Background

Bulimia nervosa is an eating disorder delineated in the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR).[1] The word bulimia is derived from the Greek words bous (ox) andlimos (hunger), indicating a state of excessive hunger. Among the eating disorders, bulimia nervosa and anorexia nervosa are far more common in young females, while bingeeating disorder, the most common eating disorder overall, is more common in adults. Bulimia nervosa includes regularly occurring compensatory behaviors that are intended to rid the body of the excess calories consumed during eating binges. Bulimia nervosa is distinguished from the recently delineated syndrome of binge-eating disorder, in which no regular or consistent compensatory behavior accompanies the bingeing episodes. The DSM-IV-TRrecognizes 2 major variants of bulimia nervosa: purging (ie, compensation by means of self-induced vomiting and/or excessive ingestion of laxatives to induce diarrhea) and nonpurging (ie, binge eating associated with the use of nonpurging compensatory measures such as excessive exercise, stimulant substances, and/or fasting). The frequent association of cigarette smoking with bulimia nervosa may at times reflect compensatory behavior, in that nicotine use appears to suppress, whereas smoking cessation provokes weight gain in some individuals. In up to 60% of cases, patients with bulimia nervosa report prior histories of anorexia nervosa. In contrast to individuals with uncomplicated binge-eating disorder who tend to be obese, people with bulimia nervosa are more typically of normal weight, although some degree of overlap between nonpurging bulimia nervosa and binge-eating disorder is seen. The natural history of eating disorders is such that individuals may pass through several diagnoses over time, with some meeting criteria for anorexia nervosa, bulimia nervosa, and binge-eating disorder at various points. The development of anorexia nervosa in individuals who initially present with bulimia nervosa is possible, although less common.[2]

Binge eating
Bulimia nervosa is characterized by frequent episodes of binge eating associated with emotional distress and a sense of loss of control. Binge eating: Eating, in a discrete period of time (eg, 2 h) an amount of food that is significantly larger than is typical for most people during the same defined period. This behavior is associated with a perceived loss of control of eating during this time. Overeating episode: The consumption of an unusually large amount of food in a defined period, without concomitant perception of loss of control. Subjective bulimic episode: The consumption of objectively minimal amounts of food in a defined period with a perception of loss of control.

Compensatory behaviors
Compensatory behaviors used by individuals with bulimia nervosa include self-induced vomiting, laxative abuse, excessive exercise generally experienced as being joyless and/or compulsive, episodes of fasting or strict dieting, diuretic abuse, use of appetite suppressants, failure to use insulin in those with type I diabetes, and/or the use of medications intended to speed up metabolism (eg, thyroid hormone). DSM-IV-TR diagnostic criteria require episodes of binge eating that occur at least twice weekly for 3 months. Individuals with bulimia nervosa are also dissatisfied with their body shape, weight, or both.

Self-evaluation
Anorexia nervosa and bulimia nervosa are characterized by abnormalities in eating behaviors associated with a fear of weight gain and usually some degree of body image distortion (believing one looks much fatter than is actually the case). These are accompanied by associated abnormalities in mood and in perceptions of hunger and satiety. Disordered eating and weight control efforts can manifest as dietary restriction, binge eating, and/or other compensatory behaviors intended to prevent weight gain, as noted above. For more information, see Medscape's Eating Disorders Resource Center.

Diagnostic Criteria for 307.51 Bulimia Nervosa DSM-IV-TR* [1] Recurrent episodes of binge eating. An episode of binge eating is characterized by both of the following: 1. Eating, in a discrete period of time (eg, within any 2-h period), an amount of food that is definitely larger than most people would eat during a similar period of time and under similar circumstances 2. A sense of lack of control over eating during the episode (eg, a feeling that one cannot stop eating or control what or how much one is eating) Recurrent inappropriate compensatory behavior in order to prevent weight gain, such as selfinduced vomiting; misuse of laxatives, diuretics, enemas, or other medications; fasting; or excessive exercise. The binge eating and inappropriate compensatory behaviors both occur, on average, at least twice a week for 3 months. Self-evaluation is unduly influenced by body shape and weight. The disturbance does not occur exclusively during episodes of anorexia nervosa.

2.

3. 4. 5.

Specify type: Purging type: During the current episode of bulimia nervosa, the person has regularly engaged in self-induced vomiting or the misuse of laxatives, diuretics, or enemas. Nonpurging type: During the current episode of bulimia nervosa, the person has used other inappropriate compensatory behaviors, such as fasting or excessive exercise, but has not regularly engaged in self-induced vomiting or the misuse of laxatives, diuretics, or enemas. Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision, (Copyright 2000). American Psychiatric Association. *Note: Diagnostic criteria are subject to change in the DSM-V. A release of the final, approved DSMV is expected in May 2013. Proposed changes and updates may be viewed at www.dsm5.org.[3]

Case study
A 21-year-old woman is brought into an outpatient clinic by her mother, who complains that her daughter has been demonstrating unusual eating patterns since she moved back home 6 months ago. Her mother observes her to eat large amounts of food, such as desserts, when she is alone, often finding food wrappers hidden in her daughters room. She is worried that her daughter may be engaging in vomiting after these episodes of heavy eating. She often isolates herself in the bathroom for 10-20 minutes after a large meal. This case will be discussed in the Clinical History section.

Epidemiology
Frequency
United States Bulimia nervosa is thought to be significantly underrecognized. In the United States, the prevalence of bulimia nervosa is 1%.[4] Lifetime prevalence is 0.5% for males and 1.5% for females. Those who are diagnosed with bulimia nervosa spend approximately 8.3 years with an episode. Approximately 65.3% of patients with bulimia have a body mass index (BMI) between 18.5-29.9 and only 3.5% have a BMI less than 18.5. Bulimia nervosa is more common among those whose occupation or hobbies require gaining and/or losing weight rapidly, such as wrestlers and competitive bodybuilders. [5] Athletes in certain sports (eg, runners and gymnasts, are particularly prone to eating disorders.[6] The female athlete triad of eating disorders, hypothalamic amenorrhea, and osteoporosis is now well recognized and is particularly common in sports where slimness and body shape are of great importance, such as gymnastics, long distance running, diving, and figure skating. Eating disorders are also being recognized as a problem in predominantly male sports such as cycling, weight lifting, and wrestling. Certain vocations such as acting, modeling, and ballet dancing[7] also appear to be associated with higher risk for these disorders. While overall epidemiological trends are difficult to assess given the changes in diagnostic criteria over time, most studies report a progressive increase in the prevalence of anorexia nervosa and bulimia nervosa in the last several decades of the 20th century, with the possibility that rates have been

leveling off. However, along with increases in obesity, rates of binge eating disorder are believed to be on the rise as well. Rates of bulimic symptoms (as distinct from the diagnosis of bulimia nervosa per se) may vary across geographic regions in the United States. In one small study, women from North Carolina and Virginia (South Atlantic region) reported more bulimic symptoms than women from Louisiana and Tennessee (South Central region) and Ohio and Missouri (Midwest region). [8]

