Elizabeth A Lawson and Anne Klibanski*

SUMMARY
Anorexia nervosa (AN) is a psychiatric disease associated with notable medical complications and increased mortality. Endocrine abnormalities, including hypogonadotropic hypogonadism, hypercortisolemia, growth hormone resistance and sick euthyroid syndrome, mediate the clinical manifestations of this disease. Alterations in anorexigenic and orexigenic appetite-regulating pathways have also been described. Decreases in fat mass result in adipokine abnormalities. Although most of the endocrine changes that occur in AN represent physiologic adaptation to starvation, some persist after recovery and might contribute to susceptibility to AN recurrence. In this Review, we summarize key endocrine alterations in AN, with a particular focus on the profound bone loss that can occur in this disease. Although AN is increasingly prevalent among boys and men, the disorder predominantly affects girls and women who are, therefore, the focus of this Review.

INTRODUCTION
Anorexia nervosa (AN), a disease characterized by self-induced starvation and pathologic fear of weight gain, affects 0.3% of the female population worldwide. Associated with notable medical consequences, AN has among the highest mortality of any psychiatric disorder. Hormonal abnormalities are common and affect multiple hypothalamic–pituitary pathways. Most hormonal changes are thought to represent a response to starvation and attempt to reassign limited substrate resources to the most essential functions of life. In this Review, we describe endocrine alterations that play important parts in mediating short-term and long-term medical complications of AN, particularly severe bone loss.

Keywords anorexia nervosa, appetite, hypothalamic dysregulation, osteopenia

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