8 - Disorders of Eating - Anorexia Nervosa, Bulimia Nervosa, and Binge-Eating Disorder

Editors: Shader, Richard I.

Title: Manual of Psychiatric Therapeutics, 3rd Edition

Copyright 2003 Lippincott Williams & Wilkins

> Table of Contents > 8 - Disorders of Eating: Anorexia Nervosa, Bulimia Nervosa, and Binge-Eating Disorder

8

Disorders of Eating: Anorexia Nervosa, Bulimia Nervosa, and Binge-Eating Disorder

W. Stewart Agras

Eating behavior is modulated by cultural, social, familial, and biologic factors. These influences guide taste preferences, dietary choices, and patterns of food intake. Social learning may lead to food choices that would be aversive to members of another culture and may overcome natural aversions (e.g., to bitter taste or to certain food smells, such as ripe cheeses). Thus, in any culture, a wide range of eating behavior is considered normal. Similarly, children may demonstrate marked variation in their food intake from meal to meal, sometimes consuming only a single food during a meal, but they demonstrate much less variation over successive 24-hour periods. Aversions to various foods may persist for several months during childhood, only to disappear eventually.

Some psychiatric disorders are accompanied by minor to more extreme pathologic eating patterns. In depression, for example, the most common pattern is diminished interest in food and poor appetite, accompanied by weight loss (see Chapter 18). A second pattern, which is seen less commonly in depression, consists of excessive eating that is often accompanied by sleepiness and lethargy. Anxiety disorder patients (see Chapter 14) may also have diminished appetite and weight loss, although a few may increase their food intake, often consuming junk food. Avoidance of foods that is most commonly based on a fear of choking may be seen in phobic disorders. Phobic patients typically avoid solid foods that are difficult to swallow. In paranoid disorders, food avoidances based on delusional thinking, often concerning poisoning, may also be seen.

Many neurochemical systems are involved in the regulation of feeding behavior. Serotonin, for example, modulates satiety, and high levels lead to the cessation of eating. Adrenergic compounds may either decrease or increase feeding, depending on the state of the organism at the time of feeding. Neuropeptide Y stimulates eating behavior; leptin appears to be inhibitory; and opioids and dopaminergic mechanisms are involved in the reinforcing properties of feeding. Cholecystokinin also plays a role in satiety.

Given these various control mechanisms, the fact that medications commonly used in psychiatric practice may affect eating behavior is not surprising. For example, the use of many antipsychotic agents, such as clozapine, olanzapine, and risperidone, can lead to weight gain, a troublesome problem for schizophrenic patients, who may need to be maintained on medication for many years. Some patients treated with antidepressants, such as amitriptyline or mirtazapine, may experience weight gain, presumably due to appetite stimulation. Paradoxically, patients with eating disorders often experience appetite suppression when they receive antidepressants. The benzodiazepines sometimes alter eating behavior by increasing food intake; an occasional patient will notice weight gain as a consequence. Amphetamines, most frequently those used for the treatment of attention deficit hyperactivity disorder (see Chapter 22) and occasionally those used for treatment of resistant depressions, diminish the appetite, and their use may lead to weight loss. In some patients, topiramate, an anticonvulsant that is sometimes used as a mood stabilizer, is also associated with weight loss.

Cultural preferences for body shape, particularly for women, strongly affect eating behavior. In undeveloped countries, a plump body shape is preferred. On the other hand, in the developed countries, the current cultural preference is for a thin body shape for women. In Western countries, researchers have shown that most adolescent females develop a fear of becoming fat and that they experience dissatisfaction with their body shape and weight. These fears and dissatisfactions, which are seen less frequently in males, lead most high school girls to diet from time to time in attempts to control their body shape and weight. However, relatively few young women develop an eating disorder. Thus, although a continuum of concern about body weight and shape that influences dietary behavior undoubtedly exists, eating disorders probably should be regarded as distinctly separate psychopathologic entities with risk factors that can add to the

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effects of simple dietary restriction. Such risk factors, in addition to weight and shape concerns and restrictive dieting, include genetic factors; a family or personal history of being overweight or obese; family influences, such as maternal concerns about a daughter's weight and shape; and peer teasing about weight and shape. Less specific factors include low self-esteem, sexual or physical abuse, and stressors of various types.

