CHAPTER 17

Feeding and Eating Disorders

James E. Mitchell, M.D.

Stephen A. Wonderlich, Ph.D.

In DSM-IV (American Psychiatric Association 1994) and DSM-IV-TR (American Psychiatric Association 2000), the chapter "Disorders Usually First Diagnosed During Infancy, Childhood, or Adolescence" included three disorders under the heading "Feeding and Eating Disorders of Infancy and Childhood": pica, rumination disorder, and feeding disorder of infancy or early childhood. With the elimination of that chapter in DSM-5 (American Psychiatric Association 2013), these three disorders have been moved to the renamed Feeding and Eating Disorders chapter. In addition, a new diagnosis, avoidant/restrictive food intake disorder (ARFID), subsumes and broadens the DSM-IV-TR diagnosis of feeding disorder of infancy or early childhood.

Anorexia nervosa and bulimia nervosa continue to be featured in DSM-5. In recent decades, both disorders have received considerable scrutiny that has resulted in some important changes to the criteria sets. This is particularly true for anorexia nervosa, where there have been a number of changes in the wording to clarify the intent. Binge-eating disorder, which appeared in Appendix B of DSM-IV-TR as a disorder for further study, has been fairly extensively studied in the interim and in DSM-5 is included as a full diagnostic entity. The inclusion of binge-eating disorder represents a major change in the classification system.

We review the DSM-5 feeding and eating disorders in the following sections.

Pica

Pica is the diagnostic term used to describe the ingestion of nonfood, nonnutritive substances. In DSM-5, this pattern of eating must be sustained for at least 1 month and not be accounted for by stage of development of the patient (infancy or toddlerhood) or cultural factors (DSM-5 criteria for pica are presented in Box 17-1). Pica typically displays an onset in childhood, but this is not necessary. Common substances ingested might include paper, soap, string, soil, chalk, or paint (Bryant-Waugh et al. 2010). Psychiatric comorbidities may include autism spectrum disorder and intellectual developmental disorder. When pica occurs in adults, it is most likely to occur in the context of learning disabilities or other mental disorders. If the eating behavior occurs exclusively during the course of another mental disorder, a separate diagnosis of pica should be made only if the eating behavior is sufficiently severe to warrant independent attention.

NOTICE. Criteria set above contains only the diagnostic criteria and specifiers; refer to DSM-5 for the full criteria set, including specifier descriptions and coding and reporting procedures.

Very little is known about the epidemiology of pica, and large-scale studies designed to characterize its psychopathology do not exist. Treatment is usually based on a multidisciplinary approach that includes provision of a range of nutritional interventions, behavioral techniques, consultation with schools and other involved agencies, and education and support of parents and caregivers. Careful attention to nutritional deficiencies should be part of any comprehensive medical examination. Currently, there are no recommended somatic treatments for pica.

Rumination Disorder

Rumination disorder involves the regurgitation of food (i.e., previously swallowed food is brought back into the mouth) without nausea, retching, or disgust. The food is typically rechewed and either ejected from the mouth or reswallowed. In DSM-5 (Box 17-2), this pattern of behavior must have persisted for at least 1 month and must not be attributable to the effects of another mental disorder or a gastrointestinal or other medical condition (e.g., esophageal reflux). The disorder may be diagnosed across the life span, particularly in individuals who have intellectual developmental disorder (Bryant-Waugh et al. 2010). Infants with the disorder display a straining and arching of the back with the head held back as they make sucking movements with their tongues. Malnutrition may occur despite apparent hunger and the ingestion of large amounts of food. Adolescents or adults with the disorder may attempt to disguise the regurgitation by placing a hand over the mouth or coughing. As in pica, treatment is typically multidisciplinary and includes behavioral interventions, nutritional and medical monitoring, and careful attention to caregivers' interactions with the individual, particularly in infants. Currently there is no recommended somatic treatment for rumination disorder.

NOTICE. Criteria set above contains only the diagnostic criteria and specifiers; refer to DSM-5 for the full criteria set, including specifier descriptions and coding and reporting procedures.

Avoidant/Restrictive Food Intake Disorder

The addition of avoidant/restrictive food intake disorder addresses an important group of patients who were difficult to classify in DSM-IV-TR, and also replaces the diagnosis of feeding disorder of infancy or early childhood, which was rarely utilized. The main diagnostic feature of avoidant/restrictive food intake eating disorder is avoidance or restriction of food intake that results in clinically significant reductions in nutritional intake, as evidenced by weight loss, specific nutritional deficiencies, or marked interference with psychosocial functioning. Such problems usually develop in infancy or early childhood but can also arise in older individuals and may persist into adulthood. The diagnostic features will to some extent depend on the age of the patient, with presentations ranging from agitation around feeding in infants to more generalized emotional difficulties in older children and adolescents. Avoidant/restrictive food intake disorder can be diagnosed in the presence of other conditions if the eating disturbance requires special clinical attention; examples include individuals with certain medical conditions (e.g., gastrointestinal disorders, food allergies) and individuals with autism spectrum disorder. Treatment strategies depend on the age of the patient and the presenting symptoms and will be dictated to a large extent by the findings from a careful evaluation. Currently there are no recommended somatic treatments for avoidant/restrictive food intake disorder, although comorbid conditions may require specific somatic interventions.

NOTICE. Criteria set above contains only the diagnostic criteria and specifiers; refer to DSM-5 for the full criteria set, including specifier descriptions and coding and reporting procedures.

Anorexia Nervosa

Anorexia Nervosa

Case Presentation

K.L. was a 16-year-old white female who lived at home with her parents and a younger sister. Throughout her adolescence she had been of normal weight, but she worried a great deal about her body weight and shape and frequently compared her body weight with that of other girls and women she encountered, usually deciding that she was too heavy relative to these other people. She frequently checked her body weight by looking in the mirror, pinching skin on her sides, and noticing that her thighs rubbed together. At about age 14 she began to diet, first sporadically and then more seriously. At 15 she decided to become a vegetarian and began to eliminate many foods from her diet. She was 5'6" and weighed 125 lb at age 15, but by her 16th birthday she had dropped to 110 lb. Rather than being reassured by this weight loss, she continued to see herself as too heavy. She weighed herself several times a day. She spent most of her time worrying about her weight, to the exclusion of other activities, including school work and involvement with friends. She became increasingly socially isolated. Her weight continued to decrease. Her parents became increasingly alarmed. They talked about this between themselves and started monitoring her eating behavior at meals. They began to encourage her to eat more and more often, usually unsuccessfully. Her weight continued to drop, and 6 months later she weighed slightly less than 100 pounds. She appeared very thin and sullen and often seemed distracted and preoccupied. She seemed weak, but despite this she continued to exercise twice each day and seemed to wish to stand or pace rather than to sit and relax. Because of their concerns, her parents contacted her pediatrician and arranged for her to be seen for an evaluation.

Diagnosis

Anorexia nervosa is a severe psychiatric disorder that has been the focus of study for an extended period of time, yet about which we have a limited understanding and for which the development of effective treatments has progressed very slowly (Bulik et al. 2007). The DSM-5 diagnostic criteria for anorexia nervosa are presented in Box 17-4. These remain fairly similar to the criteria set in DSM-IV, with a few notable changes. The first criterion has been reworded to emphasize that the diagnosed individual needs to attain a significantly low body weight, but the previously suggested reference point (85% ideal body weight) has been eliminated because many times this figure was interpreted as a cutoff, which was never the intention. Now it is underscored that the low body weight must be examined in the context of age, sex, developmental trajectory, and overall physical health and does not represent an absolute, although a percent body weight of less than 85%, and/or a body mass index (BMI) less than 17.5, is a reasonable approximation of low weight for most patients.