Mortality/Morbidity
A meta-analysis conducted of 36 studies by Arcelus et al suggests that individuals with eating disorders have significantly elevated mortality rates. Furthermore, the patients with anorexia nervosa had the highest mortality rate.[9]

Race
Bulimia nervosa is a cosmopolitan disorder that has been described in all ethnic, racial, and socioeconomic groups. Literature is mixed regarding ethnic differences in eating disorders. No clear consensus exists about the relative prevalence of eating disorders and associated symptoms across ethnicities. Clinicians should remain alert for possible ethnic diversity in symptom presentation or distress that could obscure the diagnosis or need for intervention.[10, 11]

Sex
As with other eating disorders, bulimia nervosa occurs predominantly in women. Most reports suggest a female-to-male ratio of 10:1, with reported ranges from 20:1 to 7:1. In some populations (eg, active duty military) body dissatisfaction and subclinical eating disorder rates among males have been reported to be in excess of 20%. Clinicians should remain aware that men also develop bulimia nervosa and other eating disorders. The psychopathology and attitudes of males with eating disorders appear on the whole to be similar to those of females with eating disorders; both are significantly associated with family histories of these disorders. Although few data are available, evidence suggests that men and women also share significant similarities in clinical course, complications, and response to treatment.

Age
The mean age of onset is 19.7, slightly older than the peak age of onset for anorexia nervosa but generally lower than the age of onset for binge-eating disorder. The prevalence of bulimia nervosa in children younger than 14 years appears to be less than 5%. Bulimia nervosa has also been reported in the elderly.[12]

History
Case study
A 21-year-old woman is brought into an outpatient clinic by her mother, who complains that her daughter has been demonstrating unusual eating patterns since she moved back home 6 months ago. Her mother observes her to eat large amounts of food, such as desserts, when she is alone, often finding food wrappers hidden in her daughters room. She is worried that her daughter may be engaging in vomiting after these episodes of heavy eating. She often isolates herself in the bathroom for 10-20 minutes after a large meal. When the patient was asked about her eating habits, she admitted to a loss of control. She described feeling deep remorse when she eats more than she would like. Furthermore, she described feeling so laden with guilt about her eating binges that she purposefully induces vomiting at least once every other day. This act gives her tremendous relief. She admits that she is unhappy with her overall appearance, and feels that she is fat and out of shape. She is preoccupied with her appearance and says that she compares herself to other women all day long. She also admits to feeling sad most days. She endorses experiencing occasional missed menstrual periods, low libido, low energy, and intermittent sore throat. Historically, the patient has memories of a chaotic childhood. She is an only child whose parents fought often and finally divorced when she was 9 years old. The patient remembers the first time she induced vomiting at 10 years old, after she felt too full after a large meal. The mother describes her

daughter as having few friends and as tending to isolate herself. However, the mother describes her as very bright; in fact, she was valedictorian of her high school. On physical examination, the patients blood pressure is 90/60, heart rate is 100, and BMI is 19. Her oropharynx appears injected without areas of erosion, and multiple dental caries are seen. Bilateral parotid enlargement with minor tenderness is present. The patient is tachycardic and bowel sounds are hyperactive. The abdomen is soft, nontender, and nondistended. Skin turgor is poor. On mental status examination, the patient presents as a young Caucasian woman with average body habitus and pale skin. She is meticulously dressed and groomed. She answers questions curtly, makes poor eye contact, and demonstrates mild foot tapping throughout the interview. Her mood is anxious and her affect is mood congruent but restricted to negative emotionality. She is highly articulate. Thought process is linear and goal directed. Methodical about her statements, she often takes time to clarify what she really means. Thought content displays themes of shame, guilt, and self-reproach. No active delusions or hallucinations are present. Her cognition is grossly intact. She denies suicidal thoughts, but sometimes wishes she was invisible. She has no violent or homicidal thoughts. Insight is limited regarding her ability to acknowledge her psychiatric illness. Her judgment is impaired considering her inability to recognize the potential negative health consequences of her eating behaviors. Prior to entering your office, laboratory assessment obtained at the suggestion of her primary care doctor reveals a serum potassium level of 3.8 Meq/L and serum amylase level of 140 Units/L. Take home points 1. The differential diagnosis of bulimia nervosa includes depression, anxiety and age-appropriate developmental problems (eg, lack of esteem). 2. A biopsychosocial treatment plan will be necessary to provide her the care she needs. 3. Collaboration with primary care providers is often necessary for short-term and sometimes long-term.

History
Bulimia nervosa is often not diagnosed for many months or even years after onset because of the patients' secretiveness about their difficulties, usually associated with a great deal of shame. These patients often see physicians for other problems, such as anxiety, depression, infertility, bowel irregularities, fatigue, or palpitations. Similarly, they may see mental health professionals for mood and anxiety problems, personality issues, relationship issues or substance abuse, without revealing the presence of an eating disorder. One common presenting scenario is that of a patient who is concerned her about weight who seeks help with weight loss. Symptoms may include bloating, constipation, and menstrual irregularities. Far less often, people may present with palpitations resulting from arrhythmias, which are often associated with electrolyte abnormalities and dehydration. Bulimia nervosa is also characterized by an inappropriate premium placed on slender physical appearance, though less prominently than in anorexia nervosa. A dietary history may reveal attempts to control weight by dieting and abstaining entirely from highcalorie foods at all times except during binge-eating episodes. Often, a morbid preoccupation with food and eating is present, and recurring cycles of extreme dieting and/or fasting may alternate with gorging behavior. Usually, bingeing episodes are well planned. High-calorie foods that are easy to swallow and to vomit are usually chosen. Patients may rapidly ingest up to 10 times (or more) of the recommended daily calorie allowance in a single binge episode. Understandably, patients often try to avoid social situations in which they might too easily lose control over their food intake (eg, parties, eating out). Patients with bulimia nervosa frequently engage in physical activity cyclically, in a fashion similar to that of the bingeing episodes. Most patients self-induce vomiting by gagging themselves with their fingers or a toothbrush. Some patients are able to regurgitate reflexively, without requiring external stimulation of the pharynx.[13] A minority of patients will chew, then regurgitate, without actually swallowing the food. One particularly dangerous form of vomiting is via induction through the use of

