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Anorexia nervosa

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Editor(s)-in-Chief: C. Michael Gibson, M.S.,M.D. [1]; Associate Editor(s)-in-Chief: Kiran Singh, M.D. [2]

Overview

Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Anorexia nervosa is a psychiatric eating disorder characterized by persistent restriction of energy intake leading to significantly low body weight, accompanied by an intense fear of gaining weight and disturbance in the perception of body weight or shape, with limited insight into the seriousness of the medical consequences.[1]

Individuals with anorexia nervosa often engage in voluntary starvation, rigid dietary rules, and excessive physical activity, and may use purging behaviors, including self-induced vomiting or misuse of laxatives or diuretics, particularly in the binge-eating/purging subtype.[1] Two subtypes are recognized: the restricting subtype and the binge-eating/purging subtype.[1]

Anorexia nervosa occurs worldwide and affects individuals across racial, ethnic, and socioeconomic groups, though it remains more common in females than males.[2][3][4][5] In the United States, approximately 175,000 adults are affected, with a female-to-male ratio of approximately 12:1.[5] While onset frequently occurs during adolescence, anorexia nervosa affects both adolescents and adults, and a substantial proportion of cases remain undiagnosed or untreated.[5]

Anorexia nervosa is a multisystem disease associated with significant medical morbidity. Common complications include bradycardia, hypotension, QT interval prolongation, electrolyte disturbances, endocrine suppression, and reduced bone mineral density, which may lead to osteoporosis and increased fracture risk.[6][7] Endocrine adaptations include hypothalamic amenorrhea and alterations in thyroid function consistent with the sick euthyroid syndrome.[7]

Psychiatric comorbidity is common. In a nationally representative US sample, the lifetime prevalence of major depressive disorder among individuals with anorexia nervosa was 49.5%, and the lifetime prevalence of anxiety disorders was 40.5% (Udo & Grilo, 2019). Suicide attempts have been reported in approximately 24.9% of individuals with anorexia nervosa.[5]

Anorexia nervosa has one of the highest mortality rates of any psychiatric disorder. A meta-analysis of 36 studies reported a mortality rate of 5.1 deaths per 1000 person-years, corresponding to a standardized mortality ratio of 5.86, with approximately 25% of deaths attributable to suicide.[8] Although weight restoration can be achieved in many patients, relapse rates of 40–50% within one year after intensive treatment have been reported.[9][10]

References

  1. ↑ 1.0 1.1 1.2 American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision. American Psychiatric Association Publishing; 2022.
  2. ↑ Lai CM, Mak KK, Pang JS, Fong SS, Ho RC, Guldan GS. The associations of sociocultural attitudes towards appearance with body dissatisfaction and eating behaviors in Hong Kong adolescents. Eat Behav. 2013;14(3):320-324. doi:10.1016/j.eatbeh. 2013.05.004
  3. ↑ Sabry, W., ElMahlawy, N., Essawy, H., Al-Saleet, G., Saad, M., & Morsy, M. (2020). Occurrence, sociodemographic, and clinical correlates of eating disorders among a sample of secondary school students in Egypt. Middle East Current Psychiatry, 27(1). https://doi.org/10.1186/s43045-020-00073-6
  4. ↑ Uchôa FNM, Uchôa NM, Daniele TMD, et al. Influence of the mass media and body dissatisfaction on the risk in adolescents of developing eating disorders. Int J Environ Res Public Health. 2019;16(9):1508. doi:10.3390/ ijerph16091508
  5. ↑ 5.0 5.1 5.2 5.3 Udo T, Grilo CM. Prevalence and correlates of DSM-5–defined eating disorders in a nationally representative sample of US adults. Biol Psychiatry. 2018;84(5):345-354. doi:10.1016/j.biopsych.2018.03. 014
  6. ↑ 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
  7. ↑ 7.0 7.1 Walsh BT, Hagan KE, Lockwood C. A systematic review comparing atypical anorexia nervosa and anorexia nervosa. Int J Eat Disord. 2023;56(4):798- 820. doi:10.1002/eat.23856
  8. ↑ Arcelus J, Mitchell AJ,Wales J, Nielsen S. Mortality rates in patients with anorexia nervosa and other eating disorders: ameta-analysis of 36 studies. Arch Gen Psychiatry. 2011;68(7):724-731. doi:10.1001/archgenpsychiatry.2011.74
  9. ↑ Walsh BT, Kaplan AS, Attia E, et al. Fluoxetine after weight restoration in anorexia nervosa: a randomized controlled trial. JAMA. 2006;295 (22):2605-2612. doi:10.1001/jama.295.22.2605
  10. ↑ Carter JC, Mercer-Lynn KB, Norwood SJ, et al. A prospective study of predictors of relapse in anorexia nervosa: implications for relapse prevention. Psychiatry Res. 2012;200(2-3):518-523. doi:10.1016/j.psychres.2012.04.037

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Historical Perspective

Historical Perspective

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor-In-Chief: Joseph Nasr, M.D.[2]

Terminology

The term anorexia is derived from the Greek an- (without) and orexis (appetite), literally meaning “loss of appetite.” However, this term is a misnomer in anorexia nervosa, as affected individuals typically retain appetite but consciously restrict food intake due to an intense fear of weight gain.[1]

The term “anorexia nervosa” was introduced in the late nineteenth century to distinguish the condition from organic causes of weight loss and to emphasize its psychological components.[2] In clinical and scientific literature, “anorexia nervosa” is often abbreviated to “anorexia,” although this is technically imprecise, as anorexia alone refers to the symptom of reduced appetite rather than the psychiatric disorder.[1]

Colloquial terms such as “ana” and “pro-ana”, commonly used in online communities, are not recognized medical terminology and are associated with the normalization or promotion of disordered eating behaviors. These terms are generally discouraged in clinical practice due to their association with increased illness severity and resistance to treatment.[3]

Background

Anorexia nervosa was first clearly described as a distinct medical condition in the late nineteenth century, independently by Sir William Gull in England and Charles Lasègue in France.[2] Early descriptions emphasized severe weight loss in young women without identifiable organic disease, establishing anorexia nervosa as a psychiatric illness rather than a gastrointestinal or endocrine disorder.

During this period, public fascination with so-called “fasting girls” blurred the boundaries between religious asceticism, superstition, and emerging medical science. While such cases attracted cultural attention, modern historical analyses caution against equating them directly with anorexia nervosa, as many lacked the defining psychopathology required for diagnosis under contemporary criteria (Brumberg, 1988).[4]

By the late twentieth century, anorexia nervosa became widely recognized in the medical literature, particularly during the 1970s and 1980s, coinciding with advances in psychiatric classification and growing public awareness in Western countries.[4][5]

Early Diagnosis and Treatment of Anorexia Nervosa

Early medical approaches to anorexia nervosa in the nineteenth and early twentieth centuries often emphasized strict supervision, isolation from family, and enforced feeding, reflecting limited understanding of the disorder’s psychological underpinnings.[4] These practices were influenced by contemporaneous beliefs regarding hysteria, moral weakness, and excessive maternal influence.

Throughout the mid-twentieth century, treatment strategies varied widely and included psychoanalysis, behavioral modification, pharmacologic experimentation, and institutional care, often with inconsistent outcomes.[4] Forced feeding was historically employed in life-threatening cases, though it was associated with significant physical and psychological distress.

