Eating Disorders

Eating disorders are serious psychiatric conditions defined by persistent disturbances in eating behaviour and the thoughts and emotions associated with eating. This document covers the three major eating disorders: Anorexia Nervosa (AN), Bulimia Nervosa (BN), and Binge-Eating Disorder (BED). AN carries the highest mortality rate of any psychiatric disorder - standardised mortality ratios reach 5-10, with approximately 5-10% of patients dying from medical complications, suicide, or starvation. References: DSM-5-TR, StatPearls (NCBI Bookshelf).

Eating disorders are serious psychiatric conditions defined by persistent disturbances in eating behaviour and the thoughts and emotions associated with eating. This document covers the three major eating disorders: Anorexia Nervosa (AN), Bulimia Nervosa (BN), and Binge-Eating Disorder (BED). AN carries the highest mortality rate of any psychiatric disorder - standardised mortality ratios reach 5-10, with approximately 5-10% of patients dying from medical complications, suicide, or starvation. BN and BED also carry significant morbidity and mortality. DSM-5-TR classifies all three under 'Feeding and Eating Disorders.' ICD-11 codes: AN = 6B80, BN = 6B81, BED = 6B82. Lifetime prevalence: AN ~0.3-1% (some studies up to 4% in women); BN ~1-2%; BED ~2-3.5% (the most common eating disorder). Onset typically occurs in adolescence or early adulthood, though all ages can be affected. Female-to-male ratio: AN 10:1, BN 10:1, BED 3:2. This information is for psychoeducation only.

ANOREXIA NERVOSA: Core features: restriction of energy intake leading to significantly low body weight (BMI <18.5 in adults, or failure to reach expected weight in children/adolescents); intense fear of gaining weight or becoming fat (or persistent behaviour interfering with weight gain, even at very low weight); disturbed body image (experiencing body size/shape as larger than reality, undue influence of weight on self-evaluation, or denial of the seriousness of low weight). Two subtypes: Restricting type (weight loss achieved through dieting, fasting, or excessive exercise without binge/purge episodes in the past 3 months); Binge-eating/purging type (recurrent binge eating or purging via vomiting, laxatives, diuretics, or enemas). Physical signs: emaciation, lanugo hair (fine downy hair on face and body), hypothermia, bradycardia (heart rate <60 bpm, sometimes <40 bpm), hypotension, peripheral oedema, hair loss, dry skin, brittle nails, parotid gland enlargement (if purging), dental erosion (if purging), Russell's sign (calluses on knuckles from self-induced vomiting), amenorrhoea (though no longer a DSM requirement). BULIMIA NERVOSA: Core features: recurrent episodes of binge eating (eating an objectively large amount of food in a discrete period with a sense of loss of control) followed by compensatory behaviour to prevent weight gain. Compensatory behaviours include self-induced vomiting (~80-90% of BN patients), laxative misuse, diuretic misuse, fasting, or excessive exercise. Both binge eating and compensatory behaviour occur at least once per week for 3 months. Self-evaluation is unduly influenced by body shape and weight. Weight is typically normal or slightly above normal (BMI 18.5-30).

Physical signs: parotid/salivary gland swelling ('chipmunk cheeks'), dental erosion (perimolysis - erosion of tooth enamel on lingual surfaces from gastric acid), Russell's sign, menstrual irregularities, oesophageal tears (Mallory-Weiss), metabolic alkalosis from vomiting, hypokalaemia (from purging - can cause cardiac arrhythmias), oedema (from laxative/diuretic misuse and rebound fluid retention). BINGE-EATING DISORDER: Core features: recurrent binge eating episodes (same definition as BN) occurring at least once per week for 3 months. Binge episodes are associated with at least 3 of: eating much more rapidly than normal; eating until uncomfortably full; eating large amounts when not physically hungry; eating alone due to embarrassment about the quantity; feeling disgusted, depressed, or very guilty after overeating. Marked distress about binge eating is present. NO regular compensatory behaviour (this is what distinguishes BED from BN). Most individuals with BED are overweight or obese (BMI >25), though normal weight is possible.