NOTICE. Criteria set above contains only the diagnostic criteria and specifiers; refer to DSM-5 for the full criteria set, including specifier descriptions and coding and reporting procedures.

The second criterion has been rewritten to reflect the fact that many patients deny a fear of gaining weight or becoming fat, but their persistent behaviors suggest that they are nonetheless actively avoiding weight gain. Thus the possibility of inferring this criterion has been added. The third criterion has been rewritten to emphasize that the persistent lack of recognition of the seriousness of the low body weight problem is now explicitly a criterion for diagnosis. The amenorrhea criterion has been eliminated, although this remains a marker for severity in some studies.

Two specific types of anorexia nervosa—restricting type and binge-eating/purging type—continue to be listed, but only to serve as a guide regarding the classification of the current clinical episode. DSM-5 acknowledges that these types may be unstable, particularly in mode of onset, which may be of the restricting type but later may shift to the binge-eating/purging type and, ultimately, to bulimia nervosa. Therefore, type specifiers should be regarded as descriptive of the current symptomatology rather than necessarily indicating long-term patterns or outcome. Overall, however, about half of patients who are seen in clinical samples will fall under the restricting type, and about half will have problems with binge-eating and/or purging behavior.

The intense fear of gaining weight in anorexia nervosa is not ameliorated by weight loss; if anything, this fear seems to increase as patients lose weight. Many individuals will initially want to lose a modest amount of weight, which will then increase in amount as the weight loss progresses. Not uncommonly, many patients desire a weight of less than 100 pounds, but upon reaching that goal, the pattern of attempting to attain a lower weight continues.

Many times the body weight and shape disturbance criterion is misinterpreted to indicate that patients with anorexia nervosa feel globally obese, when in reality this is rarely the case. Most patients will be knowledgeable that certain body parts are too thin, but nonetheless will wish to lose weight in other body areas, particularly the buttocks, thighs, and abdominal area, which notably are the areas of most concern to normal-weight adolescent girls in our society.

Some of these patients will self-induce vomiting and others will use large amounts of laxatives to induce weight loss. In particular, stimulant-type laxatives are used as a way to induce a sense of weight loss. Some also will use diuretics and diet pills, although these are less common and more likely to be seen in those that engage in bulimic behaviors. A subgroup of about one-third of patients with anorexia nervosa also engage in compulsive and excessive exercise.

Epidemiology and Course

The point prevalence of anorexia nervosa in late adolescence and young adulthood in women is about 0.4% (Smink et al. 2012). The course of this disorder is highly variable (Keel and Brown 2010). We know that the long-term morbidity and mortality are substantial, and it has been frequently stated that the long-term mortality from anorexia nervosa is the highest of any psychiatric disorder. The most common causes of mortality are suicide and multiple organ system failure, the latter of which can assume a variety of forms. Many times the response to treatment is markedly delayed, and patients may continue to have problems with remissions and exacerbations of symptoms over many years before eventually recovering. Eventually many patients with anorexia nervosa will recover, but some will continue to have residual symptoms. Commonly these will reflect what appear to be personality traits, such as rigidity and perfectionism, and some will also have problems with interpersonal relationships. Others will achieve an excellent remission, resume menstrual functioning, and live happy and productive lives. Patients with a later age of onset who are severely ill for a longer period of time before being seen are more likely to have a worse prognosis, and in some studies binge-eating and purging symptoms seem to be negative prognostic indicators. There is also some evidence that very early onset cases in the prepubertal age range may have a worse prognosis and that anorexia nervosa may be increasing in this population.

Comorbid Psychopathology

Psychiatric comorbidity occurs frequently in all of the eating disorders. The form of comorbidity most commonly seen in patients with anorexia nervosa is mood disorders, in particular major depression. The assessment of major depression in this population can be problematic and is confounded by the fact that low body weight frequently results in mood changes, which include symptoms highly suggestive of a primary mood disorder. However, these symptoms may resolve with weight regain. Nonetheless, mood disorders, both current and lifetime, are prominent among patients with anorexia nervosa, and this may help to explain the high rate of suicide seen in patients with this disorder.

Anxiety disorders are also commonly seen in anorexia nervosa. In particular, social phobia, obsessive-compulsive disorder, panic disorder, agoraphobia, and generalized anxiety disorder are relatively common. It is of note that post-traumatic stress disorder seems to cluster primarily in those with the bingeeating/purging subtype, who have a higher rate of prior exposure to traumatic stress. Higher-than-expected rates of substance use disorders are also reported, and again these frequently cluster among those in the binge-eating/purging subtype.

Medical Complications

The medical complications of anorexia nervosa are summarized in Table 17-1 (Mehler et al. 2010; Miller 2011; Mitchell and Crow 2006). All major organ systems are affected; in particular, patients will experience marked cachexia and a generalized sense of weakness, despite the fact that some remain hyperactive.

Note, ↑ = increased; ↓ decreased; rT₃=reverse triiodothyronine; T₃=triiodothyronine.

Skin changes include the development of fine, soft, downy body hair called lanugo in areas of the body where body hair is frequently not found, such as the volar surface of the forearm or over the abdomen. This is the body's attempt to thermoregulate because of problems with maintaining core body temperature; however, many also will notice hair loss in the scalp area. Some will develop Russell's sign, which involves callus or scar formation on the dorsum of the hand due to self-inducing vomiting. Some will develop yellowing of the skin because of problems in metabolizing carotenes.

Many patients will have marked evidence of muscle wasting, and some will develop a myopathy, particularly those who have problems with ipecac abuse. Osteopenia and osteoporosis are unfortunately quite common, and available data suggest that many of the treatments that seem most logical for this problem, including vitamin D and calcium supplementation, as well as the use of hormonal replacement therapy, are generally not very effective, and the best available treatment appears to be weight gain.

As a result of starvation and the associated behaviors of anorexia nervosa, a variety of fluid and electrolyte abnormalities can also develop. Many of these involve dehydration, and in those who are self-inducing vomiting, this may include hypokalemia and hypochloremia. Metabolic alkalosis is common, but a subgroup of patients who abuse laxatives may also be periodically acidotic. Hypophosphatemia and hypomagnesemia are particularly problematic in low-weight patients early in the course of refeeding. These can be quite serious and contribute to a clinical situation known as the refeeding syndrome.

A variety of cardiovascular changes can be seen. Many of the patients will be hypotensive and bradycardic, although some will be tachycardic during periods of severe dehydration. They are at risk for various tachyarrhythymias and not uncommonly will have evidence of QT_C prolongation and ST-T wave abnormalities.

A variety of hormonal changes are seen. These patients tend to shift to reverse triiodothyronine (rT₃), which is a less metabolically active form of the thyroid hormone. Many will be hypocholesterolemic and hypercortisolemic. Amenorrhea is very common, and levels of follicle-stimulating hormone and luteinizing hormone as well as estrogen are usually quite low, as are testosterone levels in males. Libido is frequently reduced.

Renal changes include a reduction in glomerular filtration rate and impaired concentrating ability. Chronic renal disease is the long-term risk factor with this disorder.

