Anorexia nervosa risk factors
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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] 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
- ↑ 1.0 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.
- ↑ 2.0 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
- ↑ 3.0 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
- ↑ 4.0 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
- ↑ 5.0 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
- ↑ 6.0 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
- ↑ 7.0 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
- ↑ 8.0 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
- ↑ 9.0 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