Genetic: heritability 50-80% for AN, 55-65% for BN, 45-57% for BED. First-degree relatives of AN patients have a 10-fold increased risk. Genome-wide association studies (GWAS) have identified 8 significant loci for AN, with genetic correlations between AN and OCD, major depression, anxiety, and - notably - metabolic traits (low BMI, reduced insulin resistance), suggesting AN has both psychiatric and metabolic genetic underpinnings. Psychological: perfectionism and rigidity (especially AN); low self-esteem; body dissatisfaction; negative affect and emotional dysregulation; history of dieting (the single most common behavioural precursor); trauma and sexual abuse (particularly linked to BN and BED); comorbid anxiety (often precedes eating disorder onset). Sociocultural: internalisation of thin-ideal body image; media exposure emphasising thinness; peer pressure about weight and appearance; sports and activities that emphasise leanness (ballet, gymnastics, wrestling, running, modelling); weight-related teasing and bullying. Family: family history of eating disorders, obesity, mood disorders, or substance use; high-achieving/enmeshed family dynamics (AN); family conflict (BN, BED); parental dietary restriction or weight preoccupation. Developmental: puberty (body composition changes trigger vulnerability in predisposed individuals); identity formation struggles in adolescence; major life transitions (going to college, relationship changes).

AN: A gene-environment interaction disorder. The strongest genetic finding from the Eating Disorders Genetics Initiative (EDGI) GWAS is that AN has significant positive genetic correlations with OCD and negative genetic correlations with BMI and metabolic markers - it is both a psychiatric and a metabolic condition. Neurobiologically, serotonin system overactivity (elevated 5-HT2A receptor binding) underlies the anxiety, rigidity, and harm avoidance seen in AN. Starvation itself alters brain chemistry: tryptophan restriction reduces serotonin synthesis, which may temporarily relieve the dysphoric hyperserotonergia - this creates a self-reinforcing cycle where food restriction reduces anxiety. Dopamine system abnormalities in the dorsal striatum impair reward processing for food, and the insula (interoceptive cortex) shows reduced activation, impairing hunger and satiety awareness.

BN: Serotonin dysfunction is central - reduced 5-HT function produces impulsivity, mood instability, and binge-purge cycling. The dopamine reward system shows altered activation during binge episodes (initial hedonic surge followed by guilt and aversive affect). The hypothalamic regulation of appetite involves ghrelin (elevated before binges), leptin (often reduced), cholecystokinin (impaired satiety signalling), and cortisol (elevated chronically). Impulsivity traits and emotional dysregulation are more prominent than in AN. BED: Shares some neurobiological overlap with BN and addiction. The dopamine reward system shows similar alterations to substance use disorders - reduced D2 receptor availability in the striatum, heightened food-cue reactivity, and impaired inhibitory control. Emotional eating is driven by cortisol-mediated stress responses and endogenous opioid release during binge episodes. BED is strongly associated with obesity, and the metabolic consequences of both conditions interact.

Lifetime prevalence: AN 0.3-1% (up to 4% in women by some estimates); BN 1-2%; BED 2-3.5%. BED is the most common eating disorder overall. Point prevalence among adolescents: AN 0.3%; BN 0.9%; BED 1.6%. Sex distribution: AN and BN are approximately 10:1 female to male; BED is approximately 3:2 female to male. Males are increasingly recognised as affected and are consistently underdiagnosed. Male eating disorders more often involve muscularity concerns rather than thinness pursuit. Age of onset: AN peaks at 15-19 years (bimodal peak at 14 and 18); BN peaks at 18-25 years; BED peaks later, often in the 20s-30s. All three can occur at any age. Mortality: AN has a standardised mortality ratio (SMR) of 5.86, the highest of any psychiatric disorder. Approximately 5-10% of AN patients die within 10 years of diagnosis, and 20% within 20 years. Causes of death: cardiac arrhythmias from electrolyte abnormalities (33%), suicide (20%), medical complications of starvation. BN mortality is elevated but lower than AN (SMR ~1.9). BED mortality relates primarily to obesity-associated medical conditions. Comorbidity: AN - depression 40-80%, anxiety disorders 50-60%, OCD 15-40%. BN - depression 50-70%, anxiety 40-60%, substance use 20-30%, BPD 20-30%. BED - depression 50-60%, anxiety 35-50%, substance use 15-25%. All three are associated with elevated suicide risk.

