Published: July 2017
Eating disorders are syndromes characterized by severe disturbances in eating behavior and by distress or ex-cessive concern about body shape or weight and often occur with severe medical or psychiatric comorbidities. Denial of symptoms and reluctance to seek treatment make treatment especially challenging.
Major eating disorders can be classified as anorexia nervosa, bulimia nervosa, binge–eating disorder, other specified feeding and eating disorder, avoidant/restrictive food intake disorder, and unspecified feeding and eating disorder. The fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM–5), contains several important changes from the fourth edition (DSM–4) and DSM–4 Text Revision (DSM–4–TR) in the classification of eating disorders.1,2 Characteristics of each of these disorders are summarized in (Table 1) and the complete diagnostic criteria is available in the DSM–5.2 Significant updates to the eating disorder diagnostic criteria include elimination of the amenorrhea and weight requirement for a diagnosis of anorexia nervosa. Instead of the arbitrary DSM–4–TR weight requirement (85% of expected body weight), DSM–5 places low body weight in the context of age, sex, developmental trajectory, and physical health.
Similar to the DSM–4–TR, the DSM–5 includes 2 subtypes of anorexia nervosa: restrictive type (restrict intake or excessive exercise to energy deficit) and binge–eating/purging type (binge eating with compensatory weight control behaviors such as self–induced vomiting, exercising, and misue of diet pills, diuretics, or laxatives). For bulimia nervosa, the required frequency of binging and compensatory behavior is once a week for 3 months, instead of the previous DSM–4–TR requirement of twice a week. In addition, there are no longer subtypes of bulimia nervosa.1,2
The DSM–5 also added binge–eating disorder as an eating disorder diagnosis, characterized by binge eating without inappropriate compensatory behaviors. The DSM–5 also attempts to reduce unspecified eating disorder diagnoses through the introduction of the other specified feeding or eating disorder diagnostic category. Many patients did not meet strict DSM–4–TR criteria for either anorexia or bulimia nervosa, or had characteristics of both disorders. DSM–5 includes 2 new subcategories to better characterize these patients within the other specified feeding or eating disorder diagnostic category, including atypical anorexia and bulimia nervosa of low frequency or limited duration. In addition, the other specified feeding or eating disorder category also includes binge–eating disorder of low frequency or limited duration, purging disorder, and night eating syndrome. Avoidant/restrictive food intake disorder is another new DSM–5 diagnosis, characterized by failure to meet nutrition needs for reasons other than weight control. With this expansion of the eating disorder diagnoses, patients are better matched to specific diagnoses and fewer patients are classified with unspecified feeding and eating disorders.3,4
| Disorder | Characteristics |
|---|---|
| Anorexia nervosa |
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| Bulimia nervosa |
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| Binge-eating disorder |
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| Avoidant/restrictive food intake disorder |
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| Other specified feeting or eating disorders |
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| Unspecified feeding or eating disorders |
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Based on information from the DSM–5.2 See the DSM–5 for complete diagnostic criteria.
Eating disorders have been reported in approximately 3% of adolescents and young adults.5 The prevalence of subthreshold eating disorders is even higher, estimated at 11%.6 The most common age of onset for anorexia nervosa is during adolescence, although eating disorders can occur in patients of any age, sex, race, or ethnicity. Similarly, the onset of bulimia nervosa is usually in adolescence7 and the onset of binge–eating disorder is slightly later, most commonly in the mid–20s.8
Screening and treatment of eating disorders has focused on young white females, but more recent estimates suggest that males may make up 10% to 25% of patients.9 In addition, this percentage may increase as clinicians become more familiar with DSM–5 diagnostic criteria for eating disorders.10,11
Eating disorders are the third most common chronic illness among adolescents and the prevalence of anorexia nervosa in female adolescents is estimated at 1% to 4%.2, 8-9,12-16 A recent report of DSM–5 eating disorders among adolescent females revealed a lifetime prevalence of 1.7% for anorexia nervosa, 0.8% for bulimia nervosa, and 2.3% for binge eating disorder.17 In adolescent males, the lifetime prevalence of any DSM–5 eating disorder diagnosis approaches 3% by age 20, highlighting that these disorders are common in other populations.