emetics (eg, ipecac). Ipecac is a tightly binding and slowly released myotoxin that may lead to fatal cardiomyopathy in habitual users. o o o o o Patients with bulimia nervosa may experience the following symptoms: General - Dizziness, lightheadedness, palpitations (due to dehydration, orthostatic hypotension, possibly hypokalemia) Gastrointestinal symptoms - Pharyngeal irritation, abdominal pain (more common among persons who self-induce vomiting), blood in vomitus (from esophageal irritation and more rarely actual tears, which may be fatal), difficulty swallowing, bloating, flatulence, constipation, and obstipation Pulmonary symptoms - Uncommonly aspiration pneumonitis or, more rarely, pneumomediastinum Amenorrhea - Occurs in up to 50% of women with bulimia nervosa; significant proportion of remaining patients have irregular periods A high index of suspicion is required in any depressed or anxious weight-conscious young woman. A set of screening questions, such as the SCOFF mnemonic questionnaire [14] , is useful to obtain a quick impression as to the potential need for further in-depth questioning. The SCOFF questionnaire includes the following 5 questions: 1. Do you make yourself S ick because you feel uncomfortably full? 2. Do you worry you have lost C ontrol over how much you eat? 3. Have you recently lost more than O ne stone (about 14 lbs or 6.35 kg) in a 3-month period? 4. Do you believe yourself to be F at when others say you are too thin? 5. Would you say that F ood dominates your life? The Eating Disorder Screen for Primary Care (ESP) questionnaire is an alternative screening tool.[15] It contains the following 5 questions: 1. Are you satisfied with your eating patterns? 2. Do you ever eat in secret? 3. Does your weight affect the way you feel about yourself? 4. Have family members suffered from an eating disorder? 5. Do you currently suffer with or have you in the past suffered with an eating disorder? The Eating Attitudes Test (EAT) is a self-report population-based screening instrument that patients can complete in the waiting room prior to seeing the health care provider. [16] (See Psych Central for more information.) Family history of eating disorders, anxiety, mood disorders, and alcohol and/or substance abuse/dependence may contribute to the risk of bulimia nervosa and should be investigated. Generally, patients with bulimia nervosa are more likely than controls to view their families as conflicted, badly organized, noncohesive, and lacking in nurturance and caring. These patients have also been shown to more often appear to be angrily submissive to hostile and neglectful parents. Perceptions of appearance-related teasing by family members may be present.[17] For individuals still living with their parents, careful assessment of the familys dynamics should be undertaken.

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Physiological abnormalities
Many physiological abnormalities may be seen in association with eating disorders, but virtually all appear to be consequences of the abnormal behaviors, not their causes. In most cases of bulimia nervosa, laboratory abnormalities are relatively minor. In cases of very frequent purging (eg, daily or multiple times per day), abnormalities in electrolyte and serum amylase levels occur, but these and most other laboratory abnormalities are reversible with weight restoration and cessation of compensatory behaviors. Among the identified metabolic consequences sometimes seen in bulimia nervosa are low plasma insulin, C peptide, triiodothyronine, and glucose values, as well as increased beta-hydroxybutyrate and free fatty acid levels. Both fasting and postbinge/postvomiting hypoglycemia are sometimes seen in some patients with bulimia nervosa. Some studies suggest increased secretory diurnal amplitudes in cortisol and adrenocorticotropic hormone (ACTH) in bulimia nervosa as well as blunted responses to corticotrophin-releasing hormone (CRH). However, these findings have been inconsistent among research studies. Reports have also suggested abnormal responses to dexamethasone suppression similar to those seen in anorexia nervosa and major depressive disorder, more common among individuals with significant dietary restriction. Some authors have attributed these abnormalities to impaired dexamethasone absorption, which is demonstrated in some patients with bulimia nervosa. Similar to

findings in anorexia nervosa, patients with bulimia nervosa tend to have higher growth hormone levels at night, while nocturnal prolactin levels tend to be less than those seen in controls. Episodes of amenorrhea may occur in as many as 50% of women with bulimia nervosa. [18] About half of women with bulimia nervosa have anovulatory cycles while about 20% have luteal phase defects. Patients with anovulatory cycles generally have impaired luteinizing hormone pulsatile secretion patterns and associated reduced estradiol and progesterone pulse amplitudes.[18, 19] Although the implications of many research findings are still unclear, and none of the following offer clinical tests of any merit, reports suggest involvement of the serotonin transporter [20, 21] , autoantibodies against neuropeptides[22] , various chromosome regions[23] , brain-derived neurotrophic factor[24] , and peptides leptin and ghrelin.[25] In a few instances, cerebral hemispheric lesions may be involved in pathogenesis.[26]Regional cerebral blood flow abnormalities have been noted in adolescents.[27] Endogenous opioids and beta-endorphins have been implicated in the maintenance of binge eating.

