org/licenses/by/4.0/"
}