Eating disorder
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Editor(s)-in-Chief: C. Michael Gibson, M.S.,M.D. [1],Mark J. Warren, M.D. Associate Editor-In-Chief: Joseph Nasr, M.D.[2]
Overview
Eating disorders are psychiatric disorders characterized by a persistent disturbance in eating or eating-related behavior that results in altered consumption or absorption of food and leads to clinically significant impairment in physical health, psychosocial functioning, or both.
The etiology of eating disorders is multifactorial, involving the interaction of genetic vulnerability and environmental influences, including psychological stressors and sociocultural pressures related to body weight and shape.
Eating disorders occur worldwide and across all racial, ethnic, and socioeconomic groups, but they are more common in females than males and frequently emerge during adolescence or early adulthood.
According to the DSM-5-TR, the primary eating disorders include anorexia nervosa, bulimia nervosa, binge-eating disorder, and avoidant/restrictive food intake disorder.
Types
- According to the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision (DSM-5-TR), eating disorders are classified as follows:[1]
Recognized eating disorders
- Anorexia nervosa
- Bulimia nervosa
- Binge-eating disorder
- Avoidant/restrictive food intake disorder (ARFID)
- Other specified feeding or eating disorder (OSFED)
- Unspecified feeding or eating disorder (UFED)
Conditions not formally recognized as distinct eating disorders in DSM-5-TR
These terms are used descriptively in clinical and research contexts but do not constitute formal diagnostic categories.
Risk Factors
Eating disorders arise from the interaction of genetic vulnerability and environmental influences. Twin and family studies demonstrate a substantial heritable component, with heritability estimates ranging from approximately 0.38 to 0.74 for anorexia nervosa, 0.55 to 0.62 for bulimia nervosa, and 0.39 to 0.45 for binge-eating disorder.[2]
Environmental risk factors include childhood maltreatment, particularly emotional, physical, and sexual abuse, which has been consistently associated with increased risk of eating disorder pathology in a dose-response manner.[3] Family history of eating disorders also increases risk, reflecting both genetic susceptibility and shared environmental influences.[2]
Psychological and sociocultural factors contribute to risk, including body dissatisfaction and internalization of thin-ideal appearance standards. Exposure to sociocultural pressures emphasizing body shape or weight, as well as participation in activities that prioritize leanness such as gymnastics, ballet, or modeling, has been associated with the development of anorexia nervosa and bulimia nervosa.[4][5]
Eating disorders occur across all populations; however, higher prevalence has been observed among sexual and gender minority individuals compared with majority groups, suggesting that minority stress and social stigma may contribute to vulnerability.[6]
Anorexia Nervosa
Anorexia nervosa is an eating disorder characterized by restriction of energy intake relative to requirements, resulting in significantly low body weight for age, sex, developmental trajectory, and physical health. Individuals exhibit an intense fear of gaining weight or becoming fat, or persistent behavior that interferes with weight gain, accompanied by a disturbance in the way body weight or shape is experienced or a lack of recognition of the seriousness of the current low body weight.[1]
The DSM-5-TR recognizes two subtypes: the restricting subtype, in which weight loss is achieved primarily through dieting, fasting, or excessive exercise, and the binge-eating/purging subtype, in which individuals engage in recurrent binge eating or purging behaviors such as self-induced vomiting or misuse of laxatives, diuretics, or other medications.[1]
Anorexia nervosa is associated with medical complications related to malnutrition, including bradycardia, hypotension, electrolyte abnormalities, hypogonadotropic hypogonadism, amenorrhea or oligomenorrhea, and reduced bone mineral density, increasing the risk of fractures.[7][8]
The etiology is multifactorial and reflects the interaction of genetic susceptibility and environmental influences. Twin and family studies demonstrate substantial heritability, while environmental risk factors include childhood maltreatment and sociocultural pressures related to body shape and weight.[2][3]
