Anorexia nervosa 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]

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]

• 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.

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]}

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]

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 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]

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]

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]

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]

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.

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