Eating disorders are more common in industrialized societies where there is an abundance of food and being thin, especially for women, is considered attractive.18 Eating disorders are most common in the United States, Canada, Europe, Australia, New Zealand, and South Africa. However, rates are increasing in Asia, especially in Japan and China, where women are exposed to cultural change and modernization. In the U.S., eating disorders are common in young Latin American, Native American, and African American women, but the rates are still lower than in white women. African American women are more likely to develop bulimia and more likely to purge. Female athletes involved in running, gymnastics, or ballet and male body builders or wrestlers are at increased risk.
Biologic and psychosocial factors are implicated in the pathophysiology of eating disorders, but the underlying causes and mechanisms remain unknown.7,18,19
First–degree female relatives and monozygotic twin offspring of patients with anorexia nervosa have higher rates of anorexia nervosa and bulimia nervosa. Children of patients with anorexia nervosa have a lifetime risk for anorexia nervosa that is tenfold that of the general population (5%).20-23 Families of patients with bulimia nervosa have higher rates of substance abuse, particularly alcoholism, affective disorders, and obesity.24
Endogenous opioids might contribute to denial of hunger in patients with anorexia nervosa. Some hypothesize that dieting can increase the risk for developing an eating disorder. Increased endorphin levels have been described in patients with bulimia nervosa after purging and may induce feelings of wellbeing. Diminished norepinephrine turnover and activity are suggested by reduced levels of 3–methoxy–4–hydroxyphenylglycol in the urine and cerebrospinal fluid of some patients with anorexia nervosa. Antidepressants often benefit patients with bulimia nervosa and support a pathophysiologic role for serotonin and norepinephrine.
Starvation results in many biochemical changes such as hypercortisolemia, nonsuppression of dexamethasone, suppression of thyroid function, and amenorrhea. Several computed tomography studies of the brain have revealed enlarged sulci and ventricles, a finding that is reversed with weight gain. In one study using positron emission tomography, metabolism was higher in the caudate nucleus during the anorectic state than after hyperalimentation.
Anorexia risk may increase with a polymorphism of the promoter region of serotonin 2a receptor. The melanocortin 4 receptor gene is hypothesized to regulate weight and appetite. Polymorphism in the gene for agouti–related peptide might also play a role at the melanocortin receptor. In bulimia nervosa, there is excessive secretion of ghrelin. Ghrelin receptor gene polymorphism is associated with both hyperphagia of bulimia and Prader–Willi syndrome.
Perhaps some of the most fascinating new research addresses the overlap between uncontrolled compulsive eating and compulsive drug seeking in drug addiction.19 Reduction in ventral striatal dopamine is found in both of these groups. Lower frequency of dopamine D2 receptors was associated with higher body mass index. Obese persons might eat to temporarily increase activity in these reward circuits. Frequent visual food stimuli paired with increased sensitivity of right orbitofrontal brain activity is likely to initiate eating behavior. Marijuana’s well–known appetite stimulant effect is likely due to its agonist activity at cannabinoid receptors, and cannabinoid receptor antagonism has been associated with reduced binge eating.
High levels of hostility, chaos, and isolation and low levels of nurturance and empathy are reported in families of children presenting with eating disorders.7,18 Anorexia has been postulated as a reaction to demands on adolescents to behave more independently or to respond to societal pressures to be slender. Anorexia nervosa patients are usually high achievers, and two–thirds live at home with their parents. Many consider their bodies to be under the control of their parents. Young Asian female immigrants are at increased risk for anorexia or bulimia as compared with peers living in their homeland. First generation daughters of Asian immigrants are at higher risk than U.S. females of the same age. Family dynamics alone, however, do not cause anorexia nervosa. Self–starvation may be an effort to gain validation as a unique person. Patients with bulimia nervosa have been described as having difficulties with impulse regulation.