Hematologically, the bone marrow undergoes atrophy with mucopolysaccharide deposition and loss of stem cells. White cell counts are generally reduced (in the range of approximately 3,500), although many patients will have evidence of a relative lymphocytosis because this cell type is relatively maintained. Some will have lowering of serum platelet levels.

A variety of gastrointestinal problems can be seen, including enlargement of the salivary glands. Superior mesenteric artery syndrome involves occlusion of the third portion of the duodenum during starvation because of the loss of the fat around the superior mesenteric neurovascular bundle, which crosses the duodenum. Patients who vomit regularly usually evidence dental enamel erosion. Gastric dilatation and rupture can occur, usually associated with binge eating, and esophageal rupture can occur in the context of self-induced vomiting. Some of these patients will report hematemesis. Intermittent constipation and diarrhea are quite common.

Peripheral neuropathies can develop. On magnetic resonance imaging scans many of these patients will show mild cerebral atrophy, and many also will evidence cognitive impairment that may or may not correlate with the degree of atrophy seen on scanning.

Overall, these are medically compromised patients who require very careful medical assessment and intervention, and medical stabilization remains the first priority.

Etiology and Pathogenesis

Anorexia nervosa is highly heritable, with a genetic risk higher than many psychiatric disorders, and this has led to a great interest in attempting to isolate particular genetic polymorphisms that may increase the risk for this disorder (Clarke et al. 2012; Helder and Collier 2011). In addition to genetic factors, cultural factors also seem to be extremely important. For many years anorexia nervosa was thought to be seen almost exclusively in Western industrialized societies where a very high value was placed on slimness as a model of attractiveness among young women. However, as American culture and Western ideas about the importance of thinness as an ideal of attractiveness have spread, cases of anorexia nervosa have increasingly been seen where they were thought to be relatively uncommon before, such as in China and India. Therefore, the model that is usually posited for anorexia nervosa implies that certain individuals at high genetic risk who also experience a high-risk environment may be at greatest risk to develop the disorder. Although many theories on the causes of anorexia nervosa in the past have focused on family pathology as an etiological factor, there are few data supporting this notion, and families in general are not regarded as the pathological mechanism that causes the disorder; however, families are clearly important in the treatment and recovery of patients.

Early family studies suggested the clustering of cases of anorexia nervosa within certain families, and subsequent twin studies suggest this may be the result of additive genetic effects. More recently there has been an emphasis on attempting to identify specific genes that might be involved. Various candidate genes have been studied, particularly those related to neurotransmitters and in neurodevelopment systems as well as those involved in regulatory peptides and their receptors and with body-weight regulation and obesity. Studies thus far have been replicated infrequently, and because of this the field now has moved on to focusing on genomewide association studies, which unfortunately require very large sample sizes and are also extremely expensive to conduct. Genes that have received particular attention involve the gene for brain-derived neurotrophic factor (BDNF), the agouti related peptide gene (AgRP), and the opioid delta receptor gene (OPDR1). There is also considerable interest in the glucagon-like peptide 2 receptor (GLP 2), which produces the gut-derived 33 amino acid glucagon-peptide. These studies thus far have suggested an association of certain genes with restricting-type anorexia nervosa, including the HTR1D gene, which codes for the serotonin receptor ID, and the OPRD1 delta opioid receptor gene as well as various other novel risk loci. There is also growing interest in focusing on epigenetic factors in the development of anorexia nervosa; this field is largely in its infancy but is of particular interest given the role of nutrition in anorexia nervosa and in particular prenatal and postnatal nutritional factors that may be involved.

Brain imaging studies have found through structural magnetic resonance imaging and voxel-base morphometry image analysis that people with anorexia nervosa appear to have reduced gray matter in a range of brain areas, which differs from what is seen in patients with bulimia nervosa. Given sample heterogeneity and sample sizes, the data are far from revealing a clear pattern at this point, although significant decreases have been seen in the best available studies fairly consistently.

Other work continues to focus on alteration in the function of neurocircuits in anorexia nervosa (Kaye et al. 2009), in particular, ventral versus dorsal neurocircuit dysfunction that may relate to the primary neurotransmitters serotonin and dopamine. There is also interest in the possibility that altered insular activity could explain the interoceptive dysfunction seen in these patients and that altered striatal activity may be important in understanding deficits in reward modulation.

There has also been a great deal of interest in peripheral peptidergic regulation of feeding in patients with eating disorders, including those with anorexia nervosa (Tong and DiAlessio 2011). A variety of hormone systems in the periphery are important in regulating both hunger and satiety, and a growing literature suggests that there may be changes in these appetite-regulating hormones in the periphery in this group of patients. In particular, peptide YY, cholecystokinin, various incretin peptides, and pancreatic polypeptide have been the focus of studies. Separating the findings in these studies from the effects of starvation, however, remains problematic, and this is an area in which research is only now developing.

Treatment

Anorexia nervosa has been the focus of ongoing treatment research for an extended period of time, yet it remains difficult to treat, and generalizations about the best available treatments are difficult to make (Aigner et al. 2011; Bulik et al. 2007). Several factors have contributed to these problems with effective treatment research (Halmi et al. 2005). One is the relative rarity of the disorder compared with many psychiatric conditions. A second and particularly perplexing problem is that many of these patients are not particularly motivated for treatment and are not interested in gaining weight or in actively cooperating in any psychotherapeutic interventions, including research-based interventions. This tends to result in very low compliance and very high dropout rates.

First in any treatment sequence, and of paramount importance, is medical stabilization. Frequently, when patients present with anorexia nervosa, their weight is markedly compromised and they are medically unstable; therefore, the first goal of therapy must be to ensure medical safety. Not uncommonly, a variety of organ systems will need to be addressed, including the fluid and electrolyte system and others. This can, at times, be difficult and complicated. For example, patients with anorexia nervosa are clearly at risk for developing complications during medical stabilization. The refeeding syndrome has been reported in these patients relatively frequently. Symptoms appear early in the course of the intake of additional calories; they may be precipitated by a variety of complications, including hypomagnesemia and hypophosphatemia, and may result in congestive heart failure. Consequently, the early stages of refeeding should be done in specialized settings for medically compromised patients at very low weight, and they should be regarded as requiring intensive medical monitoring.

Beyond stabilization, much of the emphasis shifts to initiating refeeding and renutrition. Although clinicians have favored approaches wherein they would progress slowly, with gradual increases in calorie counts as the patient adjusts, some more recent literature suggests that a more aggressive approach may be useful as well and may reduce hospital stay durations (Garber et al. 2012). Again, as experience continues to accumulate, it is clear that many patients are initially quite sensitive to weight gain early during refeeding, and this may be attributable to rehydration. Beyond that, energy expenditure will increase dramatically as patients ingest more calories, and therefore the kilocalories ingested must be increased as well, sometimes rather dramatically, to encourage continued weight gain.

Although attempts are made initially to treat many patients with anorexia nervosa outside of the hospital setting, inpatient treatment or partial hospital treatment often will be necessary. This is particularly true for patients at a very low weight for whom refeeding is potentially risky and requires intensive monitoring. Some patients who are initially treated as outpatients may later need transfer to inpatient or partial hospital programs. Generally, programs that specialize in the care of these patients and are staffed with clinicians who are skilled in managing refeeding paradigms and potential complications are the preferred venue for initial intervention therapy.