The disorders of eating, which range in frequency from relatively rare to quite common, consist of anorexia nervosa, bulimia nervosa, and binge-eating disorder; the latter condition is frequently observed in the overweight. Although these three conditions are usually considered the core eating disorders, a further clinical problem, ruminative vomiting, that is seen in infancy and in the institutionalized mentally retarded, is also considered in this chapter.¹ The core eating disorders are seen far more commonly in females than in males, which mirrors the dietary concerns of the general population, and, with the exception of ruminative vomiting, they have increased in prevalence during the past 30 years. The behaviors involved in the core eating disorders include overvaluation of a thin body shape and low weight, restriction of food intake, binge eating, and purging. One should note that the treatment of the eating disorders is as costly as that for conditions such as obsessive-compulsive disorder. Hence, recognition of these disorders early in their development is important.

I. Disordered Eating Behaviors

A. Definitions and Concepts

• Overvaluation of body shape and weight. The overvaluation of body shape and weight seen in the eating disorders is partly a response to the changes in the fashion cycle noted above; thinness has become desirable for women. The most recent cyclical change toward a thin body shape began in the late 1960s. Unlike a similar cycle in the 1920s in which the thin look was attained by changes in dress style that included binding the breasts to achieve a boyish silhouette, in the most recent cycle thinness is attained by dieting. This change in societal values has led most females to become dissatisfied with their body shape and weight and to diet. However, cultural and socioeconomic differences in response to these societal demands do exist, with upper-class and middle-class white women being the most responsive. The patient with an eating disorder appears to be more concerned with her body shape and weight than are normal women of the same race and socioeconomic class.

• Dietary restriction. The dietary restriction seen in anorexia nervosa, bulimia nervosa, and binge eating is a response to overvaluing body shape and weight. The degree of restriction is most extreme in the anorexic and is least in the overweight binge eater. These patients elaborate various rigid food rules, many of which are unreasonable. For the most part, the foods that are avoided are those considered fattening by each individual, and hence they vary from patient to patient. Anorexics use various techniques to enhance their control over food intake. They tend to eat slowly, and they may make food less attractive by cutting it into small pieces or sometimes by garnishing it with pepper or salt. In the bulimic and binge eaters, episodes of dietary restriction alternate with binge eating.

• Binge eating. This is defined as an eating episode that the patient perceives as being out of control as the individual is not able to resist the temptation to eat certain foods or to stop eating unless food is no longer available, unless he or she is interrupted by someone, or unless the patient is physically unable to eat more. Binge eating is a consequence of excessive caloric restriction or the attempt to attain such restriction, with the consequent disruption of normal feeding patterns. Thus, attempts at dieting precede binge eating in patients with bulimia nervosa.

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  Severe dietary restriction can usually be sustained only for a limited time, and then various factors lead to a breakdown of control and to binge eating. Factors leading to a loss of control include the sight and smell of particularly desired foods and emotional arousal secondary to stressful life events. A large amount of food is often eaten in a binge, although wide variation in size, from small (100 calories) to large (several thousand calories), is observed. Most binges occur in time-limited episodes, although some episodes may take up most of the day, with the patient typically eating small amounts of food almost continuously, a pattern sometimes referred to as grazing. The food chosen is usually easily swallowed, often consisting of breads, pastries, ice cream, or snack items. Binges are usually carried out in private for fear of discovery or interruption. Binge eating should be distinguished from overeating, which usually occurs in the context of a special social occasion, such as Thanksgiving, although overeating may be more frequent and habitual in some people. In the case of overeating, the individual has no sense of having lost control of eating. Because overeating usually is socially sanctioned, little anxiety or guilt is associated with it. In addition, the food consumed in episodes of overeating more closely resembles a normal meal than does the food eaten in a binge.