Comorbidity
A national comorbidity study examined lifetime comorbidities of other psychiatric diagnoses in conjunction with bulimia nervosa.[4] In general, the lifetime comorbidity of any psychiatric disorder is 94.5% Affective disorders: The common co-occurrence of eating disorders with affective disorders suggests a possible relationship between them.[28]Major depressive disorder (MDD) is particularly common (approximately 50%) in this regard. Whether the association is causative (primary), secondary to the bulimia nervosa itself, or represents a common set of risk factors for bulimia nervosa and MDD is still unclear. Depressive symptoms can occur during pregnancy and postpartum in women with bulimia nervosa.[29] Bipolar II disorder also appears to be more common in patients with bulimia nervosa than in patients without eating disorders. The lifetime comorbidity for bipolar I or II is 17.7%. Anxiety disorders: Obsessive-compulsive disorder (OCD) is more common in persons with bulimia nervosa (17.4% lifetime comorbidity) than in controls. Panic disorder, social phobia, specific phobias, generalized anxiety disorder (GAD), and posttraumatic stress disorder (PTSD) significantly contribute to comorbidity. Lifetime comorbidities have been reported at approximately 17.4% for OCD, 16.2% for panic disorder, 41.3% for social phobia, 50.1% for specific phobias, 11.8% for GAD, and 45.4% for PTSD. One study suggests that baseline clinical predictors such as female gender and family history of eating disorders might be specific to the later development of eating disorders in the context of childhood OCD.[30] Substance use disorders: Some evidence suggests a relationship between disorders of substance abuse and dependence and bulimia nervosa, including alcohol dependence [31] , nicotine dependence[32] , and drug dependence[33] . Studies on caffeine intake are mixed.[34]Alcohol abuse or dependence has a lifetime comorbidity with bulimia nervosa of 33.7%, whereas illicit drug abuse or dependence has a lifetime comorbidity of 26%. Impulse control disorders: In a study of lifetime prevalence of impulse control disorders in patients with bulimia nervosa, compulsive buying and intermittent explosive disorder were the most frequently reported disorders, at 17.6% and 13.2%, respectively. Higher than expected rates of kleptomania, pathological gambling, and trichotillomania have also been reported in patients with bulimia nervosa.[35] Attention deficit hyperactivity disorder (ADHD): ADHD may be associated with bulimia.[36] In one study of more than 2,000 female inpatients treated for bulimia nervosa, 9% were also diagnosed with ADHD. The average rate of ADHD in the general population of young women is approximately 3.4%.[37] Lifetime comorbidity with ADHD and bulimia nervosa has been reported to be as high as 34.9%. Other psychopathology: The role of sexual abuse in the development of eating disorders is controversial.[38] Some reports suggest a strong association, while others detect no increased association. Borderline personality disorder is found frequently. [39] These patients usually have histories of trauma and abuse and may represent a distinct subgroup. Pathologic narcissism [40] and identity impairment[41] may be present. Features of obsessive compulsive personality disorder (OCPD), particularly perfectionism, may be increased among patients with bulimia nervosa.

Suicidal behavior
Bulimia nervosa is associated with increased risk of suicide attempts and suicidal ideations. [42] In one study, all-cause mortality rate for bulimia nervosa was 3.9%, higher than other reported studies in the

past.[43] However, the standardized mortality ratio with respect to suicide was 6.51, a much higher than expected rate.

Physical
Although patients with bulimia nervosa are often unremarkable in general appearance and frequently have no signs of illness on physical examination, several characteristic findings may occur. o Physical findings may include the following: Bilateral parotid enlargement, largely consequent to noninflammatory stimulation of the salivary glands, may be seen.[44] See parotid gland swelling in following image. o
Parotid hypertrophy. Reprinted with permission from Mandel, L and Siamak, A. Diagnosing bulimia nervosa with parotid gland swelling. J Am Dent Assoc 2004, Vol 135, No 5, 613-616.

In patients with significant self-induced vomiting, erosions of the lingual surface of the teeth, loss of enamel, periodontal disease, and extensive dental caries may be observed, as in the following image.[45]
Dental caries. Reprinted with permission from Wolcott, RB, Yager, J, Gordon, G. Dental sequelae to the binge-purge syndrome (bulimia): report of cases. JADA. 1984; 109:723-725.

Russell sign (one of the few physical examination findings in psychiatry) manifests as callosities, scarring, and abrasions on the knuckles secondary to repeated self-induced vomiting.[46]
Russell sign. Reprinted with permission from Glorio R, et al. Prevalence of cutaneous manifestations in 200 patients with eating disorders. Int J Derm, 2000, 39(5), 348-353.

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Other cutaneous manifestations can include telogen effluvium (sudden, diffuse hair loss), acne, xerosis (dry skin), nail dystrophy (degeneration), and scarring resulting from cutting, burning, and other self-induced trauma.[47] Other nonspecific but suggestive findings that may reflect the severity of the disease include bradycardia or tachycardia, hypothermia, and hypotension (often associated with dehydration). Edema, particularly of the feet (and less commonly the hands), is found more often among patients with a history of diuretic abuse, laxative abuse, or both or in patients with significant protein malnourishment causing hypoalbuminemia. Some patients may be clinically obese, but morbid obesity is rare. Patients with bulimia nervosa who are overweight may have excessive fat folds that favor humidity and maceration with bacterial and fungal overgrowth, striae due to skin overextension, stasis pigmentation related to peripheral vascular disease, and plantar hyperkeratosis due to increased weight. [47] A typical Mental Status Examination for a patient with bulimia nervosa is detailed below. (The formal Folstein Mini-Mental Status Examination [MMSE] is usually unnecessary in the evaluation of patients with bulimia nervosa because symptoms of dementia and delirium are not common in these patients.) Appearance: Patients are typically neat, well dressed, and show attention to detail. Grooming is often meticulous and may further demonstrate a patient's concern about personal appearance. Behavior: Patients usually do not have kinetic abnormalities, but anxious feelings may heighten psychomotor agitation. Movements are spontaneous, and patients generally are cooperative and able to carry out requested tasks. Cooperation: Patients generally avoid eye contact due to shame and embarrassment. Mood and affect: Patients often demonstrate a depressed mood but may also have significant anxiety. Speech: Content and articulation are generally normal. Thought process: Patients likely have a linear thought process that is goal-directed. Thought content: Thoughts tend to revolve around food and concerns regarding body image and weight. Perceptual disturbances: Delusions and hallucinations are typically absent. Suicidal ideation: Suicidal ideation is a significant consideration, especially in patients with depressed moods. Although suicidal ideation is often restricted to thoughts rather than concrete plans, suicidal thinking should be taken very seriously. Homicidal ideations: Homicidal ideation is not typically associated with those diagnosed with bulimia nervosa. Cognition: Patients are generally alert, and oriented to their surroundings. Attention and concentration typically measured by serial sevens and digit span are generally normal. Immediate memory is normal, as is recent and remote memory recall. Intellect is usually judged as normal,

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and in some cases, intellect ability may surpass average. Capacity to read and write is within normal limits. Visuospatial functions are also intact. Judgment: Patients generally demonstrate poor judgment regarding self care and treatment. Weight-reducing strategies such as induced vomiting, laxative, and diuretic ingestion are often perceived as legitimate and appropriate methods of weight management. Insight: Insight regarding the presence and significance of disturbances is variable. While patients typically admit to episodes of binge eating, they often do not appreciate their inappropriate fixation on eating or their distorted ideas of body image and weight.