Modern treatment paradigms have shifted away from isolationist and punitive models toward multidisciplinary, evidence-based approaches emphasizing nutritional rehabilitation, medical stabilization, and structured psychotherapy, with particular attention to developmental stage and family involvement.[1]

Changing Attitudes About Body and Diet

Historical attitudes toward body weight and shape have varied substantially across time and cultures. During the Victorian era, thinness was not universally idealized, and anorexia nervosa was often conceptualized as a manifestation of hysteria rather than a distinct psychiatric disorder.[4]

In contrast, the late twentieth century saw increasing cultural emphasis on thinness, particularly in Western societies, coinciding with expanded media representation of narrow body ideals. While sociocultural pressures are recognized as risk modifiers, contemporary research emphasizes that anorexia nervosa cannot be attributed solely to cultural ideals, but instead arises from the interaction of genetic, neurobiological, psychological, and environmental factors.[6]

Anorexia Nervosa in Contemporary Culture

Public awareness of anorexia nervosa increased markedly in the late twentieth century, particularly following high-profile cases and media coverage. Since that time, specialized eating disorder treatment programs have expanded, and anorexia nervosa is now recognized as a severe, chronic psychiatric illness rather than a lifestyle choice or cultural phenomenon.[1]

In contemporary clinical practice, there is growing recognition that anorexia nervosa affects individuals of all genders, ages, and socioeconomic backgrounds, and that many cases remain undiagnosed due to stigma, limited access to care, or misperceptions about who is at risk.[7] (Udo & Grilo, 2018).

References

  1. ↑ 1.0 1.1 1.2 1.3 American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision. American Psychiatric Association Publishing; 2022.
  2. ↑ 2.0 2.1 Gull, W. W. (1997). V.-anorexia nervosa (apepsia hysterica, anorexia hysterica). Obesity Research, 5(5), 498–502. https://doi.org/10.1002/j.1550-8528.1997.tb00677.x
  3. ↑ Mills R, Hyam L, Schmidt U. A narrative review of early intervention for eating disorders: barriers and facilitators. Adolesc Health Med Ther. 2023;14: 217-235. doi:10.2147/AHMT.S415698
  4. ↑ 4.0 4.1 4.2 4.3 4.4 Banner, L. W. (1988). Fasting Girls. The Emergence of Anorexia Nervosa as a Modern Disease. Joan Jacobs Brumberg. Harvard University Press, Cambridge, MA, 1988. x, 366 pp., illus. $25. Science (New York, N.Y.), 240(4855), 1061. https://doi.org/10.1126/science.240.4855.1061
  5. ↑ 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
  6. ↑ Yilmaz Z, Hardaway JA, Bulik CM. Genetics and epigenetics of eating disorders. Adv Genomics Genet. 2015;5:131-150. doi:10.2147/AGG.S55776
  7. ↑ Udo T, Grilo CM. Prevalence and correlates of DSM-5–defined eating disorders in a nationally representative sample of US adults. Biol Psychiatry. 2018;84(5):345-354. doi:10.1016/j.biopsych.2018.03. 014

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Classification

Classification

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1], Associate Editor(s)-in-Chief: Joseph Nasr, M.D.[2]

Classification

Anorexia nervosa is classified as a feeding and eating disorder in both the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision (DSM-5-TR) and the World Health Organization International Classification of Diseases, 11th Revision (ICD-11). The diagnostic criteria for eating disorders in DSM-5-TR and ICD-11 are described as similar, with both systems defining anorexia nervosa by a substantial disturbance in eating behavior accompanied by characteristic psychological and behavioral features.[1] [2]

Subtypes

Two subtypes of anorexia nervosa are recognized in the DSM-5-TR classification system. The restricting subtype refers to individuals who achieve weight loss primarily through restriction of food intake and/or excessive exercise, without regular engagement in binge-eating or purging behaviors. The binge-eating/purging subtype includes individuals who, in addition to restrictive eating, engage in binge-eating episodes and/or purging behaviors such as self-induced vomiting or misuse of laxatives.[1]

These subtypes are used to describe patterns of eating-related behaviors and may change over time within the same individual rather than representing distinct disease entities.[1]

Atypical Anorexia Nervosa

The term atypical anorexia nervosa was introduced in DSM-5 in 2013 to describe individuals who experience substantial weight loss and exhibit many of the psychological, behavioral, and physiologic characteristics of anorexia nervosa but whose body weight remains within the normal or overweight range.[3][4]

Emerging epidemiologic data cited in this review suggest that the lifetime prevalence of atypical anorexia nervosa may be similar to that of typical anorexia nervosa, with reported prevalence estimates of 2.9% and 3.1%, respectively[5] (Harrop et al., 2021). However, due to limited evidence regarding the natural history and treatment response of atypical anorexia nervosa, it is not discussed further in the review.[4]

Scope and Limitations of Classification

The review does not describe formal severity staging systems, alternative phenotypic classifications, or neurobiological subtyping of anorexia nervosa. Classification is limited to diagnostic framework alignment between DSM-5-TR and ICD-11, recognition of behavioral subtypes, and acknowledgment of atypical anorexia nervosa as a related diagnostic entity.[6]

References

  1. ↑ 1.0 1.1 1.2 American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision. American Psychiatric Association Publishing; 2022.
  2. ↑ World Health Organization. ICD-11: International Classification of Diseases, 11th Revision. Accessed May 22, 2024. https://icd.who.int/en
  3. ↑ American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition. American Psychiatric Association Publishing; 2013.
  4. ↑ 4.0 4.1 Walsh BT, Hagan KE, Lockwood C. A systematic review comparing atypical anorexia nervosa and anorexia nervosa. Int J Eat Disord. 2023;56(4):798- 820. doi:10.1002/eat.23856
  5. ↑ Harrop EN, Mensinger JL, Moore M, Lindhorst T. Restrictive eating disorders in higher weight persons: a systematic review of atypical anorexia nervosa prevalence and consecutive admission literature. Int J Eat Disord. 2021;54(8): 1328-1357. doi:10.1002/eat.23519
  6. ↑ Attia, E. and Walsh, B.T. (2025) ‘Eating disorders’, JAMA, 333(14), p. 1242. doi:10.1001/jama.2025.0132.

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Pathophysiology

Pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Joseph Nasr, M.D.[2]

Pathophysiology

Anorexia nervosa has historically been conceptualized as a disorder with a multifactorial pathophysiology involving biological, psychological, and sociocultural factors. Early and subsequent theories proposed numerous causal mechanisms; however, the relative contribution of these factors has remained uncertain, and many early hypotheses have since been revised or rejected. Contemporary understanding emphasizes that no single causal mechanism exists, and that the physiological and psychological effects of starvation play a major role in perpetuating the disorder.[1]

Biological and Physiological Factors

Genetic Factors

(Historically proposed; still supported in principle)

Family and twin studies suggested that genetic factors contribute substantially to the risk of developing eating disorders, accounting for approximately 50% of the variance, and that anorexia nervosa shares genetic risk with major depressive disorder (Klump et al., 2001; Strober et al., 2000). These findings supported early views that genes influencing eating regulation, personality traits, and emotional processing contribute to disease vulnerability.

Animal models, including stress-based paradigms and gene-knockout studies, were historically used to explore biological mechanisms such as hypothalamic–pituitary–adrenal (HPA) axis dysregulation.[2] However, these models are now recognized as having significant limitations because food restriction is externally imposed and cannot replicate voluntary self-starvation or cognitive distortions, limiting their relevance to human anorexia nervosa.[1][2]

Neurobiological Factors

(Historically influential; causal role unresolved)

Early neurobiological research identified associations between anorexia nervosa and serotonergic neurotransmission, given serotonin’s role in mood, anxiety, impulse control, appetite, sleep, and emesis (Kaye et al., 2005).[3] Increased activity at 5-HT1A receptors and reduced activity at 5-HT2A receptors were proposed to contribute to anxiety, behavioral inhibition, and restrictive eating.[3][4]

It was further hypothesized that self-starvation may serve a compensatory function, as reduced tryptophan availability and altered steroid metabolism during starvation could lower serotonin synthesis and thereby reduce anxiety.[3] Subsequent work demonstrated that it is difficult to distinguish whether serotonergic abnormalities are causal risk factors or secondary consequences of malnutrition, and these findings are now interpreted as reflecting a mixture of trait vulnerabilities and state-dependent effects.[1][3]

An autoimmune hypothesis later proposed that autoantibodies directed against melanocortin peptides, which regulate appetite and stress responses, might contribute to anorexia nervosa.[5] This hypothesis remains preliminary, with limited replication, and is not considered an established causal mechanism.[5]

Nutritional and Metabolic Factors

(Historically proposed as causal; now considered secondary)

Earlier research by Bakan in 1979 proposed that micronutrient deficiencies, particularly zinc deficiency, could cause or perpetuate anorexia nervosa by suppressing appetite. Zinc supplementation was reported to improve weight gain in early trials, leading to the hypothesis that zinc deficiency might be a primary driver of anorexic symptoms.

