clinic samples. The course may be chronic or intermittent, with periods of remission alternating with recurrences of binge eating. However, over longer-term follow-up, the symptoms of many individuals appear to diminish with or without treatment, although treatment clearly impacts outcome. Periods of remission longer than 1 year are associated with better long-term outcome.
individuals with bulimia nervosa. The CMR (crude mortality rate) for bulimia nervosa is nearly 2% per decade.
Diagnostic cross-over from initial bulimia nervosa to anorexia nervosa occurs in a mi- nority of cases (10%—15%). Individuals who do experience cross-over to anorexia nervosa commonly will revert back to bulimia nervosa or have multiple occurrences of cross-overs between these disorders. A subset of individuals with bulimia nervosa continue to binge eat but no longer engage in inappropriate compensatory behaviors, and therefore their symptoms meet criteria for binge-eating disorder or other specified eating disorder. Diag- nosis should be based on the current (i.e., past 3 months) clinical presentation.
Temperamental. Weight concerns, low self—esteem, depressive symptoms, social anxi- ety disorder, and overanxious disorder of childhood are associated with increased risk for the development of bulimia nervosa.
Environmental. Internalization of a thin body ideal has been found to increase risk for developing weight concerns, which in turn increase risk for the development of bulimia nervosa. Individuals who experienced childhood sexual or physical abuse are at increased risk for developing bulimia nervosa.
Genetic and physiological. Childhood obesity and early pubertal maturation increase risk for bulimia nervosa. Familial transmission of bulimia nervosa may be present, as well as genetic vulnerabilities for the disorder.
Course modifiers. Severity of psychiatric comorbidity predicts worse long—term outcome of bulimia nervosa.
Bulimia nervosa has been reported to occur with roughly similar frequencies in most in- dustrialized countries, including the United States, Canada, many European countries,
Australia, Japan, New Zealand, and South Africa. In clinical studies of bulimia nervosa in the United States, individuals presenting with this disorder are primarily white. However, the disorder also occurs in other ethnic groups and with prevalence comparable to esti- mated prevalences observed in white samples.
Bulimia nervosa is far more common in females than in males. Males are especially under- represented in treatment-seeking samples, for reasons that have not yet been systemati- cally examined.
No specific diagnostic test for bulimia nervosa currently exists. However, several labora- tory abnormalities may occur as a consequence of purging and may increase diagnostic certainty. These include ﬂuid and electrolyte abnormalities, such as hypokalemia (which can provoke cardiac arrhythmias), hypochloremia, and hyponatremia. The loss of gastric acid through vomiting may produce a metabolic alkalosis (elevated serum bicarbonate), and the frequent induction of diarrhea or dehydration through laxative and diuretic abuse can cause metabolic acidosis. Some individuals with bulimia nervosa exhibit mildly ele— vated levels of serum amylase, probably reﬂecting an increase in the salivary isoenzyme.
Physical examination usually yields no physical findings. However, inspection of the mouth may reveal significant and permanent loss of dental enamel, especially from lin- gual surfaces of the front teeth due to recurrent vomiting. These teeth may become chipped and appear ragged and ”moth—eaten.” There may also be an increased frequency of dental caries. In some individuals, the salivary glands, particularly the parotid glands, may become notably enlarged. Individuals who induce vomiting by manually stimulating the gag reﬂex may develop calluses or scars on the dorsal surface of the hand from re- peated contact with the teeth. Serious cardiac and skeletal myopathies have been reported among individuals following repeated use of syrup of ipecac to induce vomiting.