AN - Starvation effects: the body enters a catabolic state with widespread organ system effects. Cardiac: bradycardia (often <50 bpm), QTc prolongation, mitral valve prolapse, pericardial effusion, cardiac atrophy. Endocrine: hypothalamic hypogonadism (low LH, FSH, oestrogen/testosterone → amenorrhoea/oligomenorrhoea), low T3 (euthyroid sick syndrome), elevated cortisol, low IGF-1, growth hormone resistance. Bone: reduced bone mineral density (osteopenia in 50%, osteoporosis in 20-30% of AN patients), increased fracture risk; bone loss may be irreversible. Gastrointestinal: delayed gastric emptying, constipation, superior mesenteric artery syndrome (compression of the duodenum). Haematological: pancytopenia, gelatinous bone marrow transformation.

Brain: grey matter volume reduction (partially reversible with weight restoration), white matter changes, ventricular enlargement. BN - Purging effects: self-induced vomiting causes metabolic alkalosis, hypokalaemia, and hypochloraemia (loss of HCl and KCl). Hypokalaemia is the most dangerous acute complication because it causes cardiac arrhythmias (prolonged QT, U waves, ventricular tachycardia). Dental erosion from gastric acid (perimolysis) affects lingual surfaces of upper teeth. Oesophageal tears (Mallory-Weiss) and, rarely, oesophageal rupture (Boerhaave syndrome, a surgical emergency). Parotid gland hypertrophy. Laxative misuse causes metabolic acidosis, dehydration, and 'cathartic colon' (loss of normal peristalsis). Ipecac misuse (rare now) causes irreversible cardiomyopathy. BED - Metabolic consequences: obesity-related complications include type 2 diabetes, hypertension, dyslipidaemia, cardiovascular disease, obstructive sleep apnoea, non-alcoholic fatty liver disease, and osteoarthritis. The metabolic profile of BED patients is often worse than weight-matched controls without BED, suggesting BED-specific metabolic effects beyond weight alone. Refeeding syndrome: a dangerous complication of refeeding in severely malnourished AN patients. When carbohydrates are reintroduced, insulin secretion drives potassium, phosphate, and magnesium into cells, causing profound hypophosphataemia (the hallmark), hypokalaemia, and hypomagnesaemia. This can cause cardiac failure, arrhythmias, respiratory failure, seizures, and death. Risk is highest in the first 72-96 hours of refeeding. Prevention: start refeeding at low caloric levels (initially 10-20 kcal/kg/day in high-risk patients), supplement phosphate, potassium, and magnesium prophylactically, and monitor electrolytes every 12 hours for the first 3-5 days.

History taking should be conducted sensitively. Many patients minimise or deny symptoms. Use validated screening tools: SCOFF questionnaire (5 questions, score >=2 suggests eating disorder; sensitivity ~85% for AN and BN); EDE-Q (Eating Disorder Examination Questionnaire, 28 items, self-report). Key history questions: (1) Relationship with food and eating: restricting, binge eating, compensatory behaviours (vomiting, laxative/diuretic use, excessive exercise), food rituals, fear of certain foods. (2) Weight history: lowest and highest adult weight, desired weight, recent weight changes. (3) Body image: how do you see your body?