This interpretation is now considered outdated. Contemporary evidence indicates that micronutrient deficiencies, including zinc, thiamine, and amino acid precursors such as tryptophan and tyrosine, are consequences of prolonged starvation, not primary causes of anorexia nervosa. While these deficiencies may exacerbate metabolic and neurochemical disturbances and influence recovery, they are insufficient to explain disease onset.[1]

Starvation produces profound metabolic and endocrine adaptations, including electrolyte disturbances, hypoglycemia, and suppression of reproductive and thyroid hormones. These physiological changes contribute significantly to medical complications and may reinforce restrictive behaviors but are understood as state effects of malnutrition rather than etiologic mechanisms.[1]

Psychological Factors

(Historically proposed and largely retained)

Psychological theories proposed that restrictive eating behaviors arise from feelings of fatness and unattractiveness and are maintained by cognitive biases affecting how individuals evaluate their bodies, food, and eating behaviors.[6]

A consistent finding is body image distortion, now understood not as a sensory perceptual deficit but as a bias in cognitive evaluation. Individuals with anorexia nervosa tend to overestimate body size and lack positive self-evaluative biases commonly observed in unaffected individuals.[7][8][9] Personality traits frequently reported in anorexia nervosa include perfectionism, obsessionality, behavioral restraint, rigidity, and a strong need for control. These traits often precede illness onset and persist after recovery, supporting their role as predisposing characteristics rather than consequences of starvation.[10]

Psychiatric comorbidity is common, with depression, anxiety disorders, obsessive–compulsive disorder, substance use disorders, and personality disorders frequently co-occurring and contributing to illness severity and chronicity.[1][10]

Neuropsychological Findings

(Historically observed; interpretation refined)

Neuropsychological studies have produced variable findings, partly due to the confounding effects of starvation. A relatively consistent observation is reduced cognitive flexibility, reflecting difficulty shifting cognitive strategies, which may contribute to behavioral rigidity. This impairment is now interpreted as reflecting both trait vulnerability and starvation effects, rather than a disease-specific deficit.[11]

Additional studies suggested attentional and memory biases toward body- and weight-related information. These findings are limited and inconsistent and are considered maintaining rather than causal factors.[12][13]
Fairburn and colleagues psychological model of anorexia

Psychological Models

(Maintenance models, not etiologic)

Fairburn and colleagues proposed a transdiagnostic cognitive-behavioral model, suggesting that eating disorders are maintained by shared psychopathological processes including clinical perfectionism, low self-esteem, mood intolerance, and interpersonal difficulties. This model has been influential in guiding treatment but is understood as a maintenance framework rather than an explanation of disease origin.[14]

Social and Environmental Factors

(Historically emphasized; causal role revised)

Early sociocultural theories emphasized media-driven ideals of thinness as a primary cause of anorexia nervosa, supported by higher prevalence in professions with strong pressures to maintain low body weight.[15] Subsequent evidence indicates that sociocultural factors act as risk modifiers rather than primary causes.[1]

Anorexia nervosa occurs across cultures, and in some non-Western populations restrictive eating may occur without prominent fear of fatness, indicating that sociocultural influences shape symptom expression rather than disease origin.[1]

Adverse life experiences, including childhood sexual abuse, have been associated with greater illness severity and chronicity but are not specific causal factors for anorexia nervosa.[16]

The internet has facilitated both recovery-oriented communities and pro-ana groups that reject medical models of anorexia nervosa. While most online resources promote treatment, pro-ana communities have raised concerns regarding reinforcement of disordered eating behaviors, particularly among adolescents.[17][18]

Understanding as of 2025

A review by Attia and Walsh (2025) synthesizes available evidence and emphasizes that anorexia nervosa is best understood as a multifactorial disorder arising from the interaction of genetic vulnerability, psychological traits, sociocultural influences, and the physiological consequences of starvation. They explicitly caution against attributing causality to any single biological, nutritional, or psychological mechanism and highlights that many abnormalities observed in anorexia nervosa represent state-dependent effects of malnutrition, while others may reflect pre-existing trait vulnerabilities.[1]

References

  1. ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 1.8 Attia, E. and Walsh, B.T. (2025a) ‘Eating disorders’, JAMA, 333(14), p. 1242. doi:10.1001/jama.2025.0132.
  2. ↑ 2.0 2.1 Siegfried Z, Berry EM, Hao S, Avraham Y. (2003) Animal models in the investigation of anorexia. Physiol Behav, 79 (1), 39-45. PMID 12818708.
  3. ↑ 3.0 3.1 3.2 3.3 Kaye WH, Frank GK, Bailer UF, Henry SE, Meltzer CC, Price JC, Mathis CA, Wagner A. (2005) Serotonin alterations in anorexia and bulimia nervosa: new insights from imaging studies. Physiol Behav, 85 (1), 73-81. PMID 15869768.
  4. ↑ Kaye WH, Bailer UF, Frank GK, Wagner A, Henry SE. (2005) Brain imaging of serotonin after recovery from anorexia and bulimia nervosa. Physiol Behav, 86(1-2), 15-7. PMID 16102788.
  5. ↑ 5.0 5.1 Fetissov SO, Harro J, Jaanisk M, Jarv A, Podar I, Allik J, Nilsson I, Sakthivel P, Lefvert AK, Hokfelt T. (2005) Autoantibodies against neuropeptides are associated with psychological traits in eating disorders. Proc Natl Acad Sci U S A, 102 (41), 14865-70. PMID 16195379.
  6. ↑ Rosen JC, Reiter J, Orosan P. (1995) Assessment of body image in eating disorders with the body dysmorphic disorder examination. Behav Res Ther, 1, 77-84. PMID 7872941.
  7. ↑ Skrzypek S, Wehmeier PM, Remschmidt H. (2001) Body image assessment using body size estimation in recent studies on anorexia nervosa. A brief review. Eur Child Adolesc Psychiatry, 10 (4), 215-21. PMID 11794546.
  8. ↑ Wonderlich SA, Lilenfeld LR, Riso LP, Engel S, Mitchell JE. (2005) Personality and anorexia nervosa. Int J Eat Disord, 37 Suppl, S68-71. PMID 15852324.
  9. ↑ Jansen A, Smeets T, Martijn C, Nederkoorn C. (2006) I see what you see: the lack of a self-serving body-image bias in eating disorders. Br J Clin Psychol, 45 (1), 123-35. PMID 16480571.
  10. ↑ 10.0 10.1 O’Brien KM, Vincent NK. (2003) Psychiatric comorbidity in anorexia and bulimia nervosa: nature, prevalence, and causal relationships. Clin Psychol Rev, 23 (1), 57-74. PMID 12559994
  11. ↑ Tchanturia K, Campbell IC, Morris R, Treasure J. (2005) Neuropsychological studies in anorexia nervosa. Int J Eat Disord, 37 Suppl, S72-6. PMID 15852325.
  12. ↑ Tiggemann M and Pickering AS. (1996) Role of television in adolescent women’s body dissatisfaction and drive for thinness Int J Eat Disord, Sep;20(2):199-203.
  13. ↑ Cooper MJ (2005) Cognitive theory in anorexia nervosa and bulimia nervosa: progress, development and future directions. Clin Psychol Rev, 25 (4), 511-31. PMID 15914267.
  14. ↑ Fairburn CG, Cooper Z, Shafran R. (2003) Cognitive behavior therapy for eating disorders: a “transdiagnostic” theory and treatment. Behav Res Ther, 41 (5), 509-28. PMID 12711261.
  15. ↑ Garner DM, Garfinkel PE. (1980) Socio-cultural factors in the development of anorexia nervosa. Psychol Med, 10 (4), 647-56. PMID 7208724.
  16. ↑ Carter JC, Bewell C, Blackmore E, Woodside DB. (2006) The impact of childhood sexual abuse in anorexia nervosa. Child Abuse Negl, 30 (3), 257-69. PMID 16524628.
  17. ↑ Norris ML, Boydell KM, Pinhas L, Katzman DK. (2006) Ana and the internet: A review of pro-anorexia websites. International Journal of Eating Disorders, 39(6):443-7. PMID 16721839.
  18. ↑ Reaves, J. (2001). Anorexia goes high tech. Time (July). Retrieved on April 16, 2007.

