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INTRODUCTION

Adolescents as well as younger children engage in disordered eating behavior at an alarming rate, and many develop partial or full-blown eating disorders (EDs). The spectrum of EDs includes anorexia nervosa (AN), bulimia nervosa (BN), binge-eating disorder (BED), other specified feeding or eating disorder (OSFED), and avoidant/restrictive food intake disorder (ARFID). These disorders are best defined in a biopsychosocial context.

ETIOLOGY

There is strong evidence for a genetic basis for EDs. The incidence of AN is 7% in first-degree relatives of anorexic patients compared with 1%–2% in the general population. The concordance rate in monozygotic twins is 55% compared with 7% in dizygotic twins. Twin studies estimate the heritability of AN as 33%–84% and BN as 28%–83%.

There is evidence of altered serotonergic and dopaminergic function and alterations in neuropeptides and gut peptides in AN and BN. It remains unclear whether abnormalities of neurotransmitters contribute to the development of EDs or are a consequence of the physiologic changes associated with the disorders. Patients with BN or BED appear to have a blunted serotonin response to eating and satiety. With decreased satiety, patients continue to eat, leading to a binge. Treatment with selective serotonin reuptake inhibitors (SSRIs) tends to equilibrate satiety regulation. Adiponectin is elevated in AN, although it is unclear whether this is merely secondary to malnutrition. Cholecystokinin is decreased in BN, perhaps contributing to the lack of post-ingestion satiety that perpetuates a binge. Ghrelin, a gut peptide, is elevated in patients with AN, and it does not decrease normally after a meal in these patients. Obestatin, a gut peptide that inhibits appetite, is elevated in AN as well.

Leptin physiology is deranged in patients with AN. These abnormalities may mediate energy changes that affect the hypothalamic-pituitary axis and play a role in perpetuating AN. Leptin levels increase excessively as individuals with AN regain weight. The abnormally high levels of leptin may contribute to the difficulty AN patients have when trying to regain weight, as higher leptin levels signal the body to decrease energy intake.

Traditional psychological theory has suggested many environmental factors that might promote the development of EDs. Enmeshment of mother with daughter to the point that the teenager cannot develop her own identity (a key developmental marker of adolescence) may be a predisposing factor. The teenager may cope by asserting control over food, as she senses her lack of control in the developmental realm. A second theory is related to puberty. Some teenagers may fear or dislike their changing bodies. By restricting food intake, they lose weight, stop menstruating, and effectively reverse pubertal development. Related, emerging literature demonstrates that transgender youth may use food restriction and compensatory behaviors to control pubertal development. It is generally recognized that ED diagnoses are more common in trans youth compared to cisgender youth. The largest study showed that 17% of transgender American college youth reported ...

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