• Purging. This may be defined as any activity aimed at ameliorating the perceived negative effects of a binge on body shape and weight. Purging may consist of self-induced vomiting, the use of laxatives, the use of diuretics, or enemas. A rarer form consists of spitting out food that has been chewed but not swallowed. Excessive exercise or fasting may also be used to compensate for binge eating. These latter behaviors are now termed nonpurging compensatory behaviors. Patients who induce vomiting often drink large amounts of fluids during and after the binge to facilitate purging. Although most bulimics become adept at inducing vomiting without emetics, a few use ipecac; this practice occasionally results in death from ipecac toxicity.

II. Anorexia Nervosa

A. Definitions and Concepts

The cardinal features of anorexia nervosa are a weight that is at least 15% below the ideal body weight, a strong fear of gaining weight, a perception of being fat even at a low weight, and, in the female, amenorrhea. The low body weight is achieved via a relentless pursuit of thinness through dieting, excessive exercise, and often purging. The degree of weight loss and the accompanying weakness and fatigue are often denied. The differential diagnosis includes weight loss accompanying severe depression, although no preoccupation regarding body shape or size is observed in this condition; in the weight loss accompanying schizophrenia, the food avoidance is based on delusional thinking.

The initial visit by a patient with this disorder usually stems from family concern about excessive weight loss, although a few patients present with physical complaints, such as orthopedic problems due to excessive exercise or cardiovascular problems secondary to starvation and potassium deficiency.

Anorexia nervosa is a relatively rare disorder with an incidence of about 15 new cases per 100,000 population per year in the United States. The disorder is seen far more frequently in females than in males, in whom it is quite rare. Because it is a chronic disorder, the lifetime prevalence is higher, ranging from 0.1% and 0.7%. The peak onset is during adolescence, although the first episode may occur in childhood or in early adult life.

Genetic factors may play a significant etiologic role. Twin studies reveal a concordance rate of approximately 70% for monozygotic twins. Family studies reveal that anorexia nervosa is about eight times more common in the relatives of anorexics than it is in the relatives of patients without anorexia. An excess of affective disorder is also observed in the families of bulimic anorexics, but the two disorders appear to be transmitted separately.

Comorbid obsessive-compulsive disorder with the usual range of obsessions and compulsions (e.g., dirt, infection, harming others, and associated

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rituals) occurs in 10% to 20% of anorexics. Because of the obsessional thinking and compulsive behavior regarding food that occur in all anorexics, some view the obsessional traits as a major contributor to the disorder (see Chapter 6). A concurrent episode of major depression is seen frequently, as is social phobia.

Many of the behavioral and physiologic changes seen in anorexia nervosa are a consequence of starvation; these are also seen in any starving population. They include intense preoccupation with food; slow eating; depression; a loss of energy; a loss of sexual interest; social withdrawal; and cognitive impairments resulting in diminished concentration, diminished performance on tests of intellectual function, and poor judgment. About half of all anorexics also binge eat and purge. This behavior is more likely to occur in the impulsive, less inhibited anorexic.

Physical examination reveals the evident cachexia, slow pulse rate, hypotension, cold and blue extremities, dry skin, and, at times, the appearance of fine body hair known as lanugo. Although many alterations in metabolic function occur, all are secondary to starvation. Thus, gonadotropin levels are decreased, the luteinizing hormone levels assume a prepubertal pattern, and the follicle-stimulating hormone and estrogen levels are also low. Growth hormone levels may be high in some patients, and the resting plasma cortisol levels are elevated. Triiodothyronine levels are below normal. All of these changes may be viewed as compensatory adaptations to starvation. Osteopenia and osteoporosis are common, and they may be accompanied by fractures in severe cases. Other changes that may be noted are elevated levels of cholesterol and carotene, leukopenia, and anemia. Potassium levels may also be low, particularly in the purging anorexic. These low levels (less than 3.0 mEq per L) may, in turn, give rise to cardiac arrhythmias that can lead to death when they are not corrected by supplemental potassium and the restoration of a normal fluid balance. In the low-weight anorexic, as opposed to the bulimic, this should be accomplished by intravenous infusion.