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Causes

Causes

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Joseph Nasr, M.D.[2]

Overview

The exact cause of anorexia nervosa is unknow. Current evidence supports no single cause for anorexia, but rather that it stems from a mixture of social, psychological and biological factors. This multifactorial etiology involves an interaction between genetic vulnerability, neurological factors, psychological traits, and environmental and sociocultural influences. Research is commonly focused on explaining existing factors and uncovering new causes. However, there is considerable debate over how much each of the known causes contributes to the development of anorexia. In particular, the contribution of perceived media pressure on women to be thin has been especially contentious.[1]

Causes

  • The exact causes of anorexia nervosa are unknown.
  • Many factors probably are involved. Genes and hormones may play a role. Social attitudes promoting very thin body types may also be involved.
  • Family conflicts are no longer thought to contribute to this or other eating disorders.
  • Anorexia usually begins during the teen years or young adulthood. It is more common in females, but may also be seen in males. The disorder is seen mainly in white women who are high academic achievers and who have a goal-oriented family or personality.

Common Causes

The most common form of anorexia is simply satiation following the consumption of food. This happens in all normal humans and is called postprandial anorexia. Disorders that cause (harmful) anorexia include anorexia nervosa, severe depression, cancer, dementia, AIDS, and chronic renal failure and the use of certain drugs, particularly stimulants and narcotics. Environmentally induced disorders such as altitude sickness can also trigger an acute form of anorexia. Anorexia may also be seen in congestive heart failure, perhaps due to congestion of the liver with venous blood.

Although the presenting symptom (the one which prompts a patient to seek medical attention) in acute appendicitis is abdominal pain, patients virtually always experience anorexia as well, possibly accompanied by an early episode of vomiting.

Some medications, antidepressants for example, can have anorexia as a side effect. Most notoriously, however, chemicals that are a member of the phenethylamine family are known to have more intense anorectic properties. For this reason, many individuals suffering from anorexia nervosa may seek to use these medications to suppress appetite. Such prescription medications include Ritalin, Adderall, Dexedrine, and Desoxyn. In some cases, these medications are prescribed to patients prior to undergoing an operation requiring general anesthesia. This is a prophylactic measure taken to ensure no food will back up into the esophagus and cause the patient to stop breathing during the procedure. [2] [3]

Genetic and Biological Factors

Twin and family studies demonstrate a substantial genetic contribution to anorexia nervosa, with heritability estimates ranging from approximately 0.38 to 0.74, indicating a strong inherited susceptibility that interacts with environmental exposures. Genetic risk appears to influence traits such as rigidity, anxiety, and harm avoidance, which may predispose individuals to restrictive eating behaviors. Neuroendocrine and metabolic adaptations to starvation further reinforce restrictive behaviors once the illness has begun.[4]

Psychological and Psychiatric Factors

Anorexia nervosa is frequently associated with premorbid psychological traits, including perfectionism, compulsivity, cognitive rigidity, and heightened anxiety. Psychiatric comorbidities are common, particularly mood disorders, anxiety disorders, and obsessive-compulsive disorder, suggesting shared underlying vulnerability rather than simple causation. Individuals may also transition between eating disorder diagnoses over time, supporting a dimensional rather than categorical model of risk.[5][6][7]

Sociocultural Influences

Sociocultural pressures emphasizing thinness and weight control are consistently associated with body dissatisfaction and disordered eating behaviors, particularly among adolescents and young adults. Media exposure and internalization of thin ideals have been shown to increase drive for thinness and body dissatisfaction, especially in females.[1][3] Participation in activities that emphasize leanness or weight (such as ballet, gymnastics, modeling, and certain competitive sports) is associated with increased risk of developing anorexia nervosa.[8][9]

Developmental and Environmental Factors

Adolescence and young adulthood represent critical periods of vulnerability. Malnutrition, psychosocial stressors, and adverse life events during development may interact with genetic susceptibility to precipitate illness onset. Childhood maltreatment, including emotional, physical, or sexual abuse, has been associated with increased risk of eating disorder pathology, although many affected individuals report no identifiable trauma.[10]

Sex, Gender, and Social Context

Anorexia nervosa is more common in females than males, though it occurs across all sexes, races, and socioeconomic groups. Sexual and gender minority individuals have a higher lifetime prevalence of eating disorder diagnoses compared with heterosexual and cisgender populations, likely reflecting minority stress and psychosocial vulnerability rather than sexual orientation itself.[11]

Medical and Secondary Causes of Anorexia (Loss of Appetite)

Anorexia (loss of appetite) must be distinguished from anorexia nervosa. Reduced appetite may occur secondary to medical illnesses such as malignancy, chronic renal failure, congestive heart failure, dementia, AIDS, infections, and inflammatory gastrointestinal diseases, as well as during acute illnesses such as appendicitis, where anorexia is a common associated symptom.[2][3] Certain medications and substances, particularly stimulants, narcotics, antidepressants, and phenethylamine derivatives, may also suppress appetite and, in some cases, be misused by individuals with eating disorders.[2][3]

Summary

Anorexia nervosa arises from the convergence of genetic susceptibility, psychological traits, and environmental and sociocultural pressures, with biological adaptations to starvation perpetuating the disorder once established. No single factor is sufficient to cause the illness, and the relative contribution of each varies among individuals.

References

  1. ↑ 1.0 1.1 Tiggemann M and Pickering AS. (1996) Role of television in adolescent women’s body dissatisfaction and drive for thinness Int J Eat Disord, Sep;20(2):199-203.
  2. ↑ 2.0 2.1 2.2 Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:77 ISBN 1591032016
  3. ↑ 3.0 3.1 3.2 3.3 Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:68 ISBN 140510368X
  4. ↑ Yilmaz Z, Hardaway JA, Bulik CM. Genetics and epigenetics of eating disorders. Adv Genomics Genet. 2015;5:131-150. doi:10.2147/AGG.S55776
  5. ↑ Castellini G, Lo Sauro C, Mannucci E, et al. Diagnostic crossover and outcome predictors in eating disorders according to DSM-IV and DSM-V proposed criteria: a 6-year follow-up study. Psychosom Med. 2011;73(3):270-279. doi:10.1097/ PSY.0b013e31820a1838
  6. ↑ 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
  7. ↑ Wagner AF, Vitousek KM. Personality variables and eating pathology. Psychiatr Clin North Am. 2019;42(1):105-119. doi:10.1016/j.psc.2018.10.012
  8. ↑ 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
  9. ↑ 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
  10. ↑ 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
  11. ↑ 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


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Differentiating Anorexia Nervosa from other Diseases

Differentiating Anorexia Nervosa from other Diseases

link=https://www.wikidoc.org/index.php/Anorexia nervosa
link=https://www.wikidoc.org/index.php/Anorexia nervosa

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Kiran Singh, M.D. [2] Joseph Nasr, M.D.[3]

Overview

Anorexia nervosa should be differentiated from other diseases that cause chronic nausea and vomiting. Anorexia nervosa must also be differentiated from other diseases such as bulimia nervosa, major depressive disorder, and social anxiety disorder among others.[1]

Differential Diagnosis

Differential Diagnosis of Anorexia (Loss of Appetite)

This table lists medical, psychiatric, infectious, and pharmacologic conditions associated with anorexia (loss of appetite) and should not be confused with the etiology of anorexia nervosa, which is a distinct psychiatric disorder.