In such settings, some of the emphasis will be placed on positive reinforcement for weight gain and, when possible, the elimination or minimization of behaviors designed to compensate for food intake, such as self-induced vomiting or laxative abuse. Because of this, highly structured facilities are generally needed.

A variety of counseling approaches have been utilized, and to some extent, these appear to be differentially effective for adolescents, for whom caregivers are available at home, and adults. We discuss first the treatment of adolescents with anorexia nervosa. A growing literature suggests that this population may be best treated using family-based approaches (Fisher et al. 2010; Lock 2011). The family approach that has received the most study is the so-called Maudsley Approach, which was originally developed at the Maudsley Hospital in London and now has been widely employed in the United States and elsewhere. This is a highly structured, manual-based approach that requires a therapeutic staff highly skilled in the management of these patients and an active program of involving the family in the patients' management. Parents are encouraged initially to take control of the individual's eating behavior and other behaviors. As the patient gains weight and can assume responsibility, the focus shifts toward more traditional issues such as family and personal problems and more general adolescent issues. This approach clearly requires more research, but the empirical data base is growing impressively.

Other approaches that have been tried and appear to have some utility are largely applicable to adults with this disorder. Cognitive-behavioral therapy (CBT) is popular and is usually used as a relapse prevention approach, particularly in weight-restored individuals. This is superior to simple nutritional counseling alone (Pike et al. 2010); however, as a treatment for the low-weight anorexia nervosa patient CBT is less well established.

As opposed to many areas in psychiatry, the use of pharmacotherapy appears to have limited utility with this group of patients (Aigner et al. 2011). Historically, when antipsychotic drugs became available, they were used in some early trials, as was cyproheptadine, a drug that tends to promote weight gain. The data for these compounds were limited and have not supported the compounds' utility as ongoing therapies. The use of tricyclic antidepressants has also been employed, and the literature here indicates that many of these drugs were poorly tolerated and not particularly useful.

More recently, interest has focused on the use of serotonin reuptake inhibitors (Bulik et al. 2007). The available data do not show a significant benefit for these agents in low-weight patients with anorexia nervosa, and there are no compelling data for their utility in relapse prevention in weight-restored patients, although certain isolated patients may respond well, particularly if they have co-morbid severe depressive symptoms. The routine use of such agents, however, cannot be recommended.

There has also been a growing interest in the use of atypical antipsychotics, such as olanzapine, that promote weight gain in other populations (Attia et al. 2011). Although the literature here is limited, there are some data suggesting these agents can be helpful for some patients. Their clinical utility appears to be greatest in patients with treatment-resistant illness who have a great deal of trouble with weight regain. One of the problems is that many patients become knowledgeable about these drugs after reading about them on the Internet or hearing about them from other patients, and therefore many are not willing to take them or to be compliant with their use out of fear of weight gain.

In summary, the role of pharmacotherapy is clearly limited in patients with anorexia nervosa. Overall, much additional research is needed on the treatment of these patients both psychotherapeutically and pharmacologically; currently, the available treatment should be seen as in development, and the field is clearly in need of additional innovation.

Bulimia Nervosa

Bulimia Nervosa

Case Presentation

R.L. was a 24-year-old white female college student who presented for treatment at the student health service at her university with symptoms suggestive of bulimia nervosa. She reported that she had always worried a great deal about her weight and that despite having a normal weight for her height, she was dieting much of the time during adolescence and young adulthood. She felt that her self-esteem was solely based on her weight, and she continually worried that she would gain weight and become obese.Beginning in her early 20s, she would try to fast for extended periods of time, but then noticed she would have breakthrough periods during which she would eat large amounts of food in a very short period of time, including foods that she would normally not eat because she considered them too high in fat and calories. She had a distressing sense of loss of control during these episodes. She had read an article about bulimia nervosa and thought that perhaps a solution to her concern was to self-induce vomiting after overeating. She found she could do this relatively easily. This behavioral pattern initially occurred rarely, perhaps once a month, but the behavior continued to escalate in frequency over time, and by the time she sought evaluation and treatment, she was binge-eating and purging at least daily and sometimes several times a day. She would go to the grocery store, furtively bring the food to her dormitory room, and in secret eat large amounts of food, and then make herself vomit. Initially she believed that it would be relatively easy to control the behavior. She thought that the behavior was very helpful in terms of her weight control concerns. Eventually she came to realize that the binge-eating and purging were becoming habitual and had come to dominate her life. Because of the behavior, she frequently isolated herself from her friends and canceled social engagements. She found that she was not doing as well academically as she had been doing before the behavior began. She also found that she was developing symptoms of depression, including low mood, problems sleeping, anxiety, and feelings of hopelessness. She entertained the idea that perhaps the way out of her problem would be to take her own life. She realized that she was becoming increasingly isolated and unhappy and started noticing that she was developing physical symptoms as well. Her teeth seemed quite sensitive to the ingestion of liquids, and she started having bouts of diarrhea and constipation. In general, she did not feel healthy. Eventually she decided that the behavior was out of her control and that she needed evaluation and treatment.

Diagnosis

Bulimia nervosa is an eating disorder characterized by problems with binge eating followed by compensatory behaviors, such as self-induced vomiting and laxative abuse. This disorder was characterized as a distinct psychiatric disorder in 1979 by Russell. Since that time a fairly large literature has accumulated concerning the disorder (Crow and Brandenburg 2010).

The DSM-5 diagnostic criteria for bulimia nervosa are shown in Box 17-5. There have been some changes since DSM-IV. The criterion regarding binge eating remains essentially unchanged and describes eating, within a discrete period of time, an amount that is definitely larger than most people would eat during a similar period of time. The criterion further stipulates that the eating must be accompanied by a sense of loss of control. Clinicians and researchers are focusing on the sense of loss of control as a particularly significant variable, perhaps of even greater importance than the objective amount of food actually ingested. Some individuals will engage in what are known as subjective bingeeating episodes wherein the amount of food ingested is not objectively large but the sense of loss of control is present.

Patients with bulimia also engage in inappropriate compensatory behaviors to prevent weight gain, most commonly self-induced vomiting, which occurs in about 90% of patients, as well as using stimulant-type laxatives as a way of inducing diarrhea and causing a sense of weight loss. This is not uncommon, and in various empirical studies it seems to characterize 40%-60% of patients with bulimia nervosa. Diuretics are also occasionally used as weight-control techniques. Most often this involves the use of the over-the-counter diuretics, most of which are fairly impotent, but at times patients use prescription diuretics, which are more potent and more dangerous. Over-the-counter diet pills are frequently used, but often only for short periods because of their relative inefficacy and cost. Some patients will also fast all day or for several days. Excessive exercise is used by a subgroup of these patients as well. Also of note, insulin-dependent patients with diabetes mellitus may restrict their insulin use as a way of inducing glucosuria and causing weight loss, a particularly dangerous behavior that can result in severe sequelae of the diabetes such as neuropathy and retinopathy. Other behaviors that are sometimes seen include the rumination (i.e., regurgitation and reswallowing) of food, the use of enemas in an attempt to get rid of calories and weight, and rarely the use of saunas as a weight-control technique.