Earlier diagnostic frameworks, including DSM-IV and ICD-10, required fixed weight thresholds, commonly a body mass index (BMI) of 17.5 or lower, and the presence of amenorrhea in postmenarchal females. These criteria were removed in DSM-5 and retained in DSM-5-TR to reflect evidence that anorexia nervosa occurs across sexes and age groups and that significant medical and psychological impairment may be present in individuals who do not meet strict BMI cutoffs or who continue to menstruate. The removal of amenorrhea as a criterion also improved diagnostic inclusivity for males, premenarchal females, postmenopausal females, and individuals receiving hormonal therapy.[1][9][10]
Bulimia Nervosa
Bulimia nervosa is an eating disorder characterized by recurrent episodes of binge eating, defined as consuming an objectively large amount of food within a discrete period of time accompanied by a sense of lack of control, followed by inappropriate compensatory behaviors to prevent weight gain. These behaviors include self-induced vomiting, misuse of laxatives, diuretics, or other medications, fasting, or excessive exercise.[1]
To meet DSM-5-TR criteria, binge eating and compensatory behaviors must occur at least once weekly for three months, and self-evaluation is unduly influenced by body shape and weight. Unlike anorexia nervosa, individuals with bulimia nervosa typically maintain a body weight within or above the normal range.[1]
Bulimia nervosa is associated with medical complications primarily related to purging behaviors, including electrolyte abnormalities such as hypokalemia and hyponatremia, metabolic alkalosis, dehydration, dental enamel erosion, salivary gland hypertrophy, and, in severe cases, Mallory-Weiss esophageal tears.[11]
The disorder frequently co-occurs with other psychiatric conditions, including mood disorders, anxiety disorders, substance use disorders, and impulsive behaviors. Elevated rates of nonsuicidal self-injury and substance misuse have been reported among individuals with bulimia nervosa.[12]
Earlier diagnostic frameworks, including DSM-IV, required a higher frequency of binge eating and compensatory behaviors and placed greater emphasis on specific compensatory methods. DSM-5 reduced the frequency threshold to once weekly and retained the core features of binge eating, compensatory behaviors, and overvaluation of body shape and weight, changes that were maintained in DSM-5-TR to improve diagnostic sensitivity and clinical applicability.[1][9]
Binge Eating Disorder
Binge-eating disorder is an eating disorder characterized by recurrent episodes of binge eating, defined as consumption of an objectively large amount of food within a discrete period of time accompanied by a sense of lack of control. Episodes are associated with marked distress and occur at least once weekly for three months, in the absence of recurrent compensatory behaviors such as purging or excessive exercise.[1]
Binge-eating episodes are associated with behavioral features that may include eating rapidly, eating until uncomfortably full, eating when not physically hungry, eating alone due to embarrassment, and feelings of guilt or disgust following the episode. Unlike bulimia nervosa, self-evaluation in binge-eating disorder is not necessarily dominated by body shape or weight.[1]
Binge-eating disorder is associated with overweight and obesity and with increased risk of obesity-related medical conditions, including type 2 diabetes mellitus and hypertension. In clinical samples, the majority of individuals with binge-eating disorder meet criteria for obesity.[13][14]
Psychiatric comorbidity is common and includes mood disorders, anxiety disorders, post-traumatic stress disorder, and substance use disorders. Population-based studies have demonstrated high lifetime prevalence of major depressive disorder and anxiety disorders among individuals with binge-eating disorder.[12]
The etiology of binge-eating disorder is multifactorial and reflects the interaction of genetic susceptibility and environmental factors. Childhood adversity, including abuse and food insecurity, has been associated with increased risk of developing binge-eating disorder.[3][15]
DSM-5-TR includes severity specifiers based on the frequency of binge-eating episodes per week, ranging from mild (1–3 episodes) to extreme (14 or more episodes).[1]
Excessive or Compulsive Exercise (Associated Behavior)
Excessive or driven exercise is a common maladaptive behavior observed in individuals with eating disorders, particularly anorexia nervosa and bulimia nervosa. It is typically used as a method of weight control or to counteract perceived caloric intake and may persist despite medical illness, injury, or significant physical exhaustion.[1]
In anorexia nervosa, excessive exercise may contribute to further weight loss and medical instability, while in bulimia nervosa it may function as a compensatory behavior following binge-eating episodes. Excessive exercise is not recognized as a distinct eating disorder diagnosis in DSM-5-TR but is considered a clinically significant behavior that can exacerbate nutritional deficiency and medical complications.[1]