Cardiovascular • Congestive heart failure •Hypercalcemia
Chemical / poisoning • Chromotherapy • Retinoid • Theobromine
Dermatologic • Sporotrichosis
Drug Side Effect • Aciclovir • Amphetamine • Amphotericin B • Antidepressants •Benzodiazepine • Benzylpiperazine • Calcitriol • Chromotherapy • Cocaine•Dextromethamphetamine • Dextromethylphenidate• Diacetylmorphine • Enfuvirtide •Fluconazole • Gold salts • Hydralazine • Ketorolac • Leptoprin • Methylphenidate •Mirtazapine • Modafinil • Moxifloxacin • Pipradrol • Pyrazinamide • St John’s wort• Stimulants • Theobromine • Valaciclovir • Ziconotide• Zopiclone
Ear Nose Throat • Mastoiditis
Endocrine • Anorexia Nervosa • Binge eating • Bulimia nervosa • Carotenodermia •Diabetic neuropathy
Environmental • Acute radiation syndrome
Gastroenterologic • Acute fatty liver of pregnancy • Anorexia nervosa • Appendicitis • Binge eating • Colorectal cancer • Crohn’s Disease • Defensive vomiting • Hepatitis •Hepatitis E • Hymenolepiasis • Hypervitaminosis D • Lábrea fever • Milk-alkali syndrome • Superior mesenteric artery syndrome • Ulcerative colitis
Genetic • Acute fatty liver of pregnancy • Crohn’s Disease
Hematologic • Non-Hodgkin lymphoma
Iatrogenic No underlying causes
Infectious Disease • Acute viral nasopharyngitis (common cold) • AIDS • Astroviridae • Chagas disease • Community-acquired pneumonia • Cryptosporidium parvum • Encephalitis •Hepatitis • Hepatitis E • Mumps • Oropouche fever • Pneumonia • Pott’s disease •Relapsing fever • Rhinovirus
Musculoskeletal / Ortho • Mastoiditis
Neurologic • Chronic fatigue syndrome • Craniopharyngioma • Dementia • Encephalitis
Nutritional / Metabolic No underlying causes
Obstetric/Gynecologic • Acute fatty liver of pregnancy
Oncologic • Chromotherapy • Colorectal cancer • Craniopharyngioma• Non-Hodgkin lymphoma
Opthalmologic No underlying causes
Overdose / Toxicity • Acute radiation syndrome • Chromotherapy • Cocaine • Gold salts •Hypervitaminosis D • Vitamin A
Psychiatric • Anorexia nervosa • Binge eating • Borderline personality disorder •Bulimia nervosa • Clinical depression • Defensive vomiting • Dementia • Depression •Hangover • Obsessive-compulsive disorder • Opioid dependency • Orthorexia nervosa •Panic disorder
Pulmonary • Acute viral nasopharyngitis (common cold) • Atypical pneumonia •Community-acquired pneumonia • Pneumonia
Renal / Electrolyte • Chronic renal failure • Diabetic neuropathy• Hangover • Hypercalcemia
Rheum / Immune / Allergy • Chronic fatigue syndrome
Sexual • AIDS
Trauma No underlying causes
Urologic • Chronic renal failure • Diabetic neuropathy • Hypercalcemia
Miscellaneous • Chronic mountain sickness • High altitude

Differentiating anorexia nervosa from other diseases

Anorexia nervosa should be differentiated from other diseases that cause chronic nausea and vomiting. The differentials include the following:[2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23][24][25][26][27][28][29][30][31][32][33]

Disorder Clinical features Laboratory findings
Chronic nausea Vomiting Diarrhea Retching Lethargy Social withdrawal Photophobia Epigastric pain/burning Lanugo hair Hypogonadism Russel’s sign Body mass index (normal range: 18.5 to 24.9) Complete blood count (CBC) Electrolyte imabalance Lipase and amylase levels Gastric scintigraphy Ambulatory esophageal pH and impedance testing
Gastroparesis ✔ ✔ (within 1 hour of eating) – ✔ ✔ – – ✔ – – – ↓ ✔
  • Normal (maybe elevated if chronic renal failure is the cause of gastroparesis- usually less than threefold)
  • Periodic measurement of radiolabeled solid meal:  
    • Grade 1 (mild), 11%-20% retention at 4 h
    • Grade 2 (moderate), 21%-35% retention at 4 h
    • Grade 3 (severe), 36%-50% retention at 4 h
    • Grade 4 (very severe), > 50% retention at 4 h
  • Impedance testing (antroduodenal manometery): Loss of normal fasting migratory motor complexes (MMCs) and reduced postprandial antral contractions and, in some cases pylorospasm
Anorexia nervosa ✔ ✔ ✔ – ✔ ✔ – – ✔ ✔ – ↓ ✔
  • Increased
Bulimia nervosa ✔ ✔ ✔ ✔ ✔ ✔ – – – ✔ ✔ Normal ✔
  • Increased
Rumination syndrome ✔ ✔ (Regurgitation more common- within minutes of meal intake) ✔ – ✔ ✔ ✔ ✔ – – – ↓
  • Normal
 ✔
  • Normal
  • Esophageal pH: Fall in esophageal pH immediately after reguritation (occurs while patient is awake and erect; this is in contrast to GERD, where reflux occurs diurnally and supine position)
Functional dyspepsia ✔ ✔ ✔ ✔ – – – – – – – Normal
  • Normal
 ✔
  • Esophageal pH: May be decreased if patient develops reflux
Cyclic vomiting syndrome ✔ ✔ – ✔ ✔ – – – – – – ↓ ✔
  • Rapid or normal
  • Esophageal pH: Decreased
Pancreatitis ✔ ✔ ✔ ✔ ✔ – – ✔ – – – Normal ✔
  • Increased
  • Not indicated
  • Esophageal pH: Normal
Gastric outlet obstruction ✔ ✔ (within 1 hour of eating) – – – – – ✔ – – – ↓ ✔
  • Esophageal pH: Increased
  • Esophageal manometery:   High manoraetric score

Other differentials

Other differentials of anorexia nervosa include the following:

Diagnostic Issues and Controversies

The distinction between the diagnoses of anorexia nervosa, bulimia nervosa and eating disorder not otherwise specified (EDNOS) is often difficult to make in practice and there is considerable overlap between patients diagnosed with these conditions. Furthermore, seemingly minor changes in a patient’s overall behavior or attitude (such as reported feeling of ‘control’ over any bingeing behavior) can change a diagnosis from ‘anorexia: binge-eating type’ to bulimia nervosa. It is not unusual for a person with an eating disorder to ‘move through’ various diagnoses as his or her behavior and beliefs change over time.[34]

Additionally, it is important to note that an individual may still suffer from a health- or life-threatening eating disorder (e.g., subclinical anorexia nervosa or EDNOS) even if one diagnostic sign or symptom is still present. For example, a substantial number of patients diagnosed with EDNOS meet all criteria for diagnosis of anorexia nervosa, but lack the three consecutive missed menstrual cycles needed for a diagnosis of anorexia.[35]

Feminist writers such as Susie Orbach and Naomi Wolf have criticised the medicalisation of extreme dieting and weight-loss as locating the problem within the affected women, rather than in a society that imposes concepts of unreasonable and unhealthy thinness as a measure of female beauty.