In DSM-5, the binge-eating and compensatory behaviors must occur on average at least once a week for 3 months, because the data supporting the twice-a-week criterion in DSM-IV were really not compelling, and once a week appears to be a more useful cut point. Individuals with bulimia nervosa also are very worried about weight and shape issues, and this disorder cannot occur during the course of anorexia nervosa. The subtype diagnoses of purging versus nonpurging bulimia nervosa have been eliminated in DSM-5 due to the lack of data supporting the nonpurging construct.

Epidemiology and Course

All of the available literature suggests that bulimia nervosa is more common than anorexia nervosa and develops in approximately 2% of women as they traverse late adolescence and young adulthood, although the figures vary widely across cultures and, to some extent, over time.

The course of bulimia nervosa appears to be more benign than the course of anorexia nervosa, and long-term outcome studies suggest that many patients with bulimia nervosa will eventually recover (Steinhausen and Weber 2009). However, available data also suggest that many patients with bulimia nervosa will recover more quickly with treatment and that in long-term follow-up studies a number of patients, particularly those who have not been exposed to effective treatment, will remain symptomatic. Although onset of the disorder tends to occur in late adolescence or young adulthood, both earlier-onset and later-onset cases have been reported. The male-to-female ratio is approximately 10:1 to 20:1, but it must be underscored that bulimia nervosa can occur in males, and some of the epidemiological data suggest that the disorder appears more commonly in males than would be assumed based on clinical studies, suggesting that many males do not seek treatment, although they may be symptomatic.

Although generally regarded as more medically benign than anorexia nervosa, recent research suggests that the mortality and morbidity from bulimia nervosa are also substantial and that the rate of premature death is significantly higher than in control populations. Consequently, bulimia nervosa should also be regarded as a potentially lethal disorder (Crow et al. 2009).

Comorbid Psychopathology

Lifetime rates of mood disorders are particularly high in patients with bulimia nervosa. Of interest, many of the treatments that have been designed for bulimia nervosa, including CBT and antidepressant treatment, can be quite effective in improving mood symptoms as well, although their mechanism of action is not necessarily dependent on comorbid depression. Suicidality is also higher than expected in this population.

A high rate of anxiety disorders is also seen, including posttraumatic stress disorder, with as many as 37% of adults with bulimia nervosa reporting unwanted sexual experiences early in life. Substance use disorders are also increased among bulimia nervosa patients, and this can be a major problem in organizing successful treatment efforts.

Medical Complications

Medical complications occurring in bulimia nervosa are summarized in Table 17-1. Significantly fewer medical complications are associated with bulimia nervosa than with anorexia nervosa, and the complications themselves are usually less severe. Problems with malnutrition are generally minimal, if present at all. However, some patients will still have lost a significant amount of weight and will have problems with complaints such as weakness and dizziness.

As with anorexia nervosa, Russell's sign can be seen in those who self-induce vomiting and use their hand to induce the gag reflex. Hair loss is common. Some data suggest that osteopenia can also develop in these patients, although usually the degree of severity is much less than that seen in those with anorexia nervosa.

Given the compensatory behaviors involved, a variety of fluid and electrolyte abnormalities can occur, including dehydration, hypochloremia, hypokalemia, and metabolic alkalosis, although acidosis can also be seen in those who abuse laxatives or diuretics. The cardiovascular effects again are usually attenuated relative to those seen in patients with anorexia nervosa, but hypotension can been seen, as can tachycardia with the associated dehydration. Arrhythmias can rarely result from fluid and electrolyte abnormalities, and occasionally electrocardiographic changes are seen as well.

The neuroendocrine axes are usually much better preserved in these patients compared with those with anorexia nervosa, although there is some evidence that many patients will develop hypercortisolemia, and irregular menses is common, although frank amenorrhea is usually not seen. Renal complications are usually modest, although some patients will report symptoms suggestive of urine concentrating ability problems.

The hematological system is usually not severely affected. However, a variety of gastrointestinal symptoms are seen, including parotidomegaly and dental enamel erosion (which is quite common in patients who self-induce vomiting and usually is one of the easiest identifiable signs). Gastric dilatation and esophageal rupture are rarely seen, although both can be quite severe and should be considered medical emergencies. Constipation and diarrhea, at times alternating, also can be seen.

Therefore, given the fact that medical complications are usually modest, the need for medical intervention in this condition is more limited, although medical screening is clearly necessary. Fluid and electrolyte abnormalities may be particularly common and problematic and may require intervention.

Etiology and Pathogenesis

Bulimia nervosa is also significantly heritable, although in most of the available literature the heritability is lower than that calculated for anorexia nervosa. Some literature suggests that there is a heritable diathesis toward the development of either anorexia nervosa or bulimia nervosa and that both tend to cluster in the same families.

Again, cultural issues appear to be quite important in the development of bulimia nervosa. This is a disorder that tends to be seen primarily in societies where a very high value is placed on slimness as a model of attractiveness for women. As a result, bulimia nervosa also appears to have been increasing in prevalence in areas of the world where it was seen relatively infrequently before Western media became such a dominant influence, although some data suggest this trend may be leveling off.

Given the right genetic susceptibility and environmental conditions, why certain individuals develop bulimia nervosa and others do not remains a source of considerable interest and controversy. It does appear that a number of girls during their teenage years will be quite preoccupied with weight and shape issues, and many may be dieting unnecessarily even if they are at normal weight. However, precipitation of the full pattern of bulimia nervosa appears to be relatively rare, and why this seems to develop in only a subgroup of this population remains the focus of considerable research.

The genetic findings in bulimia nervosa are relatively modest compared with the data on anorexia nervosa; however, both twin and family studies suggest significant heritability. Candidate gene studies have focused on systems involved in the release of or metabolism of the various monoaminergic neurotransmitters and, more recently, peptidergic regulatory systems. None of the associations thus far can be considered unequivocally established, although this is an area of great research. More recently, genome-wide association studies have been used, and this may be particularly fruitful in bulimia nervosa as well as anorexia nervosa.

Dysregulation of gastrointestinal peptides may be operative in patients with bulimia nervosa, and the results thus far have been fairly wide ranging. Overall, studies of the appetite-stimulating peptide ghrelin have not yielded significantly different levels in patients with bulimia nervosa compared with healthy control subjects, but suppression of cholecystokinin and ghrelin postprandially may be reduced in bulimia nervosa, suggesting a finding that may predispose to the continuation of the eating behavior and an impaired sense of satiety.

In brain imaging studies, the available literature suggests that those with bulimia nervosa have increased gray matter volumes in frontal and ventral striatal regions. A number of limitations may have contributed to the lack of consistent findings in this literature, including the heterogeneity of samples and the small sample sizes often studied as well as variations in the methodologies involved. However, the findings in bulimia nervosa appear to be quite divergent from those with anorexia nervosa.

In summary, relative to patients with anorexia nervosa, the data on the psychobiology of bulimia nervosa are less well developed, although many of the same systems and anatomic structures are of interest, and research in this area remains active and ongoing. As our understanding of the biology of feeding, appetite, satiety, and weight control continues to expand, this will prove to be an exciting area of research.

Treatment

The treatment literature on bulimia nervosa has blossomed since the original description of this disorder in 1979, and a considerable amount of information is available concerning what treatments are effective, particularly for adults. Much of the treatment literature for bulimia nervosa has focused on either pharmacotherapy or psychotherapy, with some literature addressing the relative efficacy of these approaches in combination.