Causes
Environmental
Environmental and sociocultural factors contribute to the risk of developing eating disorders by interacting with underlying genetic vulnerability. Sociocultural pressures that emphasize thinness or particular body ideals have been associated with increased body dissatisfaction and disordered eating behaviors, particularly during adolescence.[4][5]
Exposure to appearance-focused social environments, including peer groups and activities that prioritize leanness or weight control, has been associated with increased risk of anorexia nervosa and bulimia nervosa. Experiences of bullying, particularly weight-related teasing, have also been linked to higher risk of eating disorder psychopathology.[4]
Environmental stressors do not act independently but interact with biological susceptibility. Evidence from genetic and epidemiologic studies supports a gene–environment interaction model, in which environmental exposures may precipitate or exacerbate eating disorder symptoms in genetically vulnerable individuals.[2][16]
Biological and Genetic Factors
1. Genetic Susceptibility and Gene–Environment Interaction
Evidence supports a substantial heritable contribution to eating disorders, with both genetic and environmental factors contributing to risk. Large twin and family studies demonstrate meaningful heritability for anorexia nervosa, bulimia nervosa, and binge-eating disorder, supporting a genetic vulnerability model rather than a purely sociocultural explanation.[2]
Genetic susceptibility is best understood as interacting with environmental exposures rather than acting deterministically. Genetic risk may increase vulnerability, while environmental stressors can precipitate the onset or exacerbate symptoms in susceptible individuals.[2][3]
2. Neurobiology and the “State vs Trait” Problem
Neurobiological abnormalities involving serotonin, dopamine, and norepinephrine systems have been described in eating disorders, and early models proposed that these conditions arise from primary neurochemical imbalance. However, a major limitation of this framework is that many measured neurobiologic abnormalities in anorexia nervosa and other eating disorders may be secondary to starvation and malnutrition rather than primary causal mechanisms.
This distinction complicates interpretation of findings and makes it difficult to differentiate trait markers, which may contribute to vulnerability before illness onset, from state markers, which reflect the physiological consequences of undernutrition. Historical observations describing altered serotonin levels or receptor activity in anorexia nervosa and bulimia nervosa should therefore be interpreted cautiously in the absence of consistent replication under nutritionally restored conditions.[17][18]
What is more consistently supported is the high degree of psychiatric comorbidity observed in eating disorders, including mood disorders, anxiety disorders, and obsessive-compulsive features. These associations suggest that neurobiologic systems involved in mood regulation, anxiety, and reward processing are clinically relevant, though specific mechanistic pathways remain incompletely defined.[12]
3. Neuroendocrine and Metabolic Changes
Biological changes in eating disorders frequently involve endocrine and metabolic adaptation to altered intake and body weight. In restrictive eating disorders, undernutrition is associated with widespread physiologic disturbances, including disruption of reproductive hormones and impairment of bone metabolism.[1][8]
Clinically significant downstream consequences include reduced bone mineral density and an increased risk of fractures in individuals with anorexia nervosa, particularly with prolonged illness duration. These skeletal complications represent one of the most robustly established biological consequences of restrictive eating disorders.[8][7]
Proposed mechanisms in the literature have also focused on dysregulation of appetite and stress-related hormones, including cholecystokinin, neuropeptide Y, peptide YY, leptin, and cortisol. These pathways are biologically plausible and may influence hunger, satiety, and stress responses; however, much of the supporting evidence derives from older studies or nonspecialist sources. As such, these findings are best regarded as proposed mechanisms rather than established consensus pathophysiology.[19][17]
Overall, eating disorders appear to involve dysregulation of appetite, reward, and stress systems, with neuroendocrine changes that may both contribute to symptoms and arise as consequences of altered nutritional state.
