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INTRODUCTION

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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 eating disorders includes anorexia nervosa (AN), bulimia nervosa (BN), binge-eating disorder (BED), avoidant/restrictive food intake disorder (ARFID). These disorders are best defined in a biopsychosocial context. New diagnostic categories and criteria for EDs will be available upon release of DSM-V in 2013.

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ETIOLOGY

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There is strong evidence for a genetic basis for eating disorders. 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%. First-degree female relatives of males with AN have a 20-fold relative risk of AN. Most studies also find a higher incidence of eating disorders among first-degree relatives of bulimic patients. The family of neurotrophin proteins has been shown to be involved in the regulation of eating behavior and energy metabolism and has been intensively studied to assess their potential role in the genetic susceptibility to EDs. In a study of European families with EDs, Mercader and associates found a strong association between rs7180942, a neurotrophin protein encoded by the NTRK3 gene and the presence of EDs, with an undertransmission of the heterozygous genotype and an overtransmission of the homozygous genotype associated with increased phenotypic expression of EDs.

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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 a decreased satiety response, patients continue to eat, leading to a binge. Treatment with selective serotonin reuptake inhibitors (SSRIs) tends to equilibrate satiety regulation. An alteration in dopamine has also been recognized, although its significance is not clear. Adiponectin is elevated in AN, although it is unclear whether this is merely secondary to the malnourished state. Cholecystokinin is decreased in BN, perhaps contributing to the lack of postingestion 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.

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Leptin physiology is deranged in patients with AN. Abnormalities of leptin 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 ...

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