B. Treatment

The first step in the treatment of anorexia nervosa is to persuade both the patient and the family that treatment is necessary and to explain the nature of the treatment carefully. Most anorexics can be treated on an outpatient basis with short-term hospital admissions to remedy medical instability. Conceptualizing treatment as having the following two phases can be useful: an acute phase during adolescence and a more chronic phase for those who have not recovered within a few years of the initial episode. A specialized form of family therapy has been shown to be quite successful for the adolescent anorexic in controlled trials. The prime aim of this therapy is to help the parents regain control of their child's eating behavior so that he or she steadily regains weight. Once the child's weight has been stabilized, therapy enables the parents to loosen their control and to address ongoing family issues that may maintain the anorexic behaviors. In the chronic form of the disorder, therapy is aimed at increasing caloric intake and in dealing with the social isolation that characterizes the anorexic. Partial hospitalization may be useful for such patients.

Hospitalization in a specialized inpatient unit may be required in the very low weight anorexic (i.e., more than 25% below an ideal body weight). The first step is to correct metabolic abnormalities and to begin weight restoration. The usual program takes the form of systematic reinforcement of weight gain in which access to certain activities is contingent on a specified daily amount of weight gain (e.g., 0.2 kg per day). Reward activities (e.g., leaving the hospital room for a specified period of time) are limited at first. Later, they may include access to visitors other than family members, passes off the unit, and so on. A contract specifying the amount of weight gain and the contingent privileges must be worked out with the patient and should then be renegotiated at frequent intervals during hospitalization. Patients are encouraged to take an active role in such negotiations so that the reinforcements

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are personalized. Failure to gain weight usually signifies that the contingencies are not sufficiently rewarding, and it points to the need to discover more effective reinforcers.

Contingent reinforcement of this type has been shown to lead to increased caloric intake and weight gain in controlled studies. Such treatment has been shown to be more successful than the usual hospital care in a controlled study, although it may be more effective with patients who are less severely ill.

Fluid retention may occur during the initial stages of refeeding. For the first week or 10 days, the caloric intake should not exceed 2,000 calories per day and fluid intake should be carefully monitored. Once the individual's weight has begun to increase, family therapy and individual psychotherapy, if it is needed, is begun.

Medication has relatively little place in the treatment of the anorexic. One study has shown that nonbulimic anorexics respond better to cyproheptadine, a serotonin antagonist that stimulates the appetite, in doses up to 32 mg per day than to a placebo; but the response is often clinically insignificant. For the most part, the symptoms of depression usually remit with weight gain, and no pharmacologic treatment is necessary.

Tube feeding, which was once commonly used in the treatment of anorexia nervosa, is now rarely used because it may be complicated by inhalation pneumonia. The indications for parenteral feeding include dehydration and electrolyte imbalance, an intercurrent medical emergency necessitating weight gain, and failure to gain weight after an adequate trial of therapy. If parenteral feeding is indicated, it is best carried out on a medical ward so that, once the emergency has been treated, the patient can continue in a weight restoration program. Separation of medical and psychiatric treatments limits the opportunities for manipulation of the treatment system by these patients. Tube feeding may, on occasion, be used as negative reinforcement (i.e., by gaining weight at a certain rate or above a certain threshold, the patient can avoid tube feeding).

Long-term outpatient treatment should be provided after discharge from the hospital and should be continued until a satisfactory weight has been attained and has been stabilized for at least 6 months. Such treatment usually consists of cognitive-behavior therapy (CBT) aimed at providing support for the patient, modifying the distorted patterns of thinking about weight and shape, and dealing with the ongoing problems of living. Although most patients gain weight in such a treatment program, many will relapse within a few months and will require further hospitalization. Some evidence indicates that fluoxetine may be useful in enabling the maintenance of weight gains.

Less than half of the patients with this disorder recover fully, although vocational functioning is often preserved.

