Bulimia nervosa (BN) is an eating disorder with 5 key characteristics as noted by the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5).[1]
Recurrent episodes of binge eating. Eating more than the average person in a 2-hour period, accompanied by a sense of loss of control.
Repetitive inappropriate compensatory behaviors to avoid weight gain such as excessive exercise, fasting, laxative use, and diuretic use.
This eating behavior occurs at least once a week for a period of 3 months.
Body shape and weight influence self-evaluation.
This does not occur specifically with episodes of anorexia nervosa.
Signs and symptoms
Patients with BN may experience the following symptoms:[2, 3, 4]
General - Dizziness, lightheadedness, palpitations (due to dehydration, orthostatic hypotension, possibly hypokalemia), dry skin
Gastrointestinal symptoms - Pharyngeal irritation, abdominal pain (more common among persons who self-induce vomiting), blood in vomitus (from esophageal irritation; more rarely, from actual tears, which may be fatal), difficulty swallowing, bloating, flatulence, constipation, obstipation, and gastroesophageal reflux disease (GERD)[5]
Reproductive symptoms - Amenorrhea occurs in up to 50% of women with BN; significant proportion of remaining patients have irregular periods; many more will have menstrual irregularity and scanty periods
Uncommon symptoms, or in most severe cases
Water and electrolytes - Dehydration, hypokalemia, hypochloremia, metabolic alkalosis
Cardiac - Edema; EKG changes such as QT prolongation, increased PR interval, increased P wave amplitude, widened QRS, depressed ST segment
Bilateral parotid enlargement (see the image below)
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Parotid hypertrophy. Reprinted with permission from Mandel, L and Siamak, A. Diagnosing bulimia nervosa with parotid gland swelling. J Am Dent Assoc 2....
Dental damage (see the image below)
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Dental caries. Reprinted with permission from Wolcott, RB, Yager, J, Gordon, G. Dental sequelae to the binge-purge syndrome (bulimia): report of cases....
Russell sign (see the image below)
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Russell sign. Reprinted with permission from Glorio R, et al. Prevalence of cutaneous manifestations in 200 patients with eating disorders. Int J Derm....
Cutaneous manifestations, including sudden, diffuse hair loss, acne, dry skin, nail dystrophy, and scarring resulting from cutting, burning, and other self-induced trauma
Bradycardia or tachycardia, hypothermia, and hypotension (often associated with dehydration)
Edema
Clinical obesity; morbid obesity is rare
See Clinical Presentation for more detail.
Diagnosis
Laboratory studies
Lab studies that may be used for diagnosis include:
Comprehensive blood chemistry panel
Complete blood count (CBC)
Urinalysis
Urine toxicology screen
Pregnancy test
Amylase level
Electrocardiography
Because of the potential for arrhythmias and cardiomyopathy as possible complications of BN, an electrocardiogram (ECG) should be performed in patients who are very thin, complaining of palpitations, or have other signs or symptoms of cardiovascular concern.[6]
DEXA
Because of the potential for osteoporosis, a dual-energy radiographic absorptiometry (DEXA) scan may be useful, particularly for patients with irregular menses, who have mood disorders, and/or who smoke cigarettes.
See Workup for more detail.
Imaging
Imaging studies are not routinely indicated or ordered for uncomplicated or typical cases of BN. Nonetheless, there has been growing interest in the use of neuroimaging techniques to explore the structural and functional brain changes that take place in those with eating disorders, mostly focusing on patients with anorexia nervosa, but now starting in BN.
See Workup for more detail.
Management
A meta-analysis of 45 randomized controlled trials (RCTs) assessed the prevalence of patients who abstain from binge eating and/or purging following all psychological treatments for BN, and moderated impact by the type of 78 psychotherapies delivered and the trial quality.[7] At post-treatment, the total weighted percentage of treatment-completers who achieved abstinence was 35.4% (95% CI = 29.6, 41.7), while the total weighted percentage of abstinence for all randomized patients (intention-to-treat) was 29.9% (95% CI = 25.7, 33.2). Abstinence estimates were highest in trials that used CBT and BT; guided self-help interventions produced the lowest post-treatment abstinence rates. Overall, 60% of patients fail to fully abstain from core BN symptoms even after receiving empirically supported treatments.