Would gaining 5 pounds change how you feel about yourself? (4) Menstrual history in females: amenorrhoea, irregular periods. (5) Exercise: type, frequency, duration, compulsivity (exercising through illness/injury). (6) Psychiatric history: depression, anxiety, OCD, substance use, self-harm, suicidal ideation. (7) Family history: eating disorders, obesity, depression, substance use. Physical examination: Vitals: weight and height (calculate BMI), heart rate (bradycardia in AN), blood pressure (hypotension, orthostatic drop in AN), temperature (hypothermia in AN). General: body habitus, cachexia (AN), parotid enlargement (BN purging), lanugo hair (AN), hair loss, dry skin. Oral: dental erosion (perimolysis, BN), erosion of lingual surfaces of upper teeth, caries. Hands: Russell's sign (calluses on dorsal knuckles from self-induced vomiting). Cardiac: bradycardia, irregular rhythm. Abdomen: distension, tenderness. Musculoskeletal: proximal muscle wasting (AN). Neurological: peripheral neuropathy (B12/folate deficiency in AN). Skin: carotenodermia (yellowish discolouration from excess beta-carotene intake), acrocyanosis, poor wound healing.

ANOREXIA NERVOSA (DSM-5-TR, 307.1 / F50.0x): A. Restriction of energy intake relative to requirements, leading to significantly low body weight in the context of age, sex, developmental trajectory, and physical health. Significantly low weight is defined as weight that is less than minimally normal (adults) or less than minimally expected (children/adolescents). B. Intense fear of gaining weight or of becoming fat, or persistent behaviour that interferes with weight gain, even though at a significantly low weight. C. Disturbance in the way in which one's body weight or shape is experienced, undue influence of body weight or shape on self-evaluation, or persistent lack of recognition of the seriousness of the current low body weight. Subtypes: Restricting type (F50.01); Binge-eating/purging type (F50.02). Severity (BMI-based for adults): Mild >=17; Moderate 16-16.99; Severe 15-15.99; Extreme <15. BULIMIA NERVOSA (DSM-5-TR, 307.51 / F50.2): A. Recurrent episodes of binge eating (eating a definitely larger amount of food than most individuals would eat in a similar period and circumstances + sense of lack of control over eating during the episode). B. Recurrent inappropriate compensatory behaviours to prevent weight gain (self-induced vomiting, misuse of laxatives/diuretics/other medications, fasting, excessive exercise). C. Binge eating and compensatory behaviours both occur at least once a week for 3 months. D. Self-evaluation unduly influenced by body shape and weight. E. Does not occur exclusively during episodes of AN. Severity: Mild (1-3 episodes/week); Moderate (4-7); Severe (8-13); Extreme (14+ episodes of compensatory behaviour/week). BINGE-EATING DISORDER (DSM-5-TR, 307.51 / F50.81): A. Recurrent binge eating episodes (same definition as BN criterion A). B. Binge episodes associated with 3+ of: eating rapidly, eating until uncomfortably full, eating large amounts when not hungry, eating alone from embarrassment, feeling disgusted/depressed/guilty afterwards. C. Marked distress regarding binge eating. D. Binge eating occurs at least once a week for 3 months. E. NOT associated with regular compensatory behaviour (distinguishing from BN) and does not occur exclusively during AN or BN. Severity: Mild (1-3 binge episodes/week); Moderate (4-7); Severe (8-13); Extreme (14+). ICD-11 codes: AN = 6B80, BN = 6B81, BED = 6B82.

Structured clinical interviews: EDE (Eating Disorder Examination, gold-standard clinician-administered interview), SCID-5-RV eating disorders module. Self-report measures: EDE-Q, Eating Attitudes Test (EAT-26), Binge Eating Scale (BES for BED). Essential laboratory tests for all eating disorders: Electrolytes: potassium (hypokalaemia from purging - the most dangerous lab abnormality), sodium, chloride, bicarbonate, calcium, magnesium, phosphate (critical for refeeding syndrome risk assessment). Renal function: BUN, creatinine (elevated BUN in dehydration, renal impairment from chronic dehydration). Hepatic function: ALT, AST (elevated in starvation and refeeding). CBC: pancytopenia in severe AN. Thyroid function: TSH, free T4 (low T3 syndrome in AN; rule out thyroid disease as cause of weight change). Glucose: hypoglycaemia in severe AN. ECG: QTc prolongation (>450ms concerning, >500ms dangerous), bradycardia, U waves (hypokalaemia). Bone density (DEXA scan): indicated in AN if amenorrhoea >6 months or low body weight for >1 year. Additional: amylase (elevated in purging), serum cortisol, LH, FSH, oestradiol (hormonal status in AN), vitamin D, B12, folate, iron studies. Urine: specific gravity (concentrated in dehydration), urine drug screen if substance use suspected, urine pH (alkaline in vomiting). Medical stability assessment: heart rate (<40 bpm = high risk), blood pressure (systolic <90 mmHg = high risk), orthostatic vitals (drop >20 mmHg systolic or >10 bpm on standing), temperature (<35.5°C = high risk), BMI (<15 = extreme severity), potassium (<3.0 mmol/L = high risk), phosphate (<0.5 mmol/L = refeeding risk).