Causes
Some factors identified as playing potentially important roles in etiopathogenesis are as follows:

Biological factors[48, 49, 50]

Neurotransmitters Serotonin: Serotonin is possibly closely related to weight regulation and eating behaviors. There have been documented cases of elevated serotonin in the cerebral spinal fluid in patients with anorexia nervosa and bulimia nervosa. Norepinephrine: Lower levels of serum neurotransmitter are typically thought to be associated with anorexia nervosa. Dopamine: Dopamine activity is thought to be associated with distortion of body image, and a 7 repeat allele of the D4 receptor gene is thought to be associated with both bulimia nervosa and binge eating. This 7 repeat allele is thought to possibly be involved with weight gain in patients with bulimia nervosa. Hormonal: Although many reported abnormalities in bulimia nervosa may reflect consequences of binge eating and purging rather than causal factors, complex irregular interactions exists between orexigenic factors such as neuropeptide Y (NP-Y), peptide Y (PYY), and anorectic factors such as cholecystokinin (CCK) and beta-endorphin. Patients with active bulimia nervosa have normal NP-Y and PYY levels, which do increase after successful treatment. Patients with anorexia nervosa, on the other hand have elevated levels of NP-Y and lower levels of PYY (therefore, less orexigenic peptide action). Furthermore, people with bulimia nervosa have reduced beta-endorphin, normal dynorphin, and low CCK levels. Genetics: Although no definitive inheritance patterns have been identified, a familial component appears to be involved in the development of eating disorders. Patterns of transmission involving monozygotic and dizygotic twins suggest genetic contributions in both anorexia nervosa and bulimia nervosa. There have been proposed genetic links at chromosomes 1, 3, and 10p related to bulimia nervosa. Genome-wide association studies are currently ongoing to further explore this association. Unfortunately, studies to date have been small with poor power. Chromosome 10p may also be linked with obesity in addition to bulimia nervosa.

Developmental factors
Developmental factors include childhood anxiety, (eg, difficulties separating from caretakers). [51] History of childhood trauma and neglect, including subtle degrees of psychological abuse, teasing, and other interactions that generate self-doubt may increase vulnerability.

Psychological factors
Among psychological factors suggested are difficulties with self-esteem, affective self-regulation, impulsivity, perfectionism, body image distortion, susceptibility to triggers of a binge-purge cycle (which may occur around dieting and weight loss), and poor coping skills.

Sociocultural factors
Among the potential precipitating events for a binge/purge cycle in those with bulimia nervosa are anxiety states, emotional tension, boredom, environmental cues about food and eating, alcohol use, substance abuse, and exhaustion. For patients who severely restrict their usual food intake, hunger may precipitate an eating binge (in an all or none fashion). Excessive concerns about physical appearance, body image and thinness seem central to both anorexia nervosa and bulimia nervosa.

Differentials
Anorexia Nervosa Body Dysmorphic Disorder

Depression Gastric Outlet Obstruction Insulinoma Kleine-Levin Syndrome Kluver-Bucy Syndrome Obesity Obsessive-Compulsive Disorder

Laboratory Studies
Comprehensive blood chemistry panel: This is important in detecting possible occult metabolic complications of bulimia. With significant vomiting, hypokalemic metabolic alkalosis is possible. Among patients with significant laxative abuse, normokalemic metabolic acidosis may occur. Hyponatremia, hypocalcemia, hypophosphatemia, and hypomagnesemia should be ruled out. Those who have significant intravascular depletion may have elevated blood urea nitrogen levels. Complete blood cell count: This is used to exclude anemia or other occult hematologic abnormalities. Urinalysis: Urine specific gravity may reflect the state of hydration. Some patients may water load in an attempt to gain some weight before their health care visit. Urine toxicology: Comorbid substance abuse should be ruled out with a urine toxicology screen. [53] Pregnancy test: This should always be obtained to rule out pregnancy in female patients presenting with amenorrhea. Amylase: Hyperamylasemia is found in up to 30% of persons with significant vomiting because of hypersecretion from the salivary glands. This may offer a rough measure of purging activity or suggest the presence of purging in patients who are suspected of purging but who deny doing it. However, serial amylase levels are not sufficiently sensitive to offer a useful clinical marker to follow the course of purging.

Other Tests
Because of the potential for arrhythmias and cardiomyopathy as possible complications, an electrocardiogram (ECG) should be performed in patients who are very thin, complaining of palpitations, or have other signs or symptoms suggestive of cardiovascular concern. Prolonged QTc, especially in the setting of hypokalemia, heighten the risk for cardiac decompensation in this population.[54] Because of the potential for osteoporosis, a dual energy absorptiometry (DEXA) scan may be useful, particularly for patients with irregular menses, mood disorders, and/or who smoke cigarettes. Routine neuropsychological testing is not indicated. When specific abnormalities are found in mental status testing, or when histories of learning impairment are present, neuropsychological testing may show decision-making abnormalities, as well as impairment in word recall, abstraction, attention, visuospatial functioning, and problem solving.[55, 56]

Medical Care
Triage of care
Initial care for bulimia nervosa is usually provided in outpatient settings. Factors that may indicate a need for inpatient care include significant metabolic abnormalities, medical complications, risk of suicide, failed outpatient treatment, and inability to care for self. For guidelines regarding patient level of care, refer to the table from the APA Practice Guidelines for Eating Disorders.[57]

Interdisciplinary approach
Bulimia nervosa is best managed using an interdisciplinary approach. Care providers who should be involved include the primary care provider, psychiatrist, psychotherapist, and nutritionist/dietitian. If the psychiatrist is not skilled in this area, involvement of a psychotherapist with expertise in the management of eating disorders is strongly recommended. Dietary review and nutritional rehabilitation counseling should be provided by a nutritionist/registered dietitian. Dental care merits attention. Depending on complications, those with bulimia nervosa may also require the services of other specialists. The goals of treatment are as follows:[58] Reduce and, where possible, eliminate binge eating and purging.

Treat physical complications and restore nutritional health. Enhance patients' motivation to cooperate in the restoration of healthy eating patterns and participate in treatment. Provide education regarding healthy nutrition and eating patterns. Help patients reassess and change core dysfunctional thoughts, attitudes, motives, conflicts, and feelings related to bulimia nervosa. Treat associated psychiatric conditions and psychological difficulties, including deficits in mood and impulse regulation, and factors contributing to poor self-esteem. Enlist family support and provide family counseling and therapy where appropriate. Prevent relapse.