Pharmacotherapy

A growing and impressive literature suggests that antidepressant medications can be quite effective in suppressing many of the symptoms of bulimia nervosa. Studies suggest this is true for a variety of agents, including tricyclic antidepressants, monoamine oxidase inhibitors, and—more recently and of particular clinical importance—serotonin reuptake inhibitors. The only drug that is currently approved by the U.S. Food and Drug Administration for treatment of bulimia nervosa is fluoxetine. Of note, in using serotonin reuptake inhibitors, higher dosages than are frequently used for depression are usually employed and appear to have some advantage over lower dosages. For example, a dosage of 60 mg/day of fluoxetine hydrochloride is used for bulimia nervosa, versus 20 mg/day for depression, and patients can be initiated at this dosage if desired.

Although the results with antidepressants are impressive in terms of reductions in the frequencies of target symptoms, the number of patients who are actually free of bulimic symptoms at the end of treatment remains a minority, and long-term follow-up studies suggest that many patients may be noncompliant with these medications over time. Therefore, although the drugs clearly have a place in the treatment of bulimia nervosa, overall they are regarded as less effective than psychotherapy approaches, which are usually the recommended treatment of choice (Mitchell et al. 1990). Pharmacotherapy is indicated for patients who do not respond adequately to psychotherapy approaches, who are severely depressed at baseline, or who have some other indication for these medications. Other medications also are being studied in bulimia nervosa, with a few studies focusing on the use of topiramate, which appears to have efficacy although it can be difficult to use.

Psychotherapy

A wide variety of psychotherapies with various theoretical bases have been employed in bulimia nervosa. CBT has been most widely utilized in both group and individual formats and is generally considered to be the best-established therapy for bulimia nervosa. It appears to result in higher remission rates than are commonly seen in pharmacotherapy approaches for this disorder (Fairbum 1981). Interpersonal therapy has also been shown to be quite effective for bulimia nervosa, although the research data base here is more limited. This is quite interesting both clinically and theoretically and suggests that an approach that does not directly target eating behaviors might be effective in the treatment of these patients. A growing literature suggests that dialectical behavior therapy also may be effective for some patients with bulimia nervosa. Patients who have problems with impulse control and who may have comorbidity that includes personality disorders may be a group of interest to target with this approach.

Given the fact that remission rates with CBT and other available therapies are lower than one would desire, a new generation of studies is developing that examines modifications of existing therapies or new therapies. One of these is enhanced cognitive-behavioral therapy (CBT-E), developed by Fairburn et al. (2009), which expands on previous CBT techniques to include more attention to depression tolerance, perfectionism, interpersonal problems, and low self-esteem. The available literature on the efficacy of this approach remains limited. Another approach that is receiving increased attention is integrative cognitive affective therapy, which in preliminary reports appears to offer great promise, although additional work regarding this approach is needed.

When one examines the components of various cognitive-behavioral approaches, some generalizations can be made regarding the ingredients that seem to be important. These include the following

1. Self-monitoring. Most experts in the field agree that self-monitoring is an extremely important part of therapy. Many patients are not particularly cognizant of their behaviors, and although most are resistant to self-monitoring, this exercise can be very helpful in allowing the patient and the therapist to understand the details of the individual patient's behavioral pattern.
2. Meal planning. The implementation of highly structured meal plan techniques can be quite useful, because many of these patients are eating inadequately at times when not overeating. Many have developed elaborate rituals regarding feeding and are convinced that if they eat regular balanced meals they will gain weight. The substitution of a regular meal pattern and regular balanced meals and snacks can go a long way in terms of improving eating behavior.
3. Cues and consequences. There is usually a strong emphasis placed on the examination of cues and consequences of bulimic behaviors, in particular the antecedents that may precede the behaviors, which commonly include boredom and strong affective states.
4. Cognitive restructuring. Some patients take readily to this approach, whereas others have more difficulty understanding and employing it and tend to do better with a more clearly delineated behavioral paradigm. However, cognitive restructuring particularly related to weight and shape issues and attitudes toward food can be very useful for the majority of patients, whose self-esteem many times relies on body weight issues and who have peculiar attitudes toward food.

Additional elements that are commonly used include assertiveness training, specific work on body image, and a focus on problem-solving skills. Therapy generally concludes with a period of focus on relapse prevention techniques, with the hope of preventing redevelopment of symptoms at a later time. The available data suggest that, analogous to several other kinds of problematic behavior patterns, the relapse rate is highest in the first few months after treatment; therefore, patients are encouraged to be vigilant during this time and to pay particular attention to maintaining normal eating behavior. Additional therapy visits during this time also can be quite useful (Mitchell et al. 2002).

Binge-Eating Disorder

Binge-Eating Disorder

Case Presentation

S.J. was a 62-year-old married mother of one who lived at home with her husband. Her adult son had a chronic physical illness but lived independently. She grew up in a family consisting of both parents, a sibling, and an uncle who lived with the family frequently. She described her early family life as disengaged and fundamentally nonsupportive. Her mother had died when she was a teenager, and her uncle had sexually assaulted her during her adolescence on several occasions. She indicated that after leaving the home she became increasingly concerned about her appearance and her relationships with men. She frequently dieted throughout her teenage years and continued into young adulthood. She entered a relationship with a man that was emotionally very significant to her, and she was committed to this man for a number of years. However, they never married, which was a significant disappointment to her. She began binge eating during this period of her life in what she considers an effort to "numb out." She continued to be concerned about her appearance. She never lost a considerable amount of weight and never engaged in any significant purging behaviors. Eventually, she entered into several other relationships, one of which involved the father of her son. As she raised her son as a single mother, she gained weight, which was very distressing to her and resulted in frequent dieting behavior. Ultimately, she met her current husband and had been happily married for more than 15 years. Over the past decade, she had struggled more significantly with weight gain and periodic binge eating. Her binges included relatively large amounts of food, such as 10 cookies, 3 cans of soda pop, and a piece of pie. Following such eating episodes, she felt ashamed and embarrassed. As she reached 60 years of age, she made a commitment to attempt to reduce her binge-eating behavior and stabilize her weight. This resulted in her seeking treatment at an eating disorder clinic, where she was treated with a CBT plan that helped her abstain from binge eating.

Diagnosis

Binge-eating disorder was originally included in Appendix B of DSM-IV as a diagnosis in need of further study, but it was recommended for inclusion in DSM-5 as a diagnosis in the category of feeding and eating disorders. In the 19 years since publication of DSM-IV, there has been a substantial amount of empirical research clarifying the psychopathology of this condition, as well as refinements in diagnostic criteria and treatment approaches.

The DSM-5 diagnostic criteria for binge-eating disorder are presented in Box 17-6. The DSM-5 diagnostic criteria are identical to those included in DSM-IV, with the exception that the minimum frequency of binge eating has been reduced from 2 days per week over a period of 6 months to one binge-eating episode per week for a period of 3 months. Similar to bulimia nervosa, binge eating is defined as eating an amount of food that is definitely larger than most people would eat in a similar period of time, and such episodes are characterized by a sense of loss of control over eating. As can be seen in the diagnostic criteria, binge-eating episodes also are characterized by at least three variables thought to reflect the essence of binge eating (i.e., rapid eating, disgust after binge eating, eating until uncomfortable). Additionally, individuals with binge-eating disorder experience significant distress after the episode and, by and large, do not engage in inappropriate compensatory behavior.