References

  1. ↑ 1.0 1.1 1.2 1.3 1.4 1.5 Diagnostic and statistical manual of mental disorders : DSM-5. Washington, D.C: American Psychiatric Association. 2013. ISBN 0890425558.
  2. ↑ Parkman HP (2015). “Idiopathic gastroparesis”. Gastroenterol. Clin. North Am. 44 (1): 59–68. doi:10.1016/j.gtc.2014.11.015. PMC 4324534. PMID 25667023.
  3. ↑ Werlin SL, Fish DL (2006). “The spectrum of valproic acid-associated pancreatitis”. Pediatrics. 118 (4): 1660–3. doi:10.1542/peds.2006-1182. PMID 17015559.
  4. ↑ Noddin L, Callahan M, Lacy BE (2005). “Irritable bowel syndrome and functional dyspepsia: different diseases or a single disorder with different manifestations?”. MedGenMed. 7 (3): 17. PMC 1681633. PMID 16369243.
  5. ↑ Gupta R, Kalla M, Gupta JB (2012). “Adult rumination syndrome: Differentiation from psychogenic intractable vomiting”. Indian J Psychiatry. 54 (3): 283–5. doi:10.4103/0019-5545.102434. PMC 3512372. PMID 23226859.
  6. ↑ Sağlam F, Sivrikoz E, Alemdar A, Kamalı S, Arslan U, Güven H (2015). “Bouveret syndrome: A fatal diagnostic dilemma of gastric outlet obstruction”. Ulus Travma Acil Cerrahi Derg. 21 (2): 157–9. PMID 25904280.
  7. ↑ Talley NJ (2011). “Rumination syndrome”. Gastroenterol Hepatol (N Y). 7 (2): 117–8. PMC 3061016. PMID 21475419.
  8. ↑ Tutuian R, Castell DO (2004). “Rumination documented by using combined multichannel intraluminal impedance and manometry”. Clin. Gastroenterol. Hepatol. 2 (4): 340–3. PMID 15067630.
  9. ↑ Kessing BF, Smout AJ, Bredenoord AJ (2014). “Current diagnosis and management of the rumination syndrome”. J. Clin. Gastroenterol. 48 (6): 478–83. doi:10.1097/MCG.0000000000000142. PMID 24921208.
  10. ↑ Parkman HP (2009). “Assessment of gastric emptying and small-bowel motility: scintigraphy, breath tests, manometry, and SmartPill”. Gastrointest. Endosc. Clin. N. Am. 19 (1): 49–55, vi. doi:10.1016/j.giec.2008.12.003. PMID 19232280.
  11. ↑ Waseem S, Moshiree B, Draganov PV (2009). “Gastroparesis: current diagnostic challenges and management considerations”. World J. Gastroenterol. 15 (1): 25–37. PMC 2653292. PMID 19115465.
  12. ↑ Mearin F, Camilleri M, Malagelada JR (1986). “Pyloric dysfunction in diabetics with recurrent nausea and vomiting”. Gastroenterology. 90 (6): 1919–25. PMID 3699409.
  13. ↑ Abell TL, Camilleri M, Donohoe K, Hasler WL, Lin HC, Maurer AH, McCallum RW, Nowak T, Nusynowitz ML, Parkman HP, Shreve P, Szarka LA, Snape WJ, Ziessman HA (2008). “Consensus recommendations for gastric emptying scintigraphy: a joint report of the American Neurogastroenterology and Motility Society and the Society of Nuclear Medicine”. Am. J. Gastroenterol. 103 (3): 753–63. doi:10.1111/j.1572-0241.2007.01636.x. PMID 18028513.
  14. ↑ Jiang CF, Ng KW, Tan SW, Wu CS, Chen HC, Liang CT, Chen YH (2002). “Serum level of amylase and lipase in various stages of chronic renal insufficiency”. Zhonghua Yi Xue Za Zhi (Taipei). 65 (2): 49–54. PMID 12014357.
  15. ↑ Szmukler, G. I.; Young, G. P.; Lichtenstein, M.; Andrews, J. T. (1990). “A serial study of gastric emptying in anorexia nervosa and bulimia”. Australian and New Zealand Journal of Medicine. 20 (3): 220–225. doi:10.1111/j.1445-5994.1990.tb01023.x. ISSN 0004-8291.
  16. ↑ Diamanti A, Bracci F, Gambarara M, Ciofetta GC, Sabbi T, Ponticelli A, Montecchi F, Marinucci S, Bianco G, Castro M (2003). “Gastric electric activity assessed by electrogastrography and gastric emptying scintigraphy in adolescents with eating disorders”. J. Pediatr. Gastroenterol. Nutr. 37 (1): 35–41. PMID 12827003.
  17. ↑ Ferholt J, Provence S (1976). “Diagnosis and treatment of an infant with psychophysiological vomiting”. Psychoanal Study Child. 31: 439–59. PMID 981449.
  18. ↑ Lee H, Rhee PL, Park EH, Kim JH, Son HJ, Kim JJ, Rhee JC (2007). “Clinical outcome of rumination syndrome in adults without psychiatric illness: a prospective study”. J. Gastroenterol. Hepatol. 22 (11): 1741–7. doi:10.1111/j.1440-1746.2006.04617.x. PMID 17914944.
  19. ↑ Koskenpato J, Kairemo K, Korppi-Tommola T, Färkkilä M (1998). “Role of gastric emptying in functional dyspepsia: a scintigraphic study of 94 subjects”. Dig. Dis. Sci. 43 (6): 1154–8. PMID 9635600.
  20. ↑ Urbain JL, Vekemans MC, Parkman H, Van Cauteren J, Mayeur SM, Van den Maegdenbergh V, Charkes ND, Fisher RS, Malmud LS, De Roo M (1995). “Dynamic antral scintigraphy to characterize gastric antral motility in functional dyspepsia”. J. Nucl. Med. 36 (9): 1579–86. PMID 7658213.
  21. ↑ Hejazi RA, Lavenbarg TH, McCallum RW (2010). “Spectrum of gastric emptying patterns in adult patients with cyclic vomiting syndrome”. Neurogastroenterol. Motil. 22 (12): 1298–302, e338. doi:10.1111/j.1365-2982.2010.01584.x. PMID 20723071.
  22. ↑ “Gastric outlet obstruction – an overview | ScienceDirect Topics”.
  23. ↑ Minami H, McCallum RW (1984). “The physiology and pathophysiology of gastric emptying in humans”. Gastroenterology. 86 (6): 1592–610. PMID 6370777.
  24. ↑ Humphries LL, Adams LJ, Eckfeldt JH, Levitt MD, McClain CJ (1987). “Hyperamylasemia in patients with eating disorders”. Ann. Intern. Med. 106 (1): 50–2. PMID 2431640.
  25. ↑ Hempen I, Lehnert P, Fichter M, Teufel J (1989). “[Hyperamylasemia in anorexia nervosa and bulimia nervosa. Indication of a pancreatic disease?]”. Dtsch. Med. Wochenschr. (in German). 114 (49): 1913–6. doi:10.1055/s-2008-1066848. PMID 2480214.
  26. ↑ Okada R, Okada A, Okada T, Okada T, Hamajima N (2009). “Elevated serum lipase levels in patients with dyspepsia of unknown cause in general practice”. Med Princ Pract. 18 (2): 130–6. doi:10.1159/000189811. PMID 19204432.
  27. ↑ Sansone RA, Sansone LA (2012). “Hoarseness: a sign of self-induced vomiting?”. Innov Clin Neurosci. 9 (10): 37–41. PMC 3508961. PMID 23198276.
  28. ↑ Tack J, Caenepeel P, Arts J, Lee KJ, Sifrim D, Janssens J (2005). “Prevalence of acid reflux in functional dyspepsia and its association with symptom profile”. Gut. 54 (10): 1370–6. doi:10.1136/gut.2004.053355. PMC 1774686. PMID 15972301.
  29. ↑ “gut.bmj.com” (PDF).
  30. ↑ Boles RG, Williams JC (1999). “Mitochondrial disease and cyclic vomiting syndrome”. Dig. Dis. Sci. 44 (8 Suppl): 103S–107S. PMID 10490048.
  31. ↑ Ranasinghe WK, Smith M (2013). “Gastric outlet obstruction with an elevated serum pancreatic lipase secondary to an infraumbilical hernia”. Ann R Coll Surg Engl. 95 (7): 122–4. doi:10.1308/003588413X13629960047795. PMID 24112485.
  32. ↑ Ui, Takashi; Shibusawa, Hiroyuki; Tsukui, Hidenori; Sakuma, Kazuya; Takahashi, Shuhei; Lefor, Alan K.; Hosoya, Yoshinori; Sata, Naohiro; Yasuda, Yoshikazu (2015). “Pretreatment of gastric outlet obstruction with pancrelipase: Report of a case”. International Journal of Surgery Case Reports. 12: 87–89. doi:10.1016/j.ijscr.2015.05.023. ISSN 2210-2612.
  33. ↑ Gowers S, Bryant-Waugh R. (2004) Management of child and adolescent eating disorders: the current evidence base and future directions. J Child Psychol Psychiatry, 45 (1), 63-83. PMID 14959803
  34. ↑ Lask B, and Bryant-Waugh, R (eds) (2000) Anorexia Nervosa and Related Eating Disorders in Childhood and Adolescence. Hove: Psychology Press. ISBN 0-86377-804-6.