Nonpharmacologic Interventions
Treatment should be comprehensive and generally requires an interdisciplinary approach with many of the following components:[57]

Core nonpharmacologic interventions

Individual therapies Cognitive behavioral psychotherapy (CBT): CBT is an evidence-based, effective treatment for bulimia nervosa. Behavioral approaches to avoiding undesirable eating habits are used, including diary keeping; behavioral analyses of the antecedents, behaviors, and consequences (so-called ABCs) associated with binge eating and purging episodes; and exposure to food paired with progressive response prevention regarding binge eating and purging. Distorted or maladaptive thoughts regarding weight and shape are identified, examined, and addressed, and other dysfunctional irrational beliefs are explored and confronted to allow better understanding, enhanced self-control, and improved body image. The cognitive component of CBT appears to be an essential active ingredient for change, as behavioral interventions alone are often not as effective.[58] Interpersonal psychotherapy (IPT): Interpersonal psychotherapy addresses specific issues in the interpersonal arena that create the context for and stimulate dynamic tensions that spur the patient's symptoms; these generally encompass such processes as grief, role transitions, role conflicts or disputes, and interpersonal deficits. Brief focused therapy in these areas can be effective in producing improvements in mood disturbance and low self-esteem, which may trigger and maintain the symptoms of bulimia nervosa. The efficacy of IPT is roughly similar to CBT in reducing binge eating but it may be somewhat less effective in curbing purging. Nutritional rehabilitation counseling A structured meal plan provides a concrete means to help reduce episodes of dietary restriction and, consequently, urges to binge and purge. Adequate nutritional intake can prevent craving and promote satiety. Assessing nutritional intake for all patients, even those with a normal body weight (and normal BMI), is important because normal weight per se does not ensure appropriate nutritional intake or normal body composition. Nutritional counseling may not only help reduce food restriction, but may also help patients increase the variety of foods eaten and promote healthy but not compulsive exercise patterns. Family therapy Family therapy explores family attitudes and dynamics, dysfunctional relationships, communication and behavior patterns, and other factors that may precipitate or perpetuate abnormal eating behaviors in the family setting. This perspective often views eating difficulties as a form of communication within a family. Family therapy should be considered especially for adolescent patients still living with their parents or older patients with ongoing conflicted interactions with parents. A specific form of family intervention, the so-called Maudsley model, where parents are authorized to take an active and specified role in helping their child to eat, has been shown to be effective for treating anorexia nervosa in adolescents. Its efficacy for patients with bulimia nervosa is still uncertain.

Adjunctive nonpharmacologic treatments

Individual therapy

Psychodynamic psychotherapy: Some patients, particularly those with concurrent developmental and personality pathology or other co-occurring disorders, require lengthy individual treatment. Clinical reports suggest that psychodynamic and at times psychoanalytic approaches in individual or group format may help to improve overall coping once bingeing and purging improve. Supportive-expressive psychotherapy (SEP) in individual or group therapy formats may be helpful for patients with bulimia. Couples therapy Patients with marital discord may benefit from couples therapy. Although research concerning marital and cohabitation relationships in patients with bulimia nervosa is limited, many patients with bulimia nervosa are thought to experience problematic relationships with impaired intimacy, including sexuality and suboptimal communication skills. Self-consciousness and self-silencing associated with sexual activity, and anxious attachment may be associated with bulimic symptoms.[59] Group therapy Dialectical behavior therapy and integrative cognitive-affective therapy may have an emerging role in treatment, especially for patients with severe emotional dysregulation and impulsivity.[60]

Self-help and support groups

Support groups and 12-step programs such as Overeaters Anonymous may be helpful as adjuncts in initial treatment and for subsequent relapse prevention, but they are not recommended as the sole initial treatment approach for bulimia nervosa. In the most recent update of the Self-help and guided self-help for eating disorders in the Cochrane Database of Systematic Reviews[61] , efficacies of pure self-help (PSH) and guided self-help (GSH) were mixed. PSH/GSH did not significantly differ from waiting list in abstinence from bingeing or purging, although PSH/GSH produced greater improvement on other eating disorder symptoms, psychiatric symptomatology, and interpersonal functioning, but not depression. In addition to face-to-face interventions, self-help support may be available through books and online. See the APA's complete list of Self-Help Books and Internet Resources in the Patient Education section. Self-help and Patient Support Groups for Bulimia Nervosa Connect Groups Bulimia.com

Other
Bright light therapy has been shown to reduce binge frequency in several controlled trials of patients whose binge eating follows a seasonal pattern (akin to seasonal affective disorder) and may be used as an adjunct when CBT and antidepressant therapy have not been effective in reducing bingeing symptoms in such patients.[62] One study provided some support for guided imagery compared to journaling. However, long-term maintenance of treatment effects is unknown.[63]

Pharmacologic Treatments
Food and Drug Administration (FDA) approved treatments
Fluoxetine (Prozac): Initial dose 60 mg/d in the morning. Some patients may need to begin at a lower dose if side effects are intolerable. A maximum dose of 80 mg/d may be used in some cases.

Other evidence-based pharmacologic treatments

Antidepressants Antidepressants as a group are the mainstay of pharmacotherapy for bulimia nervosa. [57] These may be helpful for patients with substantial concurrent symptoms of depression, anxiety, obsessions, or certain impulse disorder symptoms. They may be particularly good for patients who have not benefited from or had suboptimal response to suitable psychosocial therapy or who have a chronic, difficult course in combination with other treatments. Among the antidepressants, the strongest evidence for efficacy with the fewest adverse effects has been associated with selective serotonin reuptake inhibitors (SSRIs). [64, 57] As mentioned above, only fluoxetine (Prozac) is approved by the FDA for the treatment of bulimia nervosa. Sertraline (Zoloft) at 100 mg or higher dose/day is the only other SSRI shown to be effective, as demonstrated in a small, randomized controlled trial. Fluvoxamine[65] and citalopram[66] have also shown benefit. The exact