Although not included in the diagnostic criteria, other characteristics of bingeeating disorder include the presence of subjective binge-eating episodes in which the person feels out of control but the quantity of food ingested is not objectively large. Also, individuals with binge-eating disorder often attempt to restrict their caloric intake early in the day and binge-eat later in the day (Raymond et al. 2003). Although concerns about shape and weight are not included in the diagnostic criteria, it is increasingly recognized that a subset of individuals with binge-eating disorder experience significant concerns about shape and weight, and this cognitive component may reflect a more severe variant of binge-eating disorder that has a more complicated course and is less responsive to available treatments (Grilo et al. 2008).

Epidemiology and Course

The prevalence of binge-eating disorder has varied across different populations (Smink et al. 2012). For example, in a European study the prevalence was estimated to be 1.9% for women and 0.3% for men (Preti et al. 2011). In a comprehensive U.S. study with a nationally representative sample, prevalence was estimated to be 3.5% among women and 2.0% among men (Hudson et al. 2006). Although the highest rates appear to be in adults, there is also evidence that adolescents between the ages of 13 and 18 years display significant binge-eating behavior, with girls at greater risk than boys (Hudson et al. 2007).

Mortality studies are relatively rare in the binge-eating disorder literature. One 12-year follow-up study of binge-eating disorder reported a crude mortality ratio of 2.9% and a standardized mortality ratio of 2.29% (95% confidence interval [CI] = 0.00-5.45) (Fichter et al. 2008). Alternatively, significantly more studies have examined the relationship of binge-eating disorder and obesity. Estimates converge in suggesting that at least two-thirds of individuals with binge-eating disorder meet criteria for obesity (BMI>30 kg/m²) and also display an increased rate of severe obesity (BMI>40 kg/m²). Attempting to separate the negative health effects of binge-eating disorder from the effects of obesity is important in understanding the health-related risks of binge-eating disorder. In fact, there is evidence to suggest that binge-eating disorder does confer risk for negative medical outcomes beyond the effects of obesity. Finally, although suicide rates appear elevated in anorexia nervosa and bulimia nervosa, the relationship of binge-eating disorder and suicide risk remains unclear. One meta-analysis found no suicides among 246 patients with binge-eating disorder after 5.3 years of follow-up (Preti et al. 2011). However, in a recent latent class analysis, Crow et al. (2012) identified a group of individuals with eating disorders that were phenotypically consistent with binge-eating disorder who displayed increased rates of early death.

Comorbid Psychopathology

Similar to other eating disorder diagnoses, binge-eating disorder is characterized by high rates of other co-occurring psychiatric disorders. Numerous empirical studies have utilized structured interviews to estimate rates of comorbid psychopathology (e.g., Crucza et al. 2007; Hudson et al. 2007), and although there is some variability, several themes are consistently identified. For example, as in bulimia nervosa and anorexia nervosa, the most common comorbid psychiatric disorder diagnosis is depression, which affects about 50% of individuals with binge-eating disorder. Additionally, there are reasonably high rates of anxiety disorders, particularly panic disorder and simple phobia, although rates of obsessive-compulsive disorder and social phobia appear somewhat lower than in other eating disorders. Approximately 20%-25% of individuals with binge-eating disorder also display significant substance use disorder, most typically alcohol use disorder. There is also epidemiological evidence suggesting that binge-eating disorder may be associated with impulse-control disorder and attention-deficit/hyperactivity disorder, but these associations are not as frequently studied as other common comorbidities.

Over the past decade, a series of studies examining the presence of personality disturbance among individuals with bingeeating disorder has been conducted (Cassin and von Ranson 2005). Typically, avoidant, borderline, and obsessive-compulsive personality diagnoses are the most common. Evidence also suggests that avoidant and obsessive-compulsive personality traits are strongly associated with the presence of mood and anxiety symptoms. Clearly, binge-eating disorder is characterized by a wide range of diverse psychiatric comorbidities, which highlights the possibility that there is considerable heterogeneity within the diagnosis based on different patterns of co-morbid psychopathology. The notion of subtypes of binge-eating disorder is beginning to emerge, similar to what has been seen in anorexia nervosa and bulimia nervosa. For example, presentations vary substantially in terms of overvaluation of shape and weight, but there is also evidence of subtypes that vary in terms of relative intensity of dimensions reflecting dieting and affective disturbance (Grilo et al. 2001). Additionally, one recent study (Peterson et al. 2012) identified three sub-types of binge-eating disorder based on personality traits and psychiatric comorbidity dimensions, all of which suggest that binge-eating disorder may be a common pathway for diverse presentations with markedly different groupings of associated psychopathology.

Medical Complications

The relationship between binge-eating disorder and various medical consequences is complicated by the tendency for binge-eating disorder individuals to be overweight or obese. Consequently, the direct contribution of binge eating to the numerous medical complaints of this patient population is difficult to ascertain. Binge-eating disorder has been associated with several metabolic, orthopedic, and sleep-related problems. Furthermore, significant evidence suggests that these patients consume more health care resources than other individuals, even after controlling for body weight. Recent evidence suggests that there is variability within the binge-eating disorder diagnosis in terms of metabolic consequences. Several studies converge to suggest that patients with binge-eating disorder who have a history of dieting and food restriction are less likely to show the key components of metabolic syndrome than are individuals without such a history. However, many of the studies examining the relationship between binge-eating disorder and medical complications are limited methodologically. For example, most studies rely on patients' self-report of various medical illnesses rather than ascertainment of illness through objective medical examinations, which limits confidence in the assessment of various illnesses (Wonderlich et al. 2009). Furthermore, very few prospective longitudinal studies have been designed to examine the long-term implications of bingeeating disorder and overall physical health. It is hoped that with the addition of binge-eating disorder to DSM-5 there will be an increase in empirical studies examining the medical consequences of this disorder.

Etiology and Pathogenesis

Like all eating disorders, the etiology of binge-eating disorder is typically considered multifactorial in nature. For example, there is recent evidence of possible genetic influences based on family history studies that indicate the disorder tends to run in families, even after controlling for levels of obesity (Hudson et al. 2006). Furthermore, examinations of these family studies imply that the similarities within families regarding bingeeating disorder behavior seem to be significantly influenced by additive genetic effects. Additionally, there is evidence of an increased risk from cultural factors, particularly regarding weight and shape ideals. Several studies suggest that a significant fraction of individuals with binge-eating disorder display marked overvaluation of shape and weight and, furthermore, that the presence of this feature seems to predict a particularly severe form of the disorder that is resistant to typical treatment. Additionally, there is evidence that individuals with binge-eating disorder may be susceptible to the effects of stress. For example, in laboratory-based studies that induced stress in participants before eating, there is some evidence that individuals with bingeeating disorder were particularly prone to display aspects of binge eating after stressful experiences.

Similarly, growing evidence suggests that individuals with the disorder are particularly likely to binge eat after periods of significant negative emotion and that they may have deficits in decision making that result in a disinhibited behavioral style that may increase the risk of binge eating (Svaldi et al. 2010). This propensity for increased levels of disinhibition is also consistent with recent functional magnetic resonance imaging studies implicating abnormalities in prefrontal circuits that influence self-regulation among individuals with bingeeating disorder (Schienle et al. 2009). Additionally, there is considerable interest in the idea that these individuals display impairments in reward-related brain circuitry much like the impairments seen in those with substance use disorders. Finally, there is also the idea that binge-eating disorder may be associated with abnormalities in various peptides and hormones that influence feeding behavior (e.g., Geliebter et al. 2004). Several studies have examined the relationship between binge-eating disorder and ghrelin, but no consistent pattern of results has yet emerged. Similarly, a variety of different studies have examined the relationship between binge-eating disorder and the stress hormone cortisol, but again there has been considerable variability in the outcomes. Consequently, the etiology and pathogenesis of binge-eating disorder remains complicated and appears influenced by a variety of genetic, cultural, and psychobiological factors.