4. Brain Circuitry and the Hypothalamus
Multiple hormones and neurochemical systems implicated in eating behavior are integrated within hypothalamic circuitry, which plays a central role in energy balance, temperature regulation, and endocrine control. Evidence from case-based studies demonstrates that hypothalamic lesions can produce abnormalities in eating behavior, including disordered intake, vomiting, and altered weight regulation.[20]
These observations support the neurobiologic plausibility that disruption of specific brain circuits can generate eating disorder–like behaviors. However, lesion studies do not imply that primary eating disorders are typically caused by structural brain damage. Instead, they provide indirect evidence that central nervous system circuitry is capable of driving pathological eating behaviors when disrupted.[20]
5. Gastrointestinal Microbiota: Emerging Hypotheses
Emerging research has proposed a role for the gastrointestinal microbiota in eating disorders through multiple hypothetical mechanisms. These include modulation of metabolic, immune, and central nervous system signaling by short-chain fatty acids; increased intestinal permeability with cytokine-mediated effects on appetite regulation; and immune cross-reactivity between microbial peptides and appetite-regulating hormones such as α-melanocyte-stimulating hormone. Additional hypotheses suggest that certain bacterial proteins may mimic appetite-regulating peptides and influence feeding behavior.[16]
These microbiota-based mechanisms remain hypothesis-generating and are not yet incorporated into guideline-level models of eating disorder pathophysiology.
6. Consensus-Level Synthesis
Taken together, current evidence supports a multifactorial model of eating disorders involving genetic susceptibility interacting with environmental exposures. Biological findings span neurotransmitter systems, stress-axis regulation, and appetite control pathways, though many observed abnormalities may be secondary to nutritional state and illness severity.[2][3][8]
Among biological consequences, endocrine disruption and skeletal complications of undernutrition, particularly reduced bone mineral density and fracture risk in anorexia nervosa, are the most consistently established. Emerging areas of investigation, including microbiota-related mechanisms, warrant further study but should be clearly distinguished from established pathophysiology.[8][7][16]
Developmental Etiology
Developmental models of eating disorders emphasize the role of early relational experiences and family dynamics in shaping vulnerability to disordered eating behaviors. From a family systems perspective, eating disorders have been conceptualized as emerging in the context of difficulties with individuation during adolescence, particularly in environments characterized by over-controlling parenting styles and disturbed patterns of communication. In such settings, adolescents may struggle to develop autonomy and effective self-regulation, increasing reliance on maladaptive coping behaviors.[21]
Critical or emotionally unaffectionate caregiving environments have been described as contributing to increased self-criticism and reduced capacity for self-care. These developmental patterns may impair the formation of a stable internal sense of self and foster dependence on external regulation, with food-related behaviors serving compensatory or regulatory functions when adaptive coping strategies are insufficiently developed.[21]
Although these family-systems formulations are theoretical, contemporary evidence supports the broader premise that eating disorders frequently emerge during adolescence and that adverse developmental experiences may interact with underlying vulnerability to increase risk.[2]
Trauma and Adverse Experiences
Trauma-informed frameworks conceptualize eating disorders as responses to adverse experiences rather than as disorders driven solely by appearance-related concerns. Within this perspective, disordered eating behaviors may function as survival strategies or attempts to regulate overwhelming emotional distress.[22]
Exposure to sexual, physical, and emotional abuse has been associated with increased risk of eating disorder psychopathology, supporting trauma as a significant environmental contributor. Meta-analytic evidence demonstrates a consistent association between childhood maltreatment and eating disorder symptoms across diagnoses.[3]