As a general guideline, it appears that a third of patients fully recover, a third retain subthreshold symptoms, and a third maintain a chronic eating disorder.2,7,18
Long–term follow–up shows recovery rates ranging from 44% to 76%, with prolonged recovery time (57 to 59 months). Mortality (up to 20%) is primarily from cardiac arrest or suicide.25,26 Good prognostic factors are admission of hunger, lessening of denial, and improved self–esteem. Poorer prognostic factors are initial lower minimum weight, presence of vomiting or laxative abuse, failure to respond to previous treatment, disturbed family relationships, and conflicts with parents.
Little long–term follow–up data exist. Short–term success is 50% to 70%, with relapse rates between 30% and 50% after 6 months.24,27-33 These patients have an overall better prognosis as compared with anorexia nervosa patients. Poor prognostic factors are hospitalization, higher frequency of vomiting, poor social and occupational functioning, poor motivation for recovery, severity of purging, presence of medical complications, high levels of impulsivity, longer duration of illness, delayed treatment, and premorbid history of obesity and substance abuse.
Recently included in the DSM–5, pica is described as the eating of nonfood substances for at least 1 month. The symptoms should be severe enough that warrant clinical attention. Some of the substances that patients ingested tend to vary according with age and environmental availability such as paper, hair, wool, starch, ice, charcoal, pebbles among others. Normally, these patients are not complaining about food aversion. Some biological abnormalities such as vitamin deficiencies or mineral deficiencies have been reported frequent in these patients. Also patients with certain medical conditions such as infections, intestinal obstruction, and mechanical bowel problems are more likely to suffer from this condition. The prevalence is unclear; in patients with developmental disability, the prevalence appears to increase with the severity of the disability. Even though pica is more frequently reported in children, it can occur at any age.
The prevalence of rumination disorders is unknown, but is certainly higher in patients with developmental disabilities. Patients under stressful situations such as neglect, stressful life, and problems in the relationship with the parents are certainly more frequent in infant and young children.
The essential features of anorexia nervosa are refusal to maintain a minimally normal body weight, intense fear of gaining weight, and significant disturbance in the perception of the shape or size of one’s body.2,7,18 Patients commonly lack insight into the problem and are brought to professional attention by a family member. DSM–5 identifies 2 subtypes of anorexia nervosa: restricting type and binge eating–purging type. Comorbid psychiatric symptoms include depressive symptoms such as depressed mood, social withdrawal, irritability, insomnia, and decreased sexual interest. Many depressive features may be secondary to the physiologic sequelae of semistarvation. Symptoms of mood disturbances need to be reassessed after partial or complete weight restoration. Obsessive–compulsive features–thoughts of food, hoarding food, picking or pulling apart small portions of food, or collecting recipes–are common. Anxiety symptoms and concerns of eating in public are also common.
The essential features are binge eating and inappropriate compensatory behavior such as fasting, vomiting, using laxatives, or exercising to prevent weight gain. Binge eating is typically triggered by dysphoric mood states, interpersonal stressors, intense hunger following dietary restraints, or negative feelings related to body weight, shape, and food. Patients are typically ashamed of their eating problems, and binge eating usually occurs in secrecy. Unlike anorexia nervosa, bulimia nervosa patients are typically within normal weight range and restrict their total caloric consumption between binges.
The essential features are eating, nonnutritive substances for at least 1 month. The eating of these substances is not appropriate for the developmental level of the patient and is also not part of a culturally supported practice. If the pica occurs associated with another mental disorder (intellectual disability, autism, schizophrenia), the significance is severe enough that requires additional clinical attention. Some of the environmental risk factors are neglect, lack of supervision by adults, or cognitive disability. Other frequent comorbid disorders are patients with obsessive-compulsive disorder, trichotillomania, skin picking.