mechanisms underlying the efficacy of antidepressants in bulimia nervosa are unclear, but the effects are presumed to be mediated through their salutary impact on cerebral serotonin systems. Higher doses of SSRIs require more vigilance regarding side effects, though they appear to be well tolerated in this population. Bupropion (Wellbutrin) is relatively contraindicated in the treatment of bulimia nervosa because of a higher risk of seizures in patients with eating disorders associated with this medication.[57] Tricyclic antidepressants (TCAs)[67] and monoamine oxidase inhibitors (MAOIs) have been shown to be effective in small randomized controlled trials in patients with bulimia nervosa, but due to higher risks of adverse effects and toxicity in overdose they are not recommended as initial treatments. [57] o Desipramine and imipramine (up to 300mg/d) The most recent update of Antidepressants versus placebo for people with bulimia nervosa in the Cochrane Database of Systematic Reviews included TCAs, SSRIs, MAOIs, and other classes of drugs (mianserin, trazodone, bupropion). Similar results were obtained in terms of efficacy for the different groups of drugs. Patients with TCAs dropped out due to any cause more frequently than patients with placebo, and the opposite was found for fluoxetine.[68] Mood stabilizers Topiramate: Small controlled trials have demonstrated efficacy of this anticonvulsant medication, but since adverse reactions are common, topiramate should be used only when other medications have proven ineffective. Since patients tend to lose weight on topiramate, its use is problematic for normal or underweight patients.[57, 69] Topiramate is useful for short-term treatment of binge eating disorder as it improves binge frequency and decreases weight. Open label studies also suggest that topiramate may be efficacious in the long term, but this remains to be conclusively demonstrated. [70] Lithium: Lithium has not been demonstrated to be effective for bulimia nervosa per se. In patients with co-occurring bipolar disorder and bulimia nervosa, lithium treatment is particularly difficult to manage because of the risk of frequent and major fluid shifts and associated toxicity. As well, some patients have weight gain with lithium, which would have to be aggressively managed if the patients stay on the medication. Valproic acid: Since weight gain is often associated with valproic acid treatment, this medication is often unacceptable to patients with eating disorders who are weight preoccupied, but it is an option for patients who fail other treatments.[57, 71] Miscellaneous In small studies, ondansetron[72] , baclofen[73] , and an antiandrogenic oral contraceptive[74] have been shown to have some use as alternative pharmacotherapeutic options in the management of bulimia nervosa. Trials investigating naltrexone (ReVia) have shown mixed results, and venlafaxine has not been shown to be beneficial. Clinicians must be aware of the black box warnings relating to antidepressants and other medications to discuss the potential benefits and risks as part of the consent process with patients and families if such medications are to be prescribed. See the statement onAntidepressant Use in Children, Adolescents, and Adults by the Food and Drug Administration. Case reports indicate that methylphenidate may be helpful for patients with bulimia nervosa and concurrent ADHD.[57] Trials of traditional and nontraditional medication treatments have to be weighed in terms of potential for drug interactions, the medical complications of BN, and the medical comorbidities of BN.

Follow-up
Treatment outcomes
CBT is the single most well-studied and effective treatment for bulimia nervosa. Some studies have reported that the combination of antidepressant therapy and CBT results in the highest remission rates. This combination is recommended initially when qualified CBT therapists are available. In addition, when CBT alone does not result in a substantial reduction in symptoms after 10 sessions, addition of fluoxetine is ordinarily recommended.[57] However, a major study found that when excellent manual-based CBT is administered, the addition of fluoxetine may not offer additional benefit. How best to treat individuals who do not respond to CBT and/or antidepressant medications remains an unsettled question.[63] Limited evidence supports the use of fluoxetine for relapse prevention, but substantial rates of relapse occur even with treatment. The optimal duration of treatment and the optimal strategies for maintaining treatment gains are unknown. In the absence of adequate data, most clinicians recommend continuing

antidepressant therapy for a minimum of 9 months and probably for at least 1 year in most patients.[57] Other medications have not been studied long term in bulimia nervosa. With CBT and maintenance treatment, as many as 50% of patients with bulimia nervosa are asymptomatic at follow-up 2-10 years after completing treatment. Rates of persistent long-term improvement following other forms of psychotherapy (eg, IPT, supportive-expressive psychotherapy) are unknown. In a recent update of Psychotherapy for bulimia nervosa and binging in the Cochrane Database of Systematic Reviews, CBT, particularly CBT-BN (a specific modification of CBT to address bulimia nervosa), noted efficacy in decreasing binge eating. However, these conclusions are limited by the fact that the clinical trials were highly variable and small sample sizes. Long-term interpersonal psychotherapy was also demonstrated to be efficacious. Self-help, alongside highly structured CBT, appeared to be promising. However, exposure and response prevention did not appear to enhance the efficacy of CBT. Psychotherapy alone was unlikely to change body weight. [75] According to the most recent update of Antidepressants versus psychological treatments and their combination for bulimia nervosa in the Cochrane Database of Systematic Reviews, combination treatments of medications plus psychotherapy were superior to psychotherapy alone. Psychotherapy appeared to be more acceptable to patients. When antidepressants were combined with psychological treatments, acceptability of the latter was significantly reduced. [76] Technology-based interventions, such as Internet prevention programs, Internet-assisted CBT, online consulting, and text messaging have shown promise in assisting in the treatment of eating disorders. [77,
78, 79]

Surgical Care
Major medical treatment requiring surgical intervention is rare, but medical care providers should be familiar with potential serious complications. Patients may develop an acute gastric obstruction and/or gastric dilatation [80] (rarely resulting in gastric perforation leading to acute peritonitis), which presents with severe, continuous projectile vomiting that occurs soon after any oral intake. This possibility should be considered in individuals with known bulimia nervosa who present complaining of uncontrollable vomiting. When the potential for gastric dilatation, outlet obstruction, or both is of concern, an urgent surgical consultation is indicated. Emergency surgical review is also required if symptoms suggestive of esophageal tear (MalloryWeiss syndrome) develop or in case of esophageal rupture, which can precipitate acute mediastinitis. (See images below). For more information, see eMedicine articles Mallory-Weiss Syndrome and Esophageal Rupture.
This chest radiograph demonstrates pneumomediastinum, which can

occur in association with esophageal rupture from forceful vomiting. Water-soluble contrast esophagram from a patient with esophageal perforation after esophageal dilation shows contrast leak (arrowheads) and normal esophageal lumen (arrows). Mallory-Weiss tear. Typical longitudinal mucosal tear with overlying fibrinous exudate extending from the distal esophagus to the gastric cardia. Courtesy of C.J. Gostout, MD.

These conditions are surgical emergencies and, although uncommon, are occasional causes of mortality related to bulimia nervosa.

Consultations
Dental consultations
Dentists and dental hygienists sometimes play a unique role in opening dialogues with patients about eating disorders. They can help with early recognition and refer patients for specialist-level eating disorders care. Similarly, dental professionals can make important contributions to recovery and longterm treatment of these patients.[81]

Diet
As described above regarding the role of the registered dietician, patient education regarding healthy, well balanced diets, exercise, and long-term maintenance of a healthy weight is important and may help reduce the risk of relapse or chronicity.