Sociological analyses further suggest that chronic environmental stressors such as racism and poverty may contribute to disconnection from the body and vulnerability to disordered eating. Individuals positioned furthest from dominant cultural beauty ideals, including women of color and other marginalized groups, may experience compounded psychological stress that increases susceptibility to eating disorder behaviors.[22]
Consistent with this framework, epidemiologic data cited in the PDF demonstrate elevated prevalence of eating disorders among sexual and gender minority individuals, supporting the role of social marginalization and minority stress in eating disorder risk.[12]
Integrated Perspective
Together, developmental and trauma-related models describe eating disorders as arising from the interaction of biological vulnerability, adverse developmental experiences, and social stressors. Within this framework, disordered eating behaviors may serve regulatory or protective functions in response to developmental disruption or trauma exposure, rather than representing isolated disturbances of eating behavior alone.[2][3][12][21][22]
Gender Differences
Gender differences have been observed in risk factors, symptom expression, and associated behaviors in eating disorders. Preventive and epidemiologic research has suggested that predictors of disordered eating behaviors may differ between females and males. In females, frequent dieting and internalization of media-driven body ideals have been identified as independent predictors of binge-eating behaviors across age groups. In contrast, in males, negative weight-related comments from fathers have been associated with the initiation of recurrent binge eating, highlighting the potential role of gender-specific interpersonal influences.[23]
Although eating disorders occur across sexes, differences in sociocultural pressures and socialization may contribute to variation in vulnerability pathways. These findings support the importance of gender-sensitive prevention and assessment strategies that account for differing sources of body image concern and weight-related stress.[23]
Compulsive or excessive exercise has been described in both males and females, particularly among individuals with eating disorders and obsessive-compulsive features. Exercise addiction has been conceptualized as a maladaptive pattern characterized by compulsive engagement in physical activity despite physical injury, illness, or social impairment. Individuals may experience anxiety or guilt when unable to exercise and may prioritize exercise over personal relationships and health.[24]
Within this framework, excessive exercise is often driven by fear of weight gain and pursuit of an idealized body type, with reinforcing effects related to perceived psychological relief or achievement. While such descriptions emphasize behavioral and motivational aspects rather than formal diagnostic criteria, they underscore the clinical relevance of exercise behaviors in the assessment of eating disorder psychopathology.[24]
Diagnosis
Clinical Evaluation
The clinical evaluation of eating disorders involves assessment of eating behaviors, weight-related concerns, and associated psychological symptoms. Screening instruments are commonly used to aid detection, particularly in primary care and adolescent populations. The Questionnaire of Eating and Weight Patterns (QEWP) is one such instrument, with versions specifically developed for adolescents (QEWP-A) and for parent report (QEWP-P). These tools assess binge-eating behaviors and associated features and may also evaluate comorbid symptoms such as depression.[25]
Primary care–based literature emphasizes the role of clinicians in recognizing eating disorder symptoms, given that patients may present with nonspecific complaints or medical complications rather than overt eating concerns. Early detection and appropriate referral are critical components of effective management.[26]
Diagnostic Criteria
Diagnostic classification of eating disorders has evolved over time. Historically, anorexia nervosa and bulimia nervosa were diagnosed using criteria from the International Classification of Diseases (ICD-10), while binge-eating disorder was recognized within the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) and later formalized in DSM-5.