The essential feature is the repeated regurgitation of food after eating for a period of at least 1 month. This is not secondary to gastrointestinal disease or other gastrointestinal issue. Rumination disorder is not associated exclusively during anorexia, bulimia or binge–eating disorder. When the patient is regurgitating previous swallowed food this might be partially digested and patient is not having nausea or involuntary retching. This disorder is also more frequent in patients with intellectual disabilities, can happen at any age.
This disorders the previously recognized feeding disorder of infancy or early childhood. The essential feature is avoidance of food intake based on the sensory characteristics of the food, patients might have at least one of the following; significant weight loss, significant nutritional deficiency, dependence on enteral feeding, marked interference with psychosocial functioning. Food avoidance can be a negative response associating food intake with a traumatic experience, such as choking, traumatic investigation, or repeated vomiting. Patients might seem not interested in food. Children might look too sleepy, too worried, or too agitated during feeding time. In older children, other emotional symptoms such as mood symptoms or anxiety symptoms might be present.
In addition to the clinical interview, the Eating Attitudes Test, Eating Disorders Inventory, Body Shape Questionnaire, and others can be used to assess eating disorders.34
Common comorbid conditions include major depressive disorder or dysthymia (50% to 75%), sexual abuse (20% to 50%), obsessive–compulsive disorder (25% with anorexia nervosa), substance abuse (12% to 18% with anorexia nervosa, especially the binge–purge subtype, and 30% to 37% with bulimia nervosa), and bipolar disorder (4% to 13%).2,18,19,28
There are many complications related to weight loss, purging and vomiting, and laxative abuse (Table 2). When obesity is associated with the eating disorder, hyperlipidemia, diabetes mellitus, sleep apnea, joint injury, hypertension, and cardiac and respiratory disorders can result.
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Based on information from references 35-38.
Medical illnesses include brain tumors, including craniopharyngioma, and other malignancies, gastrointestinal disease, and acquired immunodeficiency syndrome.39 Other medical disorders that can present with weight loss, malabsorption, or secondary amenorrhea include chronic infections, uncontrolled diabetes mellitus, primary or secondary hyperthyroidism, adrenal insufficiency, and pituitary prolactinoma.7
Other psychiatric disorders with disturbed appetite or food intake include depression, somatization disorder, and schizophrenia. Patients with depressive disorder generally do not have an intense fear of obesity or body image disturbance. Depressed patients usually have a decreased appetite, whereas anorexia nervosa patients often claim to have a normal appetite and to feel hungry. Patients with somatization disorder do not generally express a morbid fear of obesity. Severe weight loss and amenorrhea longer than 3 months are unusual in somatization disorder. Schizophrenic patients might have delusions about food being poisoned but rarely are they concerned with caloric content. They also do not express a fear of gaining weight.
Other eating disorders may share similar features to anorexia nervosa, but may not meet all diagnostic criteria. Patients with bulimia nervosa do not have an abnormally low body weight. In avoidant/restrictive food intake disorder, restriction of intake is due to a lack of interest in food, aversion to the sensory characteristics, or concern about potential adverse consequences of eating such as choking or vomiting, and will not be accompanied by intense fear of gaining weight and body image disturbance. Patients who meet some but not all of the diagnostic criteria for anorexia nervosa set out by the DSM–5 may be given a diagnosis of other specified feeding or eating disorder.2
General medical conditions of central nervous system pathology, such as brain tumors, can simulate the binging and compensatory behaviors seen in bulimia nervosa. Klüver-Bucy syndrome is a rare condition characterized by hyperphagia, hypersexuality, and compulsive licking and biting. Klein–Levin syndrome, also rare, is more common in men and consists of hyperphagia and periodic hypersomnia.