Treatment

Several recent reviews (Sysko and Walsh 2008; Vocks et al. 2010) and the guidelines from the National Institute of Clinical Excellence have documented numerous treatments with demonstrated efficacy in the treatment of binge-eating disorder. Typically, the treatments can be grouped into three broad categories: psychotherapy or behavior therapy, pharmacological interventions, and weight-loss interventions. Psychotherapeutic or behavior therapy interventions are typically thought to be the most efficacious in terms of reducing binge-eating frequency and improving comorbid conditions, such as depression and anxiety. CBT tends to focus on enhancing normal meal consumption and reducing inaccurate or unproductive cognitions about food, shape, or weight-related themes. Interpersonal psychotherapy has been shown to be efficacious as well; although short-term and structured like CBT, it focuses almost exclusively on relationship problems and interpersonal patterns of behavior thought to precipitate binge-eating episodes. Recent evidence suggests that the gains obtained through these interventions are maintained at 4-year follow-up, suggesting that such specialty treatments are not only efficacious but enduring in their effects (Hilbert et al. 2012). Another type of behavior therapy intervention is guided self-help, which generally relies on cognitive-behavioral principles, but much of the intervention is conducted in a self-help format with periodic meetings with a professional to facilitate treatment efficacy (i.e., "guided"). Recent studies suggest that guided self-help may be as efficacious as group-oriented therapies, but future studies of the utility of such a minimal resource intervention need to be conducted with active-treatment comparison conditions rather than no-treatment or minimal-treatment comparisons.

A large number of medications have been tested in binge-eating disorder treatment trials. These drugs typically have previously been used to treat comorbidity associated with the disorder, such as mood and anxiety disorders (e.g., selective serotonin reuptake inhibitors), obesity (e.g., topiramate, zonisamide), substance use disorder (e.g., acamprosate), and attention-deficit/hyperactivity disorder (e.g., atomoxetine). These drugs have targeted a variety of possible mechanisms, including systems regulating serotonin, norepinephrine, and glutamate, and recently several trials have been initiated with agents that target dopaminergic pathways (e.g., bupropion, pramipexole). However, the list of generally accepted and effective agents for the treatment of binge-eating disorder is relatively short. The task force on eating disorders of the World Federation of Societies of Biological Psychiatry (Aigner et al. 2011) suggested that imipramine, sertraline, citalopram/escitalopram, and topiramate all had significant evidence of efficacy. Findings for fluvoxamine and fluoxetine were much less supportive. Furthermore, recent trials have failed to provide support for the utility of acamprosate.

There is also evidence that weight loss strategies can reduce binge eating, at least in the short rim. For example, very-low-calorie diets not only promote weight loss but also significantly reduce binge-eating frequency despite the fact that there is no binge eating-specific intervention involved. However, treated participants tended to regain most of their weight within 1 year, although a significant fraction of the treated patients continued to display a reduction in binge-eating behavior. More recently, comparisons between specialty treatments for binge eating (CBT or interpersonal therapy) and behavioral weight loss treatments have suggested that the former do confer greater benefit in terms of binge-eating reduction than the latter (Wilson et al. 2010). However, it is important to note that although such specialty treatments do display efficacy in terms of reduction in binge-eating frequency, their impact on weight loss remains minimal and is a significant limitation of available treatments for binge-eating disorder.

Other Specified or Unspecified Feeding or Eating Disorder

The category of other specified feeding or eating disorder (Box 17-7) or unspecified feeding or eating disorder (Box 17-8) is applied to clinically significant presentations of feeding or eating disorder symptoms that are atypical, are mixed, or do not meet full criteria for a feeding or eating disorder diagnosis.

The category of other specified feeding or eating disorder is used when the clinician chooses to state why the symptoms do not meet full criteria for a specific diagnosis. Examples of presentations to which this category might be applied include atypical anorexia nervosa, bulimia nervosa of low frequency, and binge-eating disorder of limited duration. Atypical anorexia nervosa is characterized by significant weight loss, but the individual remains within or above the normal weight range for age and height. In subthreshold presentations of bulimia nervosa or binge-eating disorder, the frequency and/or duration of the eating disorder behaviors is below that required for the full syndrome diagnosis. Additional syndromes that could receive an "other specified" designation include purging disorder, characterized by recurrent purging behavior to influence weight or shape in the absence of binge eating, and night eating syndrome, which involves recurrent episodes of awakening from sleep to eat or excessive food consumption after the evening meal and into the evening.

Finally, the category of unspecified feeding or eating disorder is used in situations where the clinician does not wish to specify the reason why criteria for a specific disorder are not met, or in cases where there is insufficient information to make a more specific diagnosis.

Conclusion

There have been substantial and clinically important changes in the eating disorder diagnoses that are included in DSM-5. A particularly noteworthy addition is avoidant/restrictive food intake disorder, which based on early studies is not an uncommon problem and will allow clinicians to better understand, classify, and hopefully treat this rather heterogeneous and complex group of patients. The diagnostic criteria for anorexia nervosa and bulimia nervosa have been changed, and binge-eating disorder has now been added as a full-fledged diagnosis following 20 years of meaningful research supporting the construct as a distinct entity.

Key Clinical Points

• Binge-eating disorder is now a DSM-5 psychiatric diagnosis.
• Avoidant/restrictive food intake disorder has been given diagnostic status and should help to clarify the diagnosis and treatment of various eating problems usually seen in infancy, childhood, and sometimes later life.
• The binge-eating frequency criterion in bulimia nervosa and that in binge-eating disorder have been harmonized, and both diagnostic sets now require binge-eating episodes at least once a week for 3 months.

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Russell G: Bulimia nervosa: an ominous variant of anorexia nervosa. Psychol Med 9:429-448, 1979

Schienle A, Schafer A, Hermann A, et al: Binge-eating disorder: reward sensitivity and brain activation to images of food. Biol Psychiatry 65:651-661, 2009

Smink FRE, van Hoeken D, Hoek HW: Epidemiology of eating disorders: incidence, prevalence and mortality rates. Curr Psychiatry Rep 14:406-414, 2012

Steinhausen HC, Weber S: The outcome of bulimia nervosa: findings from one-quarter century of research. Am J Psychiatry 166:1331-1341, 2009

Svaldi J, Brand M, Tuschen-Caffier B: Decision-making impairments in women with binge eating disorder. Appetite 54:84-92, 2010

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Suggested Readings

Agras WS: The Oxford Handbook of Eating Disorders. New York, Oxford University Press, 2010

Grilo CM, Mitchell JE: The Treatment of Eating Disorders: A Clinical Handbook. New York, Guilford, 2010

Lock J, le Grange D: Treatment Manual for Anorexia Nervosa. New York, Guilford, 2013

Waller G, Mountford V, Lawson R, et al: Beating Your Eating Disorder: A Cognitive-Behavioral Self-help Guide for Adult Sufferers and Their Carers. New York, Cambridge University Press, 2010