Contemporary diagnostic practice reflects the integration of ICD and DSM frameworks, with current classifications emphasizing behavioral patterns, psychological features, and functional impairment rather than reliance on rigid thresholds alone. This evolution has improved diagnostic inclusivity and clinical applicability across age groups and sexes.[26]
Diagnostic Criteria Checklist (DSM-5-TR)
Anorexia Nervosa
Core Criteria (required):
- ☐ Restriction of energy intake relative to requirements, leading to significantly low body weight for age, sex, developmental trajectory, and physical health
- ☐ Intense fear of gaining weight or becoming fat OR persistent behavior that interferes with weight gain
- ☐ Disturbance in body image, undue influence of weight/shape on self-evaluation, or lack of recognition of seriousness of low body weight
Behavioral features (specify if present):
- ☐ Self-induced vomiting
- ☐ Misuse of laxatives, diuretics, or appetite suppressants
- ☐ Excessive exercise
Subtypes (DSM-5-TR):
- ☐ Restricting type
- ☐ Binge-eating/purging type
Severity (DSM-5-TR, BMI-based guidance not absolute):
- Mild ≥17
- Moderate 16–16.99
- Severe 15–15.99
- Extreme <15
Important updates from older criteria:
- ☐ Fixed BMI cutoffs (e.g., <17.5 or <85% expected weight) are no longer required
- ☐ Amenorrhea is NOT required for diagnosis
Still clinically relevant:
- ☐ Delayed puberty or arrested pubertal development if onset occurs before puberty
- ☐ Growth retardation and failure of secondary sexual characteristic development in early-onset cases
- ☐ Reduced libido (may occur in all sexes as a consequence of undernutrition)
Bulimia Nervosa
Core DSM-5-TR criteria (all required):
- ☐ Recurrent episodes of binge eating, defined by:
- ☐ Eating an objectively large amount of food in a discrete period
- ☐ Sense of lack of control during the episode
- ☐ Recurrent inappropriate compensatory behaviors to prevent weight gain:
- ☐ Self-induced vomiting
- ☐ Laxatives, diuretics, or other medications
- ☐ Fasting
- ☐ Excessive exercise
- ☐ Insulin restriction in individuals with diabetes
- ☐ Binge eating and compensatory behaviors occur ≥1×/week for 3 months
- ☐ Self-evaluation unduly influenced by body shape and weight
Exclusion:
- ☐ Does not occur exclusively during episodes of anorexia nervosa
Severity (based on compensatory behaviors/week):
- Mild 1–3
- Moderate 4–7
- Severe 8–13
- Extreme ≥14
Clinically relevant retained points:
- ☐ Intense fear of weight gain commonly present
- ☐ Bulimia nervosa may occur after a prior episode of anorexia nervosa
Binge-Eating Disorder
Core DSM-5-TR criteria (all required):
- ☐ Recurrent episodes of binge eating with:
- ☐ Eating an objectively large amount of food
- ☐ Sense of lack of control
- ☐ Binge episodes associated with ≥3 of the following:
- ☐ Eating much more rapidly than normal
- ☐ Eating until uncomfortably full
- ☐ Eating large amounts when not physically hungry
- ☐ Eating alone due to embarrassment
- ☐ Feeling disgusted, depressed, or guilty afterward
- ☐ Marked distress regarding binge eating
- ☐ Occurs ≥1 day/week for 3 months
- ☐ No recurrent compensatory behaviors
Severity (episodes/week):
- Mild 1–3
- Moderate 4–7
- Severe 8–13
- Extreme ≥14
Updated note:
- ☐ Older alternative frequency thresholds (e.g., 2 days/week for 6 months) are superseded by DSM-5-TR
Avoidant/Restrictive Food Intake Disorder (ARFID)
All criteria A–D must be met:
- ☐ Eating disturbance (lack of interest in eating, sensory avoidance, fear of aversive consequences) resulting in one or more:
- ☐ Significant weight loss or failure to gain expected weight
- ☐ Nutritional deficiency
- ☐ Dependence on enteral feeding or supplements
- ☐ Marked interference with psychosocial functioning
- ☐ Disturbance not explained by lack of food or culturally sanctioned practice
- ☐ Does not occur exclusively during anorexia or bulimia
- ☐ Not attributable to another medical or mental condition (or exceeds expected severity)
Other Specified Feeding or Eating Disorder (OSFED)
- ☐ Clinically significant eating disorder symptoms causing distress or impairment
- ☐ Does not meet full criteria for a specific eating disorder
Common examples:
- ☐ Atypical anorexia nervosa (normal weight)
- ☐ Bulimia nervosa of low frequency or limited duration
- ☐ Binge-eating disorder of low frequency or limited duration
- ☐ Purging disorder
- ☐ Night eating syndrome
Unspecified Feeding or Eating Disorder (UFED)
- ☐ Clinically significant eating disorder symptoms present
- ☐ Insufficient information to make a specific diagnosis
- ☐ Used in emergency or time-limited settings
Key DSM-5-TR Notes (Exam & Clinical Pearls)
- Amenorrhea is not required for anorexia nervosa
- BMI cutoffs are no longer absolute, clinical judgment is required
- Binge-eating disorder is a formal diagnosis (not a subtype of bulimia)
- Excessive exercise is a behavior, not a standalone diagnosis
References
- ↑ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision. American Psychiatric Association Publishing; 2022.