Patients with the binge–purge subtype of anorexia nervosa fail to maintain their weight within a normal range. Patients with borderline personality disorder sometimes exhibit binge–eating but do not have other criteria for bulimia nervosa. Patients with binge–eating disorder do not exhibit compensatory behaviors such as purging, excessive exercise, or diet pill, diuretic, or laxative use.
Other psychiatric disorders may present similarly to bulimia nervosa. Overeating is common in major depressive disorder with atypical features, but individuals with this disorder will not exhibit the compensatory behaviors or excessive concern with body shape and weight present in bulimia nervosa. Patients with borderline personality disorder may engage in binge–eating behavior as an impulsive act, but will exhibit other personality changes and will not be excessively concerned with body weight or shape.2
Differential diagnosis for binge–eating disorder includes bulimia nervosa, obesity, and other psychiatric conditions such as bipolar and depressive disorders and borderline personality disorder. Binge–eating disorder differs from bulimia nervosa in that binge–eating disorder is not associated with compensatory weight loss behaviors that are present in bulimia nervosa. While binge–eating disorder is associated with overweight and obesity, key features of binge–eating disorder include higher levels of overvaluation of body weight shape, increased rates of psychiatric comorbidity, and successful outcomes with evidence–based psychotherapy. Bipolar and depressive disorders include features of increases in appetite and weight gain, but episodes of overeating may not be associated with a loss of control. Similarly, patients with borderline personality disorder may exhibit binge–eating but will not meet all criteria for binge–eating disorder, although the two conditions can exist simultaneously.2
Differential diagnosis includes anorexia nervosa, factitious disorder and non–suicidal self–injury. In patients with anorexia nervosa, the eating of nonnutritive substances is done as an attempt to control the appetite. In factitious disorders, patients will ingest non–food substances as a means to create physical symptoms. In the patients with non–suicidal self–injury, the patients will swallow objects that could be potentially harmful, in the context of getting more attention, or negative coping.
Rumination disorder can certainly occur in the context of other medical conditions or other psychiatric disorders (especially in the anxiety category). If that is the case, the diagnosis is appropriate when the severity of the symptom requires additional attention.
Loss of appetite is a very nonspecific symptom that can be seen in a number of medical (gastrointestinal disorders, food allergies, intolerances, cancer) as well as psychiatric disorders (reactive attachment disorder, autism spectrum disorder, any of the anxiety disorders, anorexia, obsessive–compulsive disorder, major depressive disorder, schizophrenia, factitious disorder). The most frequent comorbidity is anxiety disorders. Children with certain neurological neuromuscular disorders might have some feeding difficulties associated with the problems in the innervation of the oropharyngeal muscles or in patients with hypotonia or problems swallowing.
A comprehensive treatment plan including a combination of nutritional rehabilitation, medical monitoring, psychotherapy, and medication is recommended (Figure 1).21,40-43 The patient’s weight and cardiac and metabolic status determines the acuteness of the illness and the need for hospitalization (Table 3). Treatment guidelines are well documented by the American Psychiatric Association in its practice guideline for treating eating disorders.40
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Treatment goals are to restore the patient’s nutritional status and establish healthy eating patterns, treat medical complications, correct core dysfunctional thoughts related to the eating disorder, enlist family support, and provide family counseling.
Expected rates of controlled weight gain should be 2 to 3 pounds per week for inpatients and 0.5 to 1 pound per week for outpatients.40 Intake levels should start at 30 to 40 kcal/kg/day (1,000–1,600 kcal/day) in divided meals and may progress to 70 to 100 kcal/kg/day during treatment in order to reach weight restoration. New studies suggest that starting at higher caloric levels (up to 1,900 calories) may promote faster weight gain with no additional risk of refeeding syndrome.45 If oral feeding is not possible, progressive nocturnal nasogastric feeding can lessen distress (physical and psychological) during early weight gain.