Medical causes of weight loss: hyperthyroidism (increased appetite, weight loss, tachycardia - elevated T4/T3 distinguishes from AN), type 1 diabetes (polyuria, polydipsia, weight loss), inflammatory bowel disease (abdominal pain, diarrhoea, weight loss), coeliac disease, malignancy, Addison's disease, HIV/AIDS. In AN, the fear of weight gain and body image disturbance are pathognomonic and absent in medical conditions. Medical causes of binge eating: Prader-Willi syndrome (hyperphagia with intellectual disability and characteristic physical features), Kleine-Levin syndrome (periodic hypersomnia and hyperphagia), hypothalamic lesions. Depression: appetite and weight changes occur in depression, but body image distortion and compensatory behaviours are absent. Depression and eating disorders frequently co-occur. OCD: food-related rituals may mimic AN, but OCD-related food rituals are typically driven by contamination fears or magical thinking rather than weight/shape concerns. AN and OCD co-occur in 15-40% of cases. Body dysmorphic disorder (BDD): appearance preoccupation, but focused on specific perceived defects (skin, nose, etc.) rather than weight/shape. When concerns focus exclusively on weight/shape, AN or BN is the more appropriate diagnosis. Avoidant/Restrictive Food Intake Disorder (ARFID): food restriction without the weight/shape concerns, fear of gaining weight, or body image disturbance that define AN. ARFID involves sensory sensitivities, fear of aversive consequences of eating (choking, vomiting), or lack of interest in eating.

Substance use disorders: stimulant use (cocaine, amphetamines) can cause severe weight loss; must be ruled out. Substance use and eating disorders frequently co-occur (20-30% of BN/BED).

Treatment of Eating Disorders is multidisciplinary, involving medical stabilisation, nutritional rehabilitation, psychotherapy, and ongoing monitoring. Anorexia Nervosa: Medical stabilisation and weight restoration are initial priorities. Nutritional rehabilitation with structured meal plans, supervised eating, and gradual caloric increase is essential. Start with approximately 1200-1500 kcal/day in outpatients (higher in inpatients under monitoring) and increase by 200-300 kcal every 2-3 days, targeting weight gain of 0.5-1 kg/week for outpatients and 1-1.5 kg/week for inpatients. Monitor for refeeding syndrome in severely malnourished patients: check phosphate, potassium, and magnesium every 12 hours for the first 3-5 days; supplement prophylactically. Family-Based Treatment (FBT / Maudsley approach) is the first-line treatment for adolescents and involves parents taking an active role in refeeding. FBT proceeds in three phases: Phase 1 (parental control of eating), Phase 2 (gradual return of eating autonomy to the adolescent), Phase 3 (establishing healthy adolescent identity). FBT has the strongest evidence base for adolescent AN, with recovery rates of 40-50% at end of treatment and up to 75% at 5-year follow-up. CBT-Enhanced (CBT-E) is effective for adults and addresses the maintaining mechanisms of the eating disorder (dietary restraint, overvaluation of shape/weight, low self-esteem, perfectionism, interpersonal difficulties). Specialist Supportive Clinical Management (SSCM) combines clinical management with supportive psychotherapy and is an effective alternative. Pharmacotherapy has limited efficacy for AN itself. Olanzapine (2.5-10mg) may help with weight gain, anxiety, and obsessive thoughts. SSRIs are not effective during the underweight phase but may help prevent relapse after weight restoration and treat comorbid depression/anxiety. Zinc supplementation (14mg elemental zinc/day) accelerates weight gain in some studies. Hospitalisation criteria: heart rate <40 bpm, systolic BP <90 mmHg, temperature <35.5°C, BMI <15 (or rapidly declining weight), electrolyte disturbance (K+ <3.0, PO4 <0.5), syncope, suicidal ideation, failure of outpatient treatment. Bulimia Nervosa: CBT-E is the first-line treatment and targets binge-purge cycles, dietary restraint, and cognitive distortions about shape and weight. Typically 20 sessions over 20 weeks. Response rate: approximately 50-60% achieve abstinence from binge-purge behaviour. Interpersonal Psychotherapy (IPT) is an evidence-based alternative that focuses on interpersonal difficulties maintaining the eating disorder. Fluoxetine 60mg/day is FDA-approved for BN and reduces binge-purge frequency by approximately 50% independently of its antidepressant effect. The effective dose (60mg) is higher than the typical antidepressant dose (20mg). Other SSRIs are used off-label. Topiramate (25-200mg) reduces binge frequency and promotes weight loss but carries cognitive side effects. Guided self-help based on CBT principles is effective for mild-to-moderate BN and can be delivered with minimal therapist contact.

