In women, the full syndrome of BN occurs with a lifetime prevalence of 1 to 3%. Variants of the disorder, such as occasional binge eating or purging, are much more common and occur in 5 to 10% of young women. The frequency of BN among men is less than one-tenth of that among women. The prevalence of BN increased dramatically in the early 1970s and 1980s but may have leveled off or declined somewhat in recent years.
As with AN, the etiology of BN is likely to be multifactorial. Patients who develop BN describe a higher-than-expected prevalence of childhood and parental obesity, suggesting that a predisposition towards obesity may increase vulnerability to this eating disorder. The marked increase in the number of cases of BN during the past 25 years and the rarity of BN in underdeveloped countries suggest that cultural factors are important. Several biologic abnormalities in patients with BN may perpetuate this disorder once it has begun. These include abnormalities of CNS serotonergic function, which is involved in the regulation of eating behavior, and disruption of peripheral satiety mechanisms, including the release of cholecystokinin (CCK) from the small intestine.
The typical patient presenting for treatment of BN is a woman of normal weight in her mid-twenties who reports binge eating and purging 5 to 10 times a week for 5 to 10 years. The disorder usually begins in late adolescence or early adulthood during or following a diet, often in association with depressed mood. The self-imposed caloric restriction leads to increased hunger and to overeating. In an attempt to avoid weight gain, the patient induces vomiting, takes laxatives or diuretics, or engages in some other form of compensatory behavior. During binges, patients with this disorder tend to consume large amounts of sweet foods with a high fat content, such as dessert items. The most frequent compensatory behaviors are self-induced vomiting and laxative abuse, but a wide variety of techniques have been described, including the omission of insulin injections by individuals with type 1 diabetes mellitus. Initially, patients may experience a sense of satisfaction that appealing food can be eaten without weight gain. However, as the disorder progresses, patients perceive diminished control over eating. Binges increase in size and frequency and are provoked by a variety of stimuli, such as transient depression, anxiety, or a sense that too much food has been consumed in a normal meal. Between binges, patients attempt to restrict caloric intake, which increases hunger and sets the stage for the next binge. Typically, patients with BN are ashamed of their behavior and endeavor to keep their disorder hidden from family and friends. Like patients with AN, those with BN place an unusual emphasis on weight and shape as a basis for their self-esteem. Many patients with BN have mild symptoms of depression. Some patients exhibit serious mood and behavioral disturbances, such as suicide attempts, sexual promiscuity, and drug and alcohol abuse. Although vomiting may be triggered initially by manual stimulation of the gag reflex, most patients with BN develop the ability to induce vomiting at will. Rarely, patients resort to the regular use of syrup of ipecac. Laxatives and diuretics are frequently taken in impressive quantities, such as 30 or 60 laxative pills on a single occasion. The resulting fluid loss produces dehydration and a feeling of emptiness but has little impact on caloric balance.
The physical abnormalities associated with BN primarily result from the purging behavior. Painless bilateral salivary gland hypertrophy (sialadenosis) may be noted. A scar or callus on the dorsum of the hand may develop due to repeated trauma from the teeth among patients who manually stimulate the gag reflex. Recurrent vomiting and the exposure of the lingual surfaces of the teeth to stomach acid lead to loss of dental enamel and eventually to chipping and erosion of the front teeth. Laboratory abnormalities are surprisingly infrequent, but hypokalemia, hypochloremia, and hyponatremia are observed occasionally. Repeated vomiting may lead to alkalosis, whereas repeated laxative abuse may produce a mild metabolic acidosis. Serum amylase may be mildly elevated due to an increase in the salivary isoenzyme.
Serious physical complications resulting from BN are rare. Oligomenorrhea and amenorrhea are more frequent than among women without eating disorders. Arrhythmias occasionally occur secondary to electrolyte disturbances. Tearing of the esophagus and rupture of the stomach have been reported, and constitute life-threatening events. Some patients who have chronically abused laxatives or diuretics develop transient peripheral edema when this behavior ceases, presumably due to high levels of aldosterone secondary to persistent fluid and electrolyte depletion.
The critical diagnostic features of BN are repeated episodes of binge eating followed by inappropriate and abnormal behaviors aimed at avoiding weight gain (Table 65-3). The diagnosis of BN requires a candid history from the patient detailing frequent, large eating binges followed by the purposeful use of inappropriate mechanisms to avoid weight gain. Most patients with BN who present for treatment are distressed by their inability to control their eating behavior but are able to provide such details if queried in a supportive and nonjudgmental fashion.
As in AN, there are two mutually exclusive subtypes of BN. Patients with the “purging” subtype utilize compensatory behaviors that directly rid the body of calories or fluids (e.g., self-induced vomiting, laxative or diuretic abuse), whereas those with the “nonpurging” subtype attempt to compensate for binges by fasting or by excessive exercise. Patients with the nonpurging subtype tend to be heavier and are less prone to fluid and electrolyte disturbances.
The prognosis of BN is much more favorable than that of AN. Mortality is low, and full recovery occurs in approximately 50% of patients within 10 years. Approximately 25% of patients have persistent symptoms of BN over many years. Few patients progress from BN to AN.
BN can usually be treated on an outpatient basis (Figure 65-1). Cognitive behavioral therapy (CBT) is a short-term (4 to 6 months) psychological treatment that focuses on the intense concern with shape and weight, the persistent dieting, and the binge eating and purging that characterize this disorder. Patients are directed to monitor the circumstances, thoughts, and emotions associated with binge/purge episodes, to eat regularly, and to challenge their assumptions linking weight to self-esteem. CBT produces symptomatic remission in 25 to 50% of patients.
Numerous double-bind, placebo-controlled trials have documented that antidepressant medications are useful in the treatment of BN but are probably somewhat less effective than CBT. Although efficacy has been established for virtually all chemical classes of antidepressants, only the selective serotonin reuptake inhibitor fluoxetine (Prozac) has been approved for use in BN by the U.S. Food and Drug Administration. Antidepressant medications are helpful even for patients with BN who are not depressed, and the dose of fluoxetine recommended for BN (60 mg/d) is higher than that typically used to treat depression. These observations suggest that different mechanisms may underlie the utility of these medications in BN and in depression.
A subset of patients with BN does not respond adequately to CBT, antidepressant medication, or their combination. More intensive forms of treatment, including hospitalization, may be required for such patients.
Revision date: June 18, 2011
Last revised: by Janet A. Staessen, MD, PhD