Daily morning weights, vital signs including orthostatic vital signs, fluid intake, and urine output should be measured. Frequent physical examinations should be performed to detect circulatory overload, refeeding edema, and bloating. Monitor serum electrolyte levels (low potassium or phosphorus), and get an electrocardiogram if needed. During the initial stages of the treatment, daily weights might be stressful for the patient. The patient can be given the choice to be informed of changes in daily weight or not be informed, especially if it causes anxiety, frustration, or distress.
Stool softeners, not laxatives, should be used to treat constipation. The diet should be supplemented with vitamins and minerals as micronutrient deficiencies are common.
Patients should be given positive reinforcement (praise) and negative reinforcement (restrictions of exercise and purging). They should be closely supervised, and access to bathrooms should be restricted for at least 2 hours after meals. After weight restoration has progressed, stretching can begin, followed by gradual reintroduction of aerobic exercise.
Psychosocial treatments are required during hospitalization as well as after discharge.21,40,41,43,46,47 For adults with eating disorders, no one specialist treatment model has been shown to be the most effective.46 Commonly used models include dynamic expressive–supportive, interpersonal psychotherapy therapy and cognitive–behavioral techniques (planned meals and self-monitoring, exposure, and response prevention). Research data more strongly support the efficacy of cognitive-behavioral and interpersonal therapies, although there are high rates of non–response to treatment.46 Although cognitive–behavioral therapy is important, its benefits increase with the addition of a nutritional component. Newer treatment models such as the Maudsley Model of Treatment for Adults with Anorexia Nervosa is aimed at addressing rigidity, cognitive distortions about the utility of anorexia nervosa, socio–emotional impairment, and interpersonal relationships, are currently under investigation to evaluate long–term efficacy.47
Group therapy, support groups, and 12-step programs like Overeaters Anonymous may be useful as adjunct treatment and for relapse prevention. Family therapy and marital therapy are helpful in cases of dysfunctional family patterns and interpersonal distress.
Guided self–help manuals can reduce the number of binge–purge episodes in at least some patients with bulimia nervosa. In fact, a manual–driven self–help approach incorporating cognitive–behavioral principles combined with keeping contact with a general practice physician in one study did as well as specialist–based treatment in reducing bulimic episodes. Computer–based health education can improve knowledge and attitudes as a patient–friendly adjunct to therapy.43 Higher self–directedness at baseline is a good predictor of improvement at the end of a variety of interventions, as well as at follow–up 6 to 12 months later. This might help explain why manual–driven self–help and psychoeducational programs that emphasize improvement of self–esteem and reassessment of body image have achieved some success. For children and adolescents with eating disorders, Maudsley family–based therapy has been shown to be the most effective treatment for weight restoration and cognitive function in anorexia nervosa, and is suggested to be efficacious in bulimia nervosa.46 Treatments capitalize on parental/family involvement and include three phases: weight restoration, returning control over eating to the adolescent, and establishing a healthy adolescent identity.48,49
Elementary school–age children with behavioral problems, disordered eating, and obesity may benefit from a behavioral family–based therapy. Children and parents were examined and tested before and after the intervention and all lost weight. Although eating disorders did not resolve, other behavioral problems did. There was less parental dissatisfaction as children developed better awareness and behavior patterns.
Treatment for pica should follow a psychoeducational treatment approach. Parents might need increased social support. Additionally, parents may need concurrent treatment for anxiety and depression of their own in some cases. Reports about behavioral treatments, environmental enrichment, with group or individual therapy have shown varying benefits. Treating the nutritional insufficiencies is key.
Very limited research is available regarding the treatment of this feeding disorder. Potentially progressive exposure to new foods is important, behavioral therapy or feeding clinics may also be helpful.
The evidence for significant efficacy of psychotropic medication is lacking, with very few methodologically sound studies.7,18,40,42,50,51 Although medication is less successful in anorexia nervosa than in bulimia nervosa, it is most often used in anorexia nervosa after weight has been restored but may begin earlier when indicated for associated psychiatric symptoms.