Binge Eating Disorder: CBT (individual or group), IPT, and guided self-help based on CBT principles are effective psychotherapies. CBT typically achieves binge abstinence in 50-60% of patients. Lisdexamfetamine (Vyvanse, 50-70mg/day) is FDA-approved for moderate-to-severe BED and reduces binge frequency by approximately 50%. It is a Schedule II controlled substance and should not be used for weight loss. SSRIs (fluoxetine, sertraline, citalopram) reduce binge frequency modestly. Topiramate reduces binge frequency and promotes weight loss but has cognitive side effects and teratogenic potential. Nutritional Counselling: Working with a dietitian to establish regular eating patterns (typically 3 meals + 2-3 snacks daily), adequate nutrition, mechanical eating (eating by plan rather than hunger/fullness cues initially), and a healthy relationship with food is a core component across all eating disorders.

AN: approximately 50% of patients recover fully, 30% improve partially, and 20% develop a chronic course. Mortality rate: 5-10% within 10 years, up to 20% at 20-year follow-up. Leading causes of death: cardiac complications, suicide (standardised mortality ratio for suicide in AN is ~30), and infections. Good prognostic indicators: adolescent onset, short duration of illness, higher minimum BMI, no binge-purge subtype, no comorbid personality disorder. Poor prognostic indicators: low initial BMI (<15), long illness duration, binge-purging subtype, comorbid depression, OCD, or substance use, chronic medical complications. BN: approximately 50-70% of treated patients recover with evidence-based treatment (CBT + fluoxetine). About 20-30% have a chronic, relapsing course. Mortality is elevated but lower than AN (SMR ~1.9). Good prognostic indicators: shorter duration before treatment, fewer comorbidities, response within the first 4 weeks of CBT. The 'rapid response' phenomenon - significant symptom reduction in weeks 1-4 of CBT - predicts good long-term outcome. BED: approximately 50-80% of treated patients achieve remission. BED tends to have a more episodic course with spontaneous remission rates higher than AN or BN. However, weight loss is often modest despite binge reduction, and many patients require additional weight management support. Medical complications related to obesity determine much of the long-term morbidity.

