Eating and Feeding Disorders

Abstract

Eating and feeding disorders are characterized by aberrant eating and weight-control behaviors and endocrine dysregulation. The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition ( American Psychiatric Association, 2013) includes specific diagnostic criteria for anorexia nervosa (AN), bulimia nervosa (BN), binge eating disorder, avoidant/restrictive food intake disorder, rumination disorder, pica, and other specified feeding and eating disorders. The majority of research is focused on AN, BN, and symptomatically similar subdiagnostic threshold presentations, and thus this chapter concentrates on AN and BN. Although eating and feeding disorders can occur across all ages and in females and males, AN and BN most often develop during adolescence and predominate in females. AN typically onsets during mid- to late-adolescence (American Psychiatric Association, 2013), while BN tends to begin in later adolescence (Fairburn et al., 2000; Le Grange et al., 2004). Patterns of extreme dietary restriction, which can be punctuated by loss of control overeating and compensatory behaviors, and weight fluctuations are common in AN and BN. Some of the endocrine alterations observed in eating and feeding disorders may be an adaptation to starvation or malnutrition, existing as a mechanism to save energy and promote survival. Hypogonadism is the most striking endocrine change in patients with eating disorders, with amenorrhea as the main manifestation. Other endocrine alterations may include low T3 syndrome, hypercortisolism, loss of bone mineral density, and changes in the somatotropic axis and the glucose homeostasis. Hypoleptinemia, caused by food restriction and by the decrease of adipose tissue mass, seems to be the mediator of these endocrine changes. Many of these deficiencies normalize with nutritional rehabilitation. However, some dysregulations in appetite-regulating hormones are counter to what would be expected as an adaptive response to malnutrition and/or persist postrecovery, suggesting the possibility that some endocrine abnormalities may play a mechanistic or etiologic role in disordered eating.