- ↑ 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 2.8 Yilmaz Z, Hardaway JA, Bulik CM. Genetics and epigenetics of eating disorders. Adv Genomics Genet. 2015;5:131-150. doi:10.2147/AGG.S55776
- ↑ 3.0 3.1 3.2 3.3 3.4 3.5 3.6 Molendijk ML, Hoek HW, Brewerton TD, Elzinga BM. Childhood maltreatment and eating disorder pathology: a systematic review and dose-response meta-analysis. Psychol Med. 2017;47 (8):1402-1416. doi:10.1017/S0033291716003561
- ↑ 4.0 4.1 4.2 Bogár N, Kővágó P, Túry F. Increased eating disorder frequency and body image disturbance among fashion models due to intense environmental pressure: a content analysis. Front Psychiatry. 2024;15:1360962. doi:10.3389/fpsyt. 2024.1360962
- ↑ 5.0 5.1 Bratland-Sanda S, Sundgot-Borgen J. Eating disorders in athletes: overview of prevalence, risk factors and recommendations for prevention and treatment. Eur J Sport Sci. 2013;13(5):499-508. doi: 10.1080/17461391.2012.740504
- ↑ Kamody RC, Grilo CM, Udo T. Disparities in DSM-5 defined eating disorders by sexual orientation among US adults. Int J Eat Disord. 2020; 53(2):278-287. doi:10.1002/eat.23193
- ↑ 7.0 7.1 7.2 SøebyM, Gribsholt SB, Clausen L, Richelsen B. Fracture risk in patients with anorexia nervosa over a 40-year period. J Bone Miner Res. 2023;38(11): 1586-1593. doi:10.1002/jbmr.4901
- ↑ 8.0 8.1 8.2 8.3 8.4 MisraM, Golden NH, Katzman DK. State of the art systematic review of bone disease in anorexia nervosa. Int J Eat Disord. 2016;49(3):276-292. doi:10.1002/eat.22451
- ↑ 9.0 9.1 American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (DSM-5 (R)) (5th ed.). American Psychiatric Association Publishing. doi.org/10.1176/appi.books.9780890425596
- ↑ Classifications, & Terminologies. (1992, January 1). The ICD-10 Classification of Mental and Behavioural Disorders: Clinical descriptions and diagnostic guidelines. Who.Int; World Health Organization. https://www.who.int/publications/i/item/9241544228
- ↑ Nitsch A, Dlugosz H, Gibson D, Mehler PS. Medical complications of bulimia nervosa. Cleve Clin J Med. 2021;88(6):333-343. doi:10.3949/ccjm.88a. 20168
- ↑ 12.0 12.1 12.2 12.3 12.4 Udo T, Grilo CM. Psychiatric and medical correlates of DSM-5 eating disorders in a nationally representative sample of adults in the United States. Int J Eat Disord. 2019;52(1):42-50. doi:10. 1002/eat.23004
- ↑ Dingemans AE, van Furth EF. Binge eating disorder psychopathology in normal weight and obese individuals. Int J Eat Disord. 2012;45(1):135- 138. doi:10.1002/eat.20905
- ↑ Wassenaar E, Friedman J, Mehler PS. Medical complications of binge eating disorder. Psychiatr Clin North Am. 2019;42(2):275-286. doi:10.1016/j. psc.2019.01.010
- ↑ Nagata JM, Chu J, Cervantez L, et al. Food insecurity and binge-eating disorder in early adolescence. Int J Eat Disord. 2023;56(6):1233-1239. doi:10.1002/eat.23944
- ↑ 16.0 16.1 16.2 Himmerich H, Bentley J, Kan C, Treasure J (2019). "Genetic risk factors for eating disorders: an update and insights into pathophysiology". Ther Adv Psychopharmacol. 9: 2045125318814734. doi:10.1177/2045125318814734. PMC 6378634. PMID 30800283.
