Eating disorders in the twenty-first century.

The first description of anorexia nervosa appeared in the literature over three hundred years ago. Since then, much has been learned about eating disorders, including the different presentations, medical complications, prognosis, and treatment strategies. In spite of this knowledge, the prevalence of eating disorders continues to grow. As well, eating disorders are seen in increasing frequency among males, children, and adults, and from all cultures and ethnicities. Of particular concern, is that patients with eating disorders often first present because of a complication such as amenorrhea, syncope, or abdominal pain, without disclosing the eating disorder. Therefore, all physicians should be aware of the various presentations of eating disorders, including the medical complications and risks, and be able to screen for a possible eating disorder. The major medical complications are due to the decreased caloric intake which leads to a hypometabolic state. While most complications are reversible with recovery, some, such as bone loss, may not be. Of particular concern during recovery is the possible development of a refeeding syndrome which occurs as the body goes from a catabolic to an anabolic state, causing hypophosphatemia, hypocalcemia and hypomagnesemia, which can lead to delirium, coma and death. Of further concern is that eating disorders have the highest mortality rate of all psychiatric disorders at 5.6% per decade. This article will review the changing demographics, medical complications, treatment options, and prognosis of eating disorders.

Effect of weight restoration on the dyslipoproteinemia of anorexia nervosa.

Dyslipoproteinemia, a risk factor for atherosclerosis, has been described in anorexia nervosa (AN). To assess whether dyslipoproteinemia is present in our AN population, and to investigate the effect of controlled refeeding, we prospectively examined lipid profiles in 16 hospitalized adolescents with anorexia nervosa on admission and at discharge with a body weight of 90% of ideal. Healthy high school females served as controls. Total cholesterol concentration was not different from controls at either time, and there was no change with weight restoration. Triglyceride levels decreased significantly with treatment, and at discharge, levels were significantly lower than controls. High-density lipoprotein-cholesterol (HDL-C) levels increased significantly with weight gain, and were significantly higher than controls at discharge. Apoprotein A1, the major structural protein of high-density lipoprotein, was also significantly higher among the AN patients after weight gain. Low-density lipoprotein-cholesterol (LDL-C) values did not change, but apoprotein B was significantly higher than controls at discharge. The dyslipoproteinemia demonstrated in our patients was characterized by elevated HDL-C and apoprotein A levels with normal LDL-C and low triglyceride concentrations. These changes were accentuated by restoring body weight.