C. Caution

Anorexia nervosa has the highest mortality rate of any psychiatric disorder. In some long-term follow-up studies, the mortality rate from anorexia nervosa has been as high as 15%, although the usual figure that is given is 5%. In about half of the cases, death is due to suicide (see Chapter 17), a reminder that mood disorder is prevalent in this population and that suicidal risk should be carefully evaluated. Obesity is a rare complication of treatment, occurring in approximately 2% of patients.

III. Bulimia Nervosa

A. Definitions and Concepts

The following two types of bulimia nervosa are now recognized: purging and nonpurging syndromes. In the nonpurging syndrome, the compensatory behaviors are fasting and/or excessive exercise. Bulimia nervosa consists of severe dietary restriction, binge eating, and compensatory behaviors, whether purging or nonpurging, combined with dissatisfaction about body weight and shape and a fear of weight gain.

Binges are preceded in some 70% of episodes by a negative mood that is often induced by faulty interpersonal interactions. In the remaining cases,

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binge eating is preceded by acute dietary restriction. Binges are followed by feelings of guilt and depressed mood. The typical dietary pattern is to eat little or no breakfast, to have a very light lunch, and then to lose control and binge eat and purge in the late afternoon or evening.

The disorder usually begins in late adolescence with dieting and binge eating that precede the onset of purging by several months. Bulimia nervosa appears to run a chronic, sometimes episodic, course. Seeing patients who have suffered from the disorder for 30 years or more is not uncommon. Most bulimics are normal weight, and about 10% are overweight. About one-fourth of bulimics have a prior history of anorexia nervosa. A history of major depressive disorder, current major depressive disorder, and borderline personality disorder or impulsive traits are common in these patients. Other comorbid conditions are alcohol and drug abuse or dependence.

Like anorexia nervosa, bulimia nervosa is far more common in females than in males, with a prevalence of approximately 1% for patients meeting strict diagnostic criteria. Although the specific etiology of the disorder is unknown, the societal value of a thin body shape clearly appears to have influenced the increase in the number of cases of bulimia nervosa that have been seen in clinics since the late 1970s. Excessive dieting leads to a loss of control over eating, as has been demonstrated in laboratory experiments, and to binge eating. When faced with the threat of weight gain, some binge eaters then begin to purge. Dysregulation of serotonin metabolism may possibly be associated with bulimia nervosa, as bulimics appear to have low serotonin levels. Binge eating leads to the intake of tryptophan (a precursor of serotonin)-containing foods, thus raising the serotonin levels. In turn, this leads to satiety and to correction of the bulimic's low mood. However, whether the serotonin abnormalities are a result of the dietary dysregulation or a cause of it is not known.

One of the most frequent complications of bulimia nervosa is dental caries and periodontal disease as a consequence of the consumption of sweet foods. Serum amylase levels are increased in about two-thirds of patients, and swollen parotid glands are a distinguishing feature in a few. About one-fourth of all bulimics suffer from menstrual irregularity or amenorrhea. About 5% of patients will have a low serum potassium level that requires oral potassium supplementation. Other rarer complications associated with self-induced vomiting are chronic hoarseness, gastrointestinal reflux, and esophageal tears and bleeding. The use of laxatives as a method of purging leads to physiologic adaptation with slowed intestinal mobility and constipation. Many bulimic patients deny their laxative use. When covert laxative use is suspected, urine testing for phenolphthalein, a common ingredient in many over-the-counter and prescription laxatives (e.g., Ex-Lax, Medilax, Modase), is useful. However, the fact that another common laxative, bisacodyl (e.g., Dulcolax), is not detected by this method should be noted.

B. Treatment

The following three treatment approaches to bulimia nervosa have been demonstrated to be successful in controlled trials: antidepressant medications, CBT, and interpersonal therapy. CBT appears to be more successful than antidepressant medication, and its onset of action is faster than interpersonal therapy. Hence, CBT is generally recognized as the first-line treatment for bulimia nervosa.