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Epidemiology and Demographics

Epidemiology and Demographics

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Joseph Nasr, M.D.[2] Kiran Singh, M.D. [3]

Overview

Anorexia nervosa is an eating disorder characterized by restrictive energy intake, intense fear of weight gain, and a disturbed perception of body weight or shape. It occurs worldwide and affects individuals across all racial, ethnic, and socioeconomic groups, although prevalence varies by sex, age, and sociocultural context. The disorder most commonly begins during adolescence or young adulthood and disproportionately affects females.[1][2]

Epidemiology and Demographics

Prevalence

Epidemiologic estimates of anorexia nervosa vary by study design, diagnostic criteria, and population. Earlier estimates reported a 12-month prevalence of approximately 0.4% (400 per 100,000) among young females in Western populations.[1] More recent population-based studies suggest that the lifetime prevalence of anorexia nervosa among adults in the United States is approximately 0.6%–2.2% in females and 0.1%–0.6% in males, with point and 12-month prevalence substantially lower than lifetime prevalence.[2]

Globally, eating disorders as a group affect approximately 2%–5% of individuals during their lifetime, with anorexia nervosa representing a smaller but clinically severe proportion of cases.[3][4][5] The majority of prevalence and incidence data originate from high-income Western countries, and epidemiologic estimates may underestimate disease burden in low- and middle-income regions due to underdiagnosis and limited access to mental health services.[3][4][5]

Incidence

The incidence of anorexia nervosa peaks during adolescence, particularly in mid-to-late teenage years. Adolescents and young adults account for the highest proportion of newly diagnosed cases, with onset before age 25 in most individuals.[2][6] Incidence rates are lower in childhood and later adulthood, but cases can occur across the lifespan.

Sex and Gender Distribution

Anorexia nervosa occurs more frequently in females than males. Approximately 85%–90% of individuals diagnosed with anorexia nervosa are female, consistent with earlier clinical observations.[6] Contemporary epidemiologic studies report a female-to-male ratio of approximately 10–12:1.[2] Despite this disparity, anorexia nervosa is increasingly recognized in males, who may be underdiagnosed due to sex-based stereotypes and differences in symptom presentation.

Sexual and gender minority individuals have a higher prevalence of eating disorder diagnoses compared with heterosexual and cisgender populations, suggesting that psychosocial stressors and minority stress may contribute to increased risk.[7]

Age Distribution

The disorder most commonly presents during adolescence, with females aged 15–19 years historically accounting for a large proportion of cases.[6] However, anorexia nervosa can occur in preadolescent children and in adults, and delayed diagnosis is common, particularly in populations with atypical presentations or normal-weight restrictive eating patterns.[8][9]

Race, Ethnicity, and Geographic Distribution

Anorexia nervosa has been documented across diverse racial and ethnic groups. While early studies suggested higher prevalence among White populations in Western countries, more recent data indicate that eating disorders occur across racial and ethnic backgrounds, with disparities in diagnosis and treatment access rather than true absence of disease accounting for observed differences.[2][3][4][5]

References

  1. ↑ 1.0 1.1 Diagnostic and statistical manual of mental disorders : DSM-5. Washington, D.C: American Psychiatric Association. 2013. ISBN 0890425558.
  2. ↑ 2.0 2.1 2.2 2.3 2.4 Udo T, Grilo CM. Prevalence and correlates of DSM-5–defined eating disorders in a nationally representative sample of US adults. Biol Psychiatry. 2018;84(5):345-354. doi:10.1016/j.biopsych.2018.03. 014
  3. ↑ 3.0 3.1 3.2 Lai CM, Mak KK, Pang JS, Fong SS, Ho RC, Guldan GS. The associations of sociocultural attitudes towards appearance with body dissatisfaction and eating behaviors in Hong Kong adolescents. Eat Behav. 2013;14(3):320-324. doi:10.1016/j.eatbeh. 2013.05.004
  4. ↑ 4.0 4.1 4.2 SabryW, ElMahlawy N, Essawy H, Al-Saleet G, Saad M, MorsyM. Occurrence, sociodemographic, and clinical correlates of eating disorders among a sample of secondary school students in Egypt. Published November 25, 2020. Accessed May 21, 2024. https://mecp.springeropen.com/articles/10. 1186/s43045-020-00073-6
  5. ↑ 5.0 5.1 5.2 Uchôa FNM, Uchôa NM, Daniele TMD, et al. Influence of the mass media and body dissatisfaction on the risk in adolescents of developing eating disorders. Int J Environ Res Public Health. 2019;16(9):1508. doi:10.3390/ ijerph16091508
  6. ↑ 6.0 6.1 6.2 Lask B, and Bryant-Waugh, R (eds) (2000) Anorexia Nervosa and Related Eating Disorders in Childhood and Adolescence. Hove: Psychology Press. ISBN 0-86377-804-6.
  7. ↑ 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
  8. ↑ Walsh BT, Hagan KE, Lockwood C. A systematic review comparing atypical anorexia nervosa and anorexia nervosa. Int J Eat Disord. 2023;56(4):798- 820. doi:10.1002/eat.23856
  9. ↑ Harrop EN, Mensinger JL, Moore M, Lindhorst T. Restrictive eating disorders in higher weight persons: a systematic review of atypical anorexia nervosa prevalence and consecutive admission literature. Int J Eat Disord. 2021;54(8): 1328-1357. doi:10.1002/eat.23519

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Risk Factors

Risk Factors

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Joseph Nasr, M.D.[2] Kiran Singh, M.D. [3]

Overview

Anorexia nervosa arises from the interaction of genetic vulnerability, psychological traits, developmental factors, and sociocultural influences. Established risk factors include female sex, family history of eating disorders, premorbid anxiety and obsessional traits, negative self-image, and exposure to environments that emphasize thinness or weight control.[1][2]

Major Risk Factors

  • Female sex, particularly during adolescence[1][2]
  • Family history of anorexia nervosa, especially in first-degree biological relatives[1]
  • Monozygotic twin status, reflecting strong genetic susceptibility[1]
  • Premorbid anxiety disorders in childhood, including obsessive-compulsive traits[1][3]
  • Perfectionism, cognitive rigidity, and obsessional personality traits[1][3]
  • Negative self-image and body dissatisfaction[4][5][6]
  • Heightened concern with weight, shape, or dietary control[1]
  • Eating or feeding problems in infancy or early childhood[1]

Sociocultural and Environmental Risk Factors

  • Cultural ideals that promote thinness as a marker of health or success[4][5][6]
  • Occupations or avocations emphasizing leanness, including:
  • High socioeconomic status and Westernized social environments, likely reflecting both true risk and increased diagnostic recognition[2][9]

Demographic Associations (Risk Modifiers)

  • White ethnicity, historically associated with higher diagnosis rates[2]
  • Higher socioeconomic status, particularly in industrialized countries[2]
  • Underdiagnosis in individuals with non-European ancestry, suggesting diagnostic and access disparities rather than reduced biological risk[2][9]

Summary

Risk factors for anorexia nervosa are cumulative and interactive. Genetic susceptibility and early psychological traits create vulnerability, while sociocultural pressures and developmental stressors influence illness onset and expression. No single risk factor is sufficient to cause the disorder.