AN medical complications: Cardiac - arrhythmias (QTc prolongation, bradycardia <40 bpm, congestive heart failure during refeeding), mitral valve prolapse, pericardial effusion. Sudden cardiac death is the leading medical cause of mortality. Skeletal - osteopenia (50%), osteoporosis (20-30%), pathological fractures; bone loss may be irreversible even after weight restoration. Endocrine - hypothalamic amenorrhoea, infertility, low oestrogen/testosterone, cortisol elevation, growth hormone resistance. Gastrointestinal - gastroparesis (delayed gastric emptying causing bloating and early satiety), constipation, superior mesenteric artery syndrome, hepatic steatosis. Neurological - brain atrophy (grey matter loss partially reversible), peripheral neuropathy, cognitive deficits. Refeeding syndrome - potentially fatal; hypophosphataemia, cardiac failure, fluid shifts. BN medical complications: Hypokalaemia (most dangerous - cardiac arrhythmias, muscle weakness, renal impairment). Metabolic alkalosis. Dental erosion (perimolysis, dental caries). Parotid gland hypertrophy. Oesophageal tears

(Mallory-Weiss). Oesophageal rupture (Boerhaave syndrome, rare but can be fatal). Aspiration during vomiting. Cathartic colon from chronic laxative abuse. Rectal prolapse. Renal impairment from chronic dehydration. BED medical complications: type 2 diabetes, cardiovascular disease, hypertension, dyslipidaemia, obstructive sleep apnoea, non-alcoholic fatty liver disease, osteoarthritis, and increased surgical risk. Psychological complications (all three): depression, anxiety, social isolation, relationship difficulties, academic/occupational impairment, substance use, self-harm, and suicide. The suicide rate across all eating disorders is markedly elevated.

Prevention programmes with evidence: body image programmes that build media literacy and challenge thin-ideal internalisation reduce eating disorder onset. The Body Project (cognitive dissonance-based, developed by Eric Stice) reduces eating disorder incidence by 60% in high-risk young women over 3-year follow-up. School-based programmes that teach critical evaluation of media messages and build self-esteem show modest but consistent preventive effects. Internet-based programmes (StudentBodies, ProYouth) show promise for broadening reach. Key patient education messages: eating disorders are serious, biologically-based mental illnesses - not choices, vanity, or phases. They affect all genders, ages, races, and body sizes. Full recovery is possible, but early treatment produces much better outcomes. Warning signs to watch for: preoccupation with food/weight/calories, skipping meals, disappearing after meals, excessive exercise, rapid weight changes, withdrawal from social eating. Families should avoid commenting on weight or appearance and should model healthy relationships with food and exercise. For patients in treatment: complete meals are as important as medication for recovery. Weight restoration (in AN) improves brain function, mood, and cognition. Relapse does not mean failure - it is common and treatable. Meal support from family or friends reduces anxiety during refeeding. If in crisis, contact 988 (US Suicide & Crisis Lifeline), text HOME to 741741 (Crisis Text Line), or contact the ANAD helpline.

AN has the longest documented history among eating disorders. 1689: Richard Morton described 'nervous consumption' - two cases of severe emaciation without medical cause. 1873: Sir William Gull coined 'anorexia nervosa' in London; simultaneously, Charles Lasègue described 'anorexie hystérique' in Paris. Late 19th-early 20th century: AN was considered a form of hysteria and treated with forced feeding and bed rest. Hilde Bruch (1960s-70s) shifted understanding toward psychodynamic models emphasising body image distortion, sense of ineffectiveness, and interoceptive awareness deficits. BN: 1979: Gerald Russell first described 'bulimia nervosa' as 'an ominous variant of anorexia nervosa,' identifying it as a distinct syndrome. DSM-III (1980) did not include BN; DSM-III-R (1987) added it as a separate diagnosis. BED: 1959: Albert Stunkard described 'binge eating' in obese patients. The concept evolved over decades. BED was included as a provisional diagnosis in DSM-IV (1994, Appendix B) and finally granted full diagnostic status in DSM-5 (2013).

DSM evolution: DSM-III (1980) - AN only. DSM-III-R (1987) - AN and BN. DSM-IV (1994) - AN, BN, and EDNOS (eating disorder not otherwise specified, which became a catch-all). DSM-5 (2013) - AN, BN, BED (now a full diagnosis), ARFID (new), OSFED (replaced EDNOS). The amenorrhoea criterion for AN was dropped in DSM-5 because it excluded males, prepubertal females, and females on hormonal contraception.