• Antidepressants were first used on the assumption that bulimia nervosa was a disorder closely related to depression. However, bulimics who are not overtly depressed and who have no history of major depressive disorder respond as well to antidepressant treatment as do depressed bulimics. Thus, the belief that the success of antidepressants in bulimia nervosa is not secondary to their efficacy in ameliorating symptoms of depression is now generally accepted. Antidepressants, including the tricyclic antidepressants (e.g., imipramine, desipramine), the monamine oxidase inhibitors (e.g., phenelzine), and the serotonin reuptake

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  inhibitors (e.g., citalopram, fluoxetine, fluvoxamine, paroxetine, sertraline), have all been found to be effective in the treatment of bulimia nervosa. The tricyclic antidepressants and the monamine oxidase inhibitors are used at usual antidepressant doses. Fluoxetine, on the other hand, is used at higher doses than is usual in the treatment of depression (e.g., 60 rather than 20 mg per day). On average, binge eating and purging decline by about 80%, and some 30% of patients become symptom free for some period of time.

  Unfortunately, relapse often occurs when medication is withdrawn and, in about one-fourth of cases, even when the medication is maintained. Thus, bulimics should be maintained on an adequate dosage of an antidepressant for at least 1 year to prevent relapse.

• The main aims of CBT are to enhance food intake; to decrease avoidance of specific foods; and to deal with distorted thinking about foods, body image, and weight. Binge eating and purging are expected to decline once dietary restriction is eased. These aims are facilitated by detailed self-monitoring of food intake and the precipitants and consequences of binge eating. In the later stages of treatment, relapse-prevention techniques are used (e.g., learning how to cope with high-risk situations). Patients are usually seen weekly for about 20 sessions over a 6-month period. Overall, half of the patients will become symptom free after treatment, and another one-fourth will demonstrate significant improvement. The treatment of laxative abuse is best accomplished by acute withdrawal. Patients should be alerted to potential side effects of such withdrawal, including constipation, bloating and bowel discomfort, and edema. These symptoms usually persist for between 7 and 10 days. A recent study found that patients who did not reduce their purging behavior by 70% after six sessions of treatment were likely to fail treatment. For such patients, the clinician might consider adding an antidepressant to CBT.

IV. Binge-Eating Disorder

A. Definitions and Concepts

As was noted above, some adolescents who binge eat do not purge. Instead, many of them go on to struggle with weight gain for much of their lives. This syndrome is now considered a disorder that requires further research in the Diagnostic and Statistical Manual of Mental Disorders, 4th edition; it is similar to that of bulimia nervosa, except the individual does not engage in compensatory behaviors and hence has no medical complications attributable to purging. Like bulimics, these patients alternate between episodes of binge eating and dietary restriction, although the degree of such restriction is less than that seen in the bulimic patient. In other respects, the psychopathology of binge-eating disorder appears similar to that of bulimia nervosa. However, these patients tend to present for treatment later in life (often in the context of weight-reduction attempts), and they are more likely to be seen in medical clinics than in psychiatry clinics. The prime medical comorbidities of this disorder are those associated with obesity, such as essential hypertension, type II diabetes mellitus, hypercholesterolemia, and cardiovascular disease.

The night eating syndrome, a relatively uncommon disorder, should be considered in the differential diagnosis of binge-eating disorder. In this syndrome, patients present with morning anorexia, evening overeating, and insomnia. Compared with obese control subjects, those with night eating syndrome consume more calories, and over 50% of their daily caloric intake is eaten after 10 p.m., compared with control subjects whose post-10 p.m. caloric intake is 15%. Recent studies have found that those with night eating syndrome lack the usual nocturnal rise in leptin levels. They also have lower than usual nocturnal melatonin levels, which perhaps explains their nighttime eating (in the absence of leptin inhibition of eating) and their sleep disturbance. No treatments for this condition have been described.

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Although the prevalence of binge-eating disorder in the general population is approximately 2%, between one-fourth and one-third of all obese people binge eat, and the frequency of binge eating increases with increasing levels of adiposity. This suggests that binge eating may be a risk factor for the development of obesity and that a significant minority of the obese has an eating disorder.