Core nonpharmacologic interventions for BN include the following:
Cognitive-behavioral therapy (CBT)
Cognitive-behavioral therapy enhanced (CBT-E) for patients with more complex cases including comorbidities involving personality
Interpersonal psychotherapy (IPT)
Nutritional rehabilitation counseling
Family therapy
Pharmacologic agents used in the treatment of BN include the following:
Fluoxetine (Prozac) - Approved by the FDA for the treatment of BN
Other antidepressants - As a group, antidepressants are the mainstay of pharmacotherapy for BN;[8] they may help patients with substantial concurrent symptoms of depression, anxiety, obsessions, or certain impulse disorder symptoms
Mood stabilizers - Topiramate, lithium, and valproic acid have been associated with adverse effects that can make these agents difficult to use in patients with BN; lithium has not been demonstrated to be effective for BN per se
Bulimia nervosa (BN) is an eating disorder delineated in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5).[1] Among the eating disorders, bulimia nervosa and anorexia nervosa (AN) are far more common in young females, while binge-eating disorder, the most common eating disorder overall, is more common in adults.
BN includes regularly occurring compensatory behaviors that are intended to rid the body of the excess calories consumed during eating binges. BN is distinguished from the recently delineated syndrome of binge-eating disorder, in which no regular or consistent compensatory behavior accompanies the bingeing episodes. Although the DSM-5 describes that compensatory behaviors may include purging and/or nonpurging behaviors (see below), in contrast to earlier DSM editions, DSM-5 no longer maintains specific purging and nonpurging subtypes. The frequent association of cigarette smoking with BN 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 BN report prior histories of AN. In contrast to individuals with uncomplicated binge-eating disorder who tend to be obese, people with BN are more typically of normal weight, although some degree of overlap between nonpurging BN 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 AN, BN, and binge-eating disorder at various points. The development of AN in individuals who initially present with BN is possible, although less common.[9]
Binge eating
BN 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 hours) 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 BN 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, stimulants). DSM-5 diagnostic criteria require episodes of binge eating that occur at least once weekly for 3 months. Individuals with BN are also dissatisfied with their body shape, weight, or both.
Self-evaluation
AN and BN 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 bulimia nervosa
DMS-5 diagnostic criteria for 307.51 (F50.2) BN are as follows:[1]
Recurrent episodes of binge eating: An episode of binge eating is characterized by both (1) eating, in a discrete period of time (eg, within any 2-hour period), an amount of food that is definitely larger than what most individuals would eat in a similar period of time under similar circumstances and (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 behaviors in order to prevent weight gain, such as self-induced vomiting; misuse of laxatives, diuretics, or other medications; fasting; or excessive exercise
The binge eating and inappropriate compensatory behaviors both occur, on average, at least once a week for 3 months
Self-evaluation is unduly influenced by body shape and weight
The disturbance does not occur exclusively during episodes of AN
Specify if either of the following applies:
In partial remission: After full criteria for bulimia nervosa were previously met, some, but not all, of the criteria have been met for a sustained period of time
In full remission: After full criteria for bulimia nervosa were previously met, none of the criteria has been met for a sustained period of time
Specify current severity. The minimum level of severity is based on the frequency of inappropriate compensatory behaviors. The level of severity may be increased to reflect other symptoms and the degree of functional disability. Specify current severity as follows:
Mild: An average of 1-3 episodes of inappropriate compensatory behaviors per week
Moderate: An average of 4-7 episodes of inappropriate compensatory behaviors per week
Severe: An average of 8–13 episodes of inappropriate compensatory behaviors per week
Extreme: An average of 14 or more episodes of inappropriate compensatory behaviors per week
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 daughter’s 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.