References

  1. ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 Diagnostic and statistical manual of mental disorders : DSM-5. Washington, D.C: American Psychiatric Association. 2013. ISBN 0890425558.
  2. ↑ 2.0 2.1 2.2 2.3 2.4 2.5 Lindberg L, Hjern A. (2003) Risk factors for anorexia nervosa: a national cohort study. International Journal of Eating Disorders, 34 (4), 397-408. PMID 14566927
  3. ↑ 3.0 3.1 Wagner AF, Vitousek KM. Personality variables and eating pathology. Psychiatr Clin North Am. 2019;42(1):105-119. doi:10.1016/j.psc.2018.10.012
  4. ↑ 4.0 4.1 Lai CM, Mak KK, Pang JS, Fong SS, Ho RC, Guldan GS. The associations of sociocultural attitudes towards appearance with body dissatisfaction and eating behaviors in Hong Kong adolescents. Eat Behav. 2013;14(3):320-324. doi:10.1016/j.eatbeh. 2013.05.004
  5. ↑ 5.0 5.1 SabryW, ElMahlawy N, Essawy H, Al-Saleet G, Saad M, MorsyM. Occurrence, sociodemographic, and clinical correlates of eating disorders among a sample of secondary school students in Egypt. Published November 25, 2020. Accessed May 21, 2024. https://mecp.springeropen.com/articles/10. 1186/s43045-020-00073-6
  6. ↑ 6.0 6.1 Uchôa FNM, Uchôa NM, Daniele TMD, et al. Influence of the mass media and body dissatisfaction on the risk in adolescents of developing eating disorders. Int J Environ Res Public Health. 2019;16(9):1508. doi:10.3390/ ijerph16091508
  7. ↑ 7.0 7.1 7.2 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
  8. ↑ 8.0 8.1 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
  9. ↑ 9.0 9.1 Udo T, Grilo CM. Prevalence and correlates of DSM-5–defined eating disorders in a nationally representative sample of US adults. Biol Psychiatry. 2018;84(5):345-354. doi:10.1016/j.biopsych.2018.03. 014

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Screening

Screening

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Joseph Nasr, M.D.[2] Please help WikiDoc by adding content here. It’s easy! Click here to learn about editing.

Overview

There is no population-wide screening program for anorexia nervosa. However, targeted screening and case-finding are recommended in clinical settings, particularly for adolescents and young adults with weight changes, growth deviation, or psychiatric comorbidity. Early identification is associated with improved outcomes and reduced medical complications.[1][2][3][4]

Who Should Be Screened (Targeted Case-Finding)

Targeted screening should be considered in individuals with clinical or demographic risk factors, including:

  • Adolescents and young adults, particularly females
  • Unexplained weight loss, failure to gain expected weight, or growth deceleration
  • Marked concern with weight, shape, or food intake
  • Psychiatric comorbidities, including anxiety, depression, or obsessive-compulsive disorder[5]
  • Participation in activities emphasizing weight or leanness, such as elite athletics, ballet, or modeling[6][7]
  • Sexual and gender minority individuals, who have higher prevalence of eating disorder diagnoses[8]

Clinical Screening Approach

Professional guidelines recommend that clinicians ask directly about eating behaviors and attitudes rather than relying on weight alone. Screening should include:

  • Dietary restriction or avoidance of foods
  • Fear of weight gain or distorted body image
  • Compensatory behaviors such as excessive exercise, vomiting, or laxative use
  • Menstrual irregularities or delayed puberty in adolescents
  • Physical signs such as bradycardia, hypotension, or lanugo[2][3][4]

Screening Tools

Brief self-report questionnaires may be used as adjuncts to clinical assessment, particularly in primary care and adolescent health settings. These tools are intended to identify individuals who require further evaluation, not to establish a diagnosis. A positive screen should prompt comprehensive medical and psychiatric assessment.[1][2][3]

Limitations

  • Screening instruments have variable sensitivity and specificity
  • Many individuals with anorexia nervosa may deny symptoms or minimize severity
  • Underdiagnosis is common, particularly in males and individuals with normal-weight restrictive eating patterns[9][10]

Summary

Routine population screening for anorexia nervosa is not currently recommended. Targeted screening based on clinical suspicion and risk factors is the preferred approach, with direct questioning and early referral for comprehensive evaluation when concerns arise.

References

  1. ↑ 1.0 1.1 Mills R, Hyam L, Schmidt U. A narrative review of early intervention for eating disorders: barriers and facilitators. Adolesc Health Med Ther. 2023;14: 217-235. doi:10.2147/AHMT.S415698
  2. ↑ 2.0 2.1 2.2 American Psychiatric Association. Practice Guideline for the Treatment of Patients With Eating Disorders. 4th ed. American Psychiatric Association Publishing; 2023.
  3. ↑ 3.0 3.1 3.2 Hornberger LL, Lane MA; Committee on Adolescence. Identification and management of eating disorders in children and adolescents. Pediatrics. 2021;147(1):e2020040279. doi:10.1542/ peds.2020-040279
  4. ↑ 4.0 4.1 Society for Adolescent Health and Medicine. Medical management of restrictive eating disorders in adolescents and young adults. J Adolesc Health. 2022;71(5):648-654. doi:10.1016/j.jadohealth.2022. 08.006
  5. ↑ 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
  6. ↑ 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
  7. ↑ 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
  8. ↑ 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
  9. ↑ Walsh BT, Hagan KE, Lockwood C. A systematic review comparing atypical anorexia nervosa and anorexia nervosa. Int J Eat Disord. 2023;56(4):798- 820. doi:10.1002/eat.23856
  10. ↑ Harrop EN, Mensinger JL, Moore M, Lindhorst T. Restrictive eating disorders in higher weight persons: a systematic review of atypical anorexia nervosa prevalence and consecutive admission literature. Int J Eat Disord. 2021;54(8): 1328-1357. doi:10.1002/eat.23519

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Natural History, Complications, and Prognosis

Natural History, Complications, and Prognosis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Complications

  • Complications can be severe. A hospital stay may be needed.
  • Complications may include:

Prognosis

  • Anorexia is thought to have the highest mortality rate of any psychiatric disorder, with approximately 6% of those who are diagnosed with the disorder eventually dying due to related causes.[1] The suicide rate of people with anorexia is also higher than that of the general population and is thought to be the major cause of death for those with the condition.[2] A recent review suggested that less than one-half recover fully, one-third improve, and 20% remain chronically ill.[3]
  • Women who develop this eating disorder at an early age have a better chance of recovering completely. However, most people with anorexia will continue to prefer a lower body weight and be very focused on food and calories.
  • Weight management may be hard. Long-term treatment may be needed to stay at a healthy weight.

References

  1. ↑ Herzog, David B; Greenwood, Dara N; Dorer, David J; Flores, Andrea T; Ekeblad, Elizabeth R; Richards, Ana; Blais, Mark A; Keller, Martin B (2000), “Mortality in eating disorders: A descriptive study”, International Journal of Eating Disorders, 28 (1): 20–26
  2. ↑ Pompili M, Mancinelli I, Girardi P, Ruberto A, Tatarelli R. (2004) Suicide in anorexia nervosa: a meta-analysis. Int J Eat Disord, 36 (1), 99-103. PMID 15185278
  3. ↑ Steinhausen HC. (2002) The outcome of anorexia nervosa in the 20th century. Am J Psychiatry, 159 (8), 1284-93. PMID 12153817.

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