B. Treatment

Antidepressant medication, CBT, and interpersonal psychotherapy all appear effective in the treatment of the overweight binge eater. Unlike the findings for bulimia nervosa, CBT and interpersonal therapy appear to be equally effective in binge-eating disorder. Antidepressant therapy appears to promote greater weight losses when it is added to CBT. Moreover, if the cessation of binge eating is maintained, it is associated with larger weight losses than for those patients who do not stop binge eating.

V. Ruminative Vomiting

A. Definitions and Concepts

As was noted earlier, this is a relatively rare disorder that usually affects infants, in whom it is life threatening. The usual presentation is early failure to thrive, accompanied by regurgitation of milk. The infant appears to have learned to provoke regurgitation so that he or she is able to enjoy the taste of milk doubly. Unfortunately, the milk then flows out of the infant's mouth, depriving him or her of needed nutrition. The etiology of this disorder is unknown, although clinical observation suggests that the maternal relationship is often unsatisfactory, sometimes bordering on outright rejection by the mother.

B. Treatment

One treatment approach, which is based on the preceding observation, is to give the infant extra attention in a hospital environment. Although successes have been reported with this treatment, no controlled studies of its effectiveness exist. An alternative approach is to follow the regurgitative behaviors with an aversive event. Regurgitative behaviors include curling the tongue into the back of the mouth, a behavior that is often accompanied by movements of the throat and facial muscles. Various aversive stimuli have been used, including sour or bitter tastes (e.g., lemon juice). These procedures have been shown to be effective in single-case controlled studies as they rapidly eliminate regurgitation and are followed by weight gain. Clearly, the maternal relationship should be carefully investigated, and educational, social, or psychotherapeutic interventions should be offered if needed.

VI. Comment

The website of the Academy for Eating Disorders provides useful information about the Academy, as well as links to sites providing information about eating disorders (http://www.aedweb.org/).

ADDITIONAL READING

Agras WS, Apple RF. Overcoming eating disorders: a cognitive-behavioral treatment for bulimia nervosa and binge eating disorder. Therapist guide. San Antonio, TX: The Psychological Corporation, 1997.

Attia E, Haiman C, Walsh BT, et al. Does fluoxetine augment the inpatient treatment of anorexia nervosa? Am J Psychiatry 1998;155:548 551.

Dare C, Eisler E, Russell GM, et al. Family therapy for anorexia nervosa: implications from the results of a controlled trial of family and individual therapy. J Marital Fam Ther 1990;16:39 57.

Fairburn CG. Overcoming binge eating. New York: The Guilford Press, 1995.

Fairburn CG, Welch SL, Doll HA, et al. Risk factors for bulimia nervosa. A community-based case-control study. Arch Gen Psychiatry 1997;54:509 517.

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Fluoxetine Bulimia Nervosa Study Group. Fluoxetine in the treatment of bulimia nervosa. Arch Gen Psychiatry 1992;49:139 147.

Herzog DB, Greenwood DN, Dorer DJ, et al. Mortality in eating disorders: a descriptive study. Int J Eating Disord 2000;28:20 26.

Keel PK, Mitchell JE, Miller KB, et al. Long-term outcome of bulimia nervosa. Arch Gen Psychiatry 1999;56:63 69.

Spitzer RL, Yanovski S, Wadden T, et al. Binge eating disorder: its further validation in a multisite study. Int J Eating Disord 1993;13:137 153.

Striegel-Moore R, Leslie D, Petrill SA, et al. One-year use and cost of inpatient and outpatient services among female and male patients with an eating disorder: evidence from a national database of health insurance claims. Int J Eating Disord 2000;27:381 389.

Walsh BT, Wilson GT, Loeb KL, et al. Medication and psychotherapy in the treatment of bulimia nervosa. Am J Psychiatry 1997;154:523 531.

Zipfel S, Lowe B, Deter HC, et al. Long-term prognosis in anorexia nervosa: lessons from a 21-year follow-up study. Lancet 2000;355:721 722.

¹Another eating disorder, pica (the persistent ingestion of non-nutritive substances such as paint, plaster, or dirt), is sometimes considered important. Its frequency in adults and adolescents, however, is quite low, and the decision to omit it was made with this chapter's author.