Anorexia nervosa is the result of a complex interplay between biological, psychological, and social factors, which tend to affect

women more than men, and adolescents more than older women. Some evidence suggests a higher rate of the disorder in monozygotic twins than in dizygotic twins, which may indicate a biologic predisposition.8 Psychologically, prepubescent patients who subsequently develop anorexia nervosa have a high incidence of premorbid anxiety disorders. The onset of the disorder during puberty has led to the theory that, by exerting control over food intake and body weight, adolescents are attempting to compensate for a lack of autonomy and selfhood. Individuals with anorexia nervosa maintain a lifelong increased incidence of anxiety, depressive disorders, and obsessive-compulsive disorder. Neurobiologists hypothesize that disruption of serotonergic pathways in the brain mediate the development of anorexia nervosa and may account for the frequent coexistence of other psychological disturbances.9 The patient's altered body image results in a perception of fatness despite being normal or underweight. Attempts to correct this flaw through food restriction or purging lead to progressive malnutrition and eventually starvation. Modern preoccupation with slenderness and beauty in the Western world may contribute to the mindset of thinness as a valued quality in adolescents; however, this link has not been proven. Malnutrition subsequent to self-starvation leads to protein deficiency and disruption of multiple organ systems. In addition to hypoglycemia and vitamin deficiencies, starvation results in release of endogenous opioids, hypercortisolemia, and thyroid function suppression. Neuroendocrine disturbances result in delayed puberty, amenorrhea, anovulation, low estrogen states, increased growth hormone, decreased antidiuretic hormone, hypercarotenemia, and hypothermia.10 Decreased gonadotropin levels and hypogonadism may occur among males who are affected. Cardiovascular effects include mitral valve prolapse, supraventricular and ventricular dysrhythmias, long QT syndrome, bradycardia, orthostatic hypotension, and shock due to congestive heart failure.11,12 Renal disturbances include decreased glomerular filtration rate (GFR), elevated BUN, edema, acidosis with dehydration, hypokalemia, hypochloremic alkalosis with vomiting, and hyperaldosteronism. Gastrointestinal findings include constipation, delayed gastric emptying, and gastric dilation and rupture when binge eating. Patients who induce vomiting develop dental enamel erosion, palatal trauma, enlarged parotids, esophagitis, Mallory-Weiss lesions, and elevated transaminase levels. Cases of superior mesenteric artery (SMA) syndrome from loss of intraperitoneal fat in AN as well as gastric rupture from bingeing and purging, leading to pneumothorax and pneumoperitoneum, have been reported.