Eating disorders sit at the intersection of psychiatry and culture. Western societies' idealisation of thinness, amplified by social media platforms (Instagram, TikTok), demonstrably increases body dissatisfaction and disordered eating behaviours. Studies show a dose-response relationship between social media use and eating disorder symptoms in adolescents. 'Pro-ana' (pro-anorexia) and 'pro-mia' (pro-bulimia) online communities actively share tips for concealing symptoms and maintaining eating disorders, though major platforms now restrict this content. Eating disorders are not limited to affluent white women, despite this stereotype. Rates are significant across all racial and ethnic groups, and Black and Hispanic individuals are less likely to be diagnosed or referred for treatment despite similar prevalence. Males account for ~25% of AN cases, ~25% of BN, and ~40% of BED but are severely underdiagnosed due to the perception of eating disorders as 'female diseases.' Muscle dysmorphia, sometimes called 'reverse anorexia,' affects males who perceive themselves as insufficiently muscular despite being highly muscular. Stigma around eating disorders includes the belief that patients are 'choosing' to be ill, that eating disorders reflect narcissism, and that treatment is simple ('just eat' for AN, 'just stop' for BN/BED). These misconceptions delay help-seeking and undermine treatment engagement. Insurance coverage for eating disorder treatment remains inadequate in many countries, with average inpatient stays far shorter than clinical recommendations.

AN genetics: the Eating Disorders Genetics Initiative (EDGI) is conducting the largest-ever GWAS for eating disorders. Prior AN GWAS (2019, Watson et al.) identified 8 genome-wide significant loci and demonstrated that AN has both psychiatric and metabolic genetic components - a finding that challenges the traditional view of AN as purely psychological. Gut microbiome research shows altered microbial composition in AN (reduced diversity, increased methane-producing archaea) that may influence appetite regulation, energy extraction, and immune function; clinical trials of microbiome-targeted interventions are underway. Novel treatments: intranasal oxytocin to improve social cognition and reduce food-related anxiety in AN (mixed results); psilocybin-assisted therapy for treatment-resistant AN (Phase II trials); repetitive transcranial magnetic stimulation (rTMS) targeting the dorsolateral PFC to reduce binge-purge behaviours; deep brain stimulation of the subcallosal cingulate for severe, enduring AN (case series). Digital therapeutics: app-based CBT-E (Recovery Record), chatbot-delivered interventions, and virtual reality exposure therapy for body image disturbance. Pharmacogenomics: research into CYP2D6 and CYP2C19 polymorphisms for SSRI dosing in BN. Biomarkers: brain-derived neurotrophic factor (BDNF), ghrelin, leptin, and inflammatory cytokines are being evaluated as treatment response predictors.

APA. (2022). Diagnostic and Statistical Manual of Mental Disorders (5th ed., text rev.; DSM-5-TR). APA Publishing. Sadock BJ, Sadock VA, Ruiz P. (Eds.). (2024). Kaplan & Sadock's Comprehensive Textbook of Psychiatry (11th ed.). Wolters Kluwer. StatPearls [Internet]. Anorexia Nervosa; Bulimia Nervosa; Binge Eating Disorder. NCBI Bookshelf. StatPearls Publishing. WHO. (2022). ICD-11 for Mortality and Morbidity Statistics. Geneva: World Health Organization.

StatPearls Anorexia Nervosa: https://www.ncbi.nlm.nih.gov/books/NBK459148/ StatPearls Bulimia Nervosa: https://www.ncbi.nlm.nih.gov/books/NBK562178/ StatPearls Binge Eating Disorder: https://www.ncbi.nlm.nih.gov/books/NBK551700/ NIMH Eating Disorders: https://www.nimh.nih.gov/health/topics/eating-disorders NEDA (National Eating Disorders Association): https://www.nationaleatingdisorders.org ANAD (National Association of Anorexia Nervosa and Associated Disorders): https://anad.org WHO ICD-11 codes 6B80, 6B81, 6B82: https://icd.who.int Crisis: 988 (US Suicide & Crisis Lifeline); Text HOME to 741741 (Crisis Text Line) Note: Educational only. Not a substitute for professional care.