- ↑ 17.0 17.1 Long, Phillip W. (1993). Eating Disorders. Retrieved March 3, 2006, from the National Institute of Mental Health website: http://www.mentalhealth.com/book/p45-eat1.html
- ↑ Yager, Joel & Anderson, Arnold E. (2005). Anorexia Nervosa. The New England Journal of Medicine, 353 (14), 1481-1488, Retrieved March 3, 2006, from Ovid web: http://mutex.gmu.edu:2076/gw1/ovidweb.cgi
- ↑ Kalat, James W (2006). Biological Psychology (8th ed.). Houston: Wadsworth Publishing. ISBN 0495090794.
- ↑ 20.0 20.1 Uher, R; Treasure, J (June 2005), "Brain Lesions and Eating Disorders", Journal of Neurology, Neurosurgery & Psychiatry, 76 (6): 852–857, doi:10.1136/jnnp.2004.048819, PMID 15897510
- ↑ 21.0 21.1 21.2 Weiner, Sydell (1998), "The Addiction of Overeating: Self-Help Groups as Treatment Models", Journal of Clinical Psychology, 54 (2): 163–167, doi:10.1002/(SICI)1097-4679(199802)54:2<163::AID-JCLP5>3.0.CO;2-T, ISSN 0021-9762
- ↑ 22.0 22.1 22.2 Hall, C. I. (1995), "Asian Eyes: Body Image and Eating Disorders of Asian and Asian-American Women", Eating Disorders, Taylor & Francis, 3 (1): 8–19, doi:10.1080/10640269508249141
- ↑ 23.0 23.1 "Risk Factors for Eating Disorders Vary by Gender: Rejecting media images, resilience to negative comments should be focus of prevention," Kevin McKeever, HealthDay, June 3, 2008.
- ↑ 24.0 24.1 "Exercise addiction and dependence" Hollyann E. Jenkins, BrainPhysics, Aug 29, 2008.
- ↑ Johnson, William G. (1998). "Measuring Binge Eating in Adolescents: Adolescent and Parent Versions of the Questionnaire of Eating and Weight Patterns". International Journal of Eating Disorders. 26: 301. doi:10.1002/(SICI)1098-108X(199911)26:3<301::AID-EAT8>3.0.CO;2-M. ISSN 0276-3478. PMID 10441246. Unknown parameter
|coauthors=ignored (help); Unknown parameter|month=ignored (help) - ↑ 26.0 26.1 Walsh JM, Wheat ME, Freund K (2000). "Detection, evaluation, and treatment of eating disorders the role of the primary care physician". J Gen Intern Med. 15 (8): 577–90. doi:10.1046/j.1525-1497.2000.02439.x. PMC 1495575. PMID 10940151.
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- Zipfel, S (2000), "Long-term prognosis in anorexia nervosa: Lessons from a 21-year follow-up study", Lancet (North American Edition), 355 (9205): 721
de:Essstörung ko:식사장애 it:Disturbi del comportamento alimentare he:הפרעת אכילה nl:Eetstoornis no:Spiseforstyrrelse fi:Syömishäiriö sv:Ätstörningar
- ↑ Sim LA, McAlpine DE, Grothe KB, Himes SM, Cockerill RG, Clark MM (2010). "Identification and treatment of eating disorders in the primary care setting". Mayo Clin Proc. 85 (8): 746–51. doi:10.4065/mcp.2010.0070. PMC 2912736. PMID 20605951.