Deterrence/Prevention

All eating disorders appear to arise within a cultural context that places too high a value on thinness and engenders unreasonable expectations regarding physical appearance. Awareness of the cultural and social forces and education for both children and their parents regarding the attitudes and behaviors that foster eating disorders may reduce the prevalence of these syndromes. Opportunities for this kind of intervention abound in primary care, athletic, and educational settings. School-based programs that emphasize health, fitness and a range of physical and psychological competences have shown promise in being able to reduce the development of eating disorder-associated attitudes in vulnerable school-age populations.[82]

Complications
Psychiatric complications
Studies suggest that patients with bulimia nervosa have increased rates of substance abuse, anxiety disorders, bipolar II disorder, and sexual abuse; these conditions should be considered and managed as necessary. Mortality and morbidity associated with depression (suicidal thoughts or self-injury) and poor impulse control (eg, substance abuse, sexually transmitted diseases, unintended pregnancy, accidental injuries) should always be anticipated and assessed.

Medical complications
The all-cause mortality rate for bulimia nervosa per se is slightly lower than for anorexia nervosa (3.9% vs 4.0%, respectively).[43] Medical complications do arise and should be assessed carefully. While the results of formal gastric emptying studies in patients with bulimia nervosa have yielded variable results (some suggesting delayed emptying time and others suggesting normal emptying time), acute gastric dilatation is a rare but concerning risk. This complication may result in gastric rupture, which may be fatal. Among other rare potential complications are Mallory-Weiss tears of the esophagus, esophageal rupture, reflux esophagitis, and cardiomyopathies secondary to ipecac use. Ipecac toxicity may be associated with skeletal myopathy, while chronic hypokalemia may also be associated with intestinal ileus, abdominal distension, exertional rhabdomyolysis, or both. Hypokalemia-related distal renal tubulopathy is very rarely associated with bulimia nervosa. Xerosis (dry skin) is a common finding in bulimia nervosa, which appears to be related to the chronic dehydration to which persons with bulimia nervosa are often prone. Skin health usually requires an overall healthy nutritional status. Dermatological treatment is ordinarily topical. Patients who chronically overuse and abuse laxatives risk chronic constipation, cathartic colon with pseudo-Hirschsprung syndrome, melanosis coli with increased risk for colon cancer, steatorrhea, and/or protein-losing enteropathy and metabolic consequences of hypophosphatemia and hypomagnesemia. Other potential complications include osteopenia or osteoporosis, menstrual irregularity and infertility, and, less commonly, cognitive changes associated with dehydration and electrolyte and metabolic abnormalities.

Prognosis
Research to date suggests a variable prognosis. The illness may pursue a long-term, fluctuating course over many years, or may be more episodic, associated with stressful life events and crises. The diagnosis may not be stable over time.[83] In the shorter term, some reports suggest a 50% improvement in binge eating and purging behavior among patients who are able to engage in treatment. In a 12-year outcome study that looked at bulimia nervosa, purging type, 28.2% of the individuals maintained the diagnosis of bulimia nervosa, purging type. Psychiatric comorbidities predicted poor outcome, specifically self-injurious behaviors.[84] In 2008, a 10-year follow-up study was published that looked at parental psychopathology as a source of predicted outcome. The paper found that substance abuse in fathers and depression in mothers was associated with poor outcome. Obesity in mothers was associated with a better long-term outcome.[85] Most eating disorders have high recovery in the first 10 years of the disease development. However, bulimia nervosa, as compared to other eating disorders, is the only eating disorder that has increased probability of recovery past 10 years.[86] This is in contrast to those with prolonged anorexia nervosa, whose chance of recovery decreases with increasing length of disease. In another study that

examined temporal patterns of recovery in bulimia nervosa, 10% of those with bulimia nervosa met recovery criteria at 10 years. At 15 years, 25% met recovery criteria. The patients had 3 times the rate of recovery at 10-14 years than matched patients with anorexia nervosa.[4] Literature is growing about the long-term outcome of bulimia. In a 5-year longitudinal study, patients with bulimia nervosa had a remission rate of approximately 74% and a relapse rate of approximately 47%. The natural course did not appear to be influenced by personality disorder psychopathology. [87] Consistent predictors of outcome have not yet been identified. However, the severity of the purging sequelae, negative self-image[88] , childhood maltreatment[89] , childhood obesity/overeating[90] , individual/family eating patterns during childhood/early adolescence [91] , and ADHD[92] may be important indicators of worse prognosis. Depression may also be associated with a worse outcome. Electrolyte imbalances, esophagitis, and hyperamylasemia reflect more severe purging and may predict a poorer outcome. Lifetime history of anorexia nervosa maybe an important indicator of prognosis in patients with bulimia nervosa. In a 9-year longitudinal study, when compared to women with bulimia nervosa who have no history of anorexia nervosa, patients diagnosed with bulimia nervosa and with a history of anorexia nervosa were more likely to cross back into anorexia nervosa and were less likely to achieve full recovery.[93]

Patient Education
Cognitive behavioral therapy remains the therapeutic method of choice for bulimia nervosa, and various modifications of this technique are actively under investigation. Most of these interventions include the premise that education about bulimia nervosa in a nonthreatening environment has a therapeutic effect. These types of therapy are conducted in either individual or group settings. Educational components of treatment address the following issues: The multifactorial etiology of eating disorders with biologic, genetic, psychological, familial, and sociocultural factors Medical complications related to vomiting, laxative, and diuretic abuse The set-point theory of weight regulation and the potential consequences of weight cycling and cyclic dieting Basic nutritional information Sociocultural and body image issues Cognitive and behavioral strategies Relapse prevention and management of occasional binge eating "slips" More than 70% of published management studies of bulimia nervosa involve some form of psychoeducational program. Although no unbundling studies have been conducted that exclude psychoeducation to assess the relative contribution of this specific strategy to overall treatment outcomes, anecdotal reports and the personal experiences of many practitioners suggest that for at least some patients the educational information helps significantly. Family members can provide perspectives on factors contributing to the onset of the disorder and issues that may help or hamper recovery efforts, and their involvement is often critical to sustained recovery. In addition to empathically listening to family members, clinicians should educate and advise them on the nature of the disorder and their interactions with the patient. When indicated, and with the patients consent, families should be involved in treatment. Such involvement may contribute to the likelihood of better outcomes.[57]