Randomized controlled trials of antidepressants, most notably selective serotonin reuptake inhibitors (SSRIs), have not shown these medications to be effective in the treatment of anorexia nervosa or in the treatment of women with anorexia nervosa and comorbid depression, SSRIs (eg, fluoxetine) are commonly considered for patients with anorexia nervosa who have depressive, anxiety, or obsessive–compulsive symptoms that persist in spite of or in the absence of weight gain. However, SSRIs are associated with serious side effects for patients with eating disorders, including bone loss and increased risk of fracture.52
Tricyclic antidepressants and monoamine oxidase inhibitors have shown modest benefits in decreasing anorexic symptoms and increasing weight. However, they should be used with caution, because they have greater risks of cardiac complications, including arrhythmias and hypotension, and psychotic symptoms.53
Limited research has suggested that second generation antipsychotics may be useful in patients with severe, unremitting resistance to gaining weight, severe obsessional thinking, and severe denial reaching delusional states. Low doses of older antipsychotics may be used for marked agitation and psychotic thinking prior to meals. Antianxiety medications, such as benzodiazepines, may be used for extreme anticipatory anxiety concerning eating or before morning weight measures.40
Estrogen replacement alone does not generally appear to reverse osteoporosis or osteopenia, and unless there is weight gain, it does not prevent further bone loss. There is very limited evidence of bisphosphonate’s efficacy in treating associated osteoporosis. In addition, return of menses is an important marker of recovery that cannot be evaluated if estrogen replacement is implemented.
Promotility agents such as metoclopramide are commonly used for bloating and abdominal pains due to gastroparesis and premature satiety, but they require monitoring for drug–related extrapyramidal side effects.40
Antidepressants are used primarily to reduce the frequency of disturbed eating and treat comorbid depression, anxiety, obsessions, and certain impulse–disorder symptoms and are shown to be efficacious in conjunction with psychotherapy.40 Medication can reduce binge episodes, but is not sufficient to be the sole treatment. The only medication approved by the U.S. Food and Drug Administration for bulimia nervosa is the SSRI fluoxetine (Prozac). Several studies have demonstrated efficacy of other SSRIs including sertraline (Zoloft), paroxetine (Paxil), and citalopram (Celexa); tricyclic antidepressants including imipramine (Tofranil), nortriptyline (Pamelor), and desipramine (Norpramin); and monoamine oxidase inhibitors including tranylcypromine (Parnate). Doses of tricyclic antidepressants and monoamine oxidase inhibitors parallel those used to treat depression, but higher doses of fluoxetine (≤80 mg/day) may be needed to treat bulimia nervosa.51 Bupropion (Wellbutrin) has been associated with seizures in patients with purging bulimia and its use is not recommended.40
Other psychotropic drugs are sometimes used. Lithium continues to be used occasionally as an adjunct for comorbid disorders. Various anticonvulsants have successfully reduced binge eating for some patients, but they can also increase appetite. Topiramate lowers appetite but has been associated with cognitive side effects. Sibutramine has also been used to reduce appetite in bulimia nervosa and binge–eating disorder.40
Antidepressant medications, particularly SSRIs, have been shown to reduce binge–eating behavior, although it is unclear if this is a long–term effect. To be effective, the medication dosage is generally at the high end of the recommended range. SSRIs, however, are not associated with substantial weight loss. Another medication option is the appetite–suppressant sibutramine, which is associated with at least a short–term reduction in binge eating, and is also associated with significant weight loss.40
Other medications used in binge–eating disorder include zonisamide and topiramate, which may be effective for binge reduction and weight loss, but have significant side effects that may limit their utility.40
Prevention programs in schools for both females and males or in organizations like the Girl Scouts have been successful in reducing risk factors for eating disorders. Often focusing on media literacy and interactive discussion, there are increasing reports of short–term and longer–term benefits in body satisfaction and acceptance of normal growth.54