Other problems to be considered
Binge-eating disorder (BED)
BED is characterized by frequent and recurrent binge eating episodes without consistent compensatory behaviors. It is the most common eating disorder overall, with a lifetime prevalence of 2.8%. BED is known to have several comorbidities with other psychiatric disorders, and is strongly associated with severe obesity. The lifetime prevalence for BED in men is 2%, while the male prevalence of BN is 0.5% and AN is 0.3%. This makes BED the most common eating disorder not only in the general population, but in men, as well.[10]
A meta-analysis of 45 studies found only moderate support for the efficacy of cognitive-behavioral therapy (CBT) and CBT guided self-help, and modest support for interpersonal psychotherapy (IPT), selective serotonin reuptake inhibitors (SSRI), and lisdexamfetamine in the treatment of adults with BED in terms of cessation of or reduction in the frequency of binge eating.[11]
Night eating syndrome (NES)
NES has only recently been defined and recognized. It is characterized by the consumption of large amounts of food (>20% of the total calorie intake) after evening meals. It is typically associated with early morning drowsiness and anorexia. No significant overlap is seen between BED or BN and night eating disorder.
Several eating disorder syndromes have been described in association with disturbances in disturbances in sleep and circadian patterns. These disorders are diagnosed under the DSM-5 “Other Specified Feeding or Eating Disorders” category.[1]
NES is distinct from sleep-related eating disorder (SRED), another syndrome in which eating and sleep disturbances have been linked. NES and SRED are quite different. NES could be considered an abnormality in the circadian rhythm of meal timing with a normal circadian timing of sleep onset, ie, with individuals eating a substantial part of their daily intake in the evening, after usual dinnertime, before they go to sleep. Conversely, the feeding behavior in SRED is characterized by recurrent episodes of eating after an arousal from nighttime sleep with or without amnesia.
In addition to eating other foods, in SRED episodes, patients will sometimes eat foods that are ordinarily unpalatable, eg, raw flour and raw bacon have been described. Both conditions are often relentless and chronic. SRED is frequently associated with other sleep disorders, in particular parasomnias, eg, sleep-walking. Case reports have linked some cases of SRED to the use of certain psychotropic medications, including tricyclic antidepressants, anticholinergics, lithium, triazolam, olanzapine, risperidone, and zolpidem. Early studies have suggested that the anti-seizure medication topiramate may be an effective treatment for SRED.[12]
Bulimia nervosa (BN) is thought to be significantly underrecognized. In the United States, the prevalence of BN is 1%.[10] Lifetime prevalence is 0.5% for males and 1.5% for females. Those who are diagnosed with BN spend approximately 8.3 years with an episode. Approximately 65.3% of patients with BN have a body mass index (BMI) between 18.5 and 29.9 and only 3.5% have a BMI less than 18.5.
BN is more common among those whose occupation or hobbies require gaining and/or losing weight rapidly, such as wrestlers and competitive bodybuilders.[13] Athletes in certain sports (eg, runners and gymnasts) are particularly prone to eating disorders.[14] Athletes' most frequent hindering factors were negative emotions/cognitions, sport pressures, and hurtful modeling, while non-athletes reported negative emotions/cognitions, lack of support, and hurtful modeling.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[15] 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 AN and BN in the last several decades of the twentieth century, with the possibility that rates have been leveling off. However, along with increases in obesity, rates of BED are believed to be on the rise as well.
Rates of bulimic symptoms (as distinct from the diagnosis of BN 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).[16]
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 (AN) had the highest mortality rate.[17]
Race
Bulimia nervosa (BN) 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.[18, 19]
Despite efforts to understand racial/ethnic differences, relatively few eating disorder models address the important sociocultural factors that exert powerful influences on beliefs and behaviors related to weight status and eating patterns in this population. Non-traditional research designs are exploring culture-specific risk factors for eating disorders (eg, African American adolescents).
Sex
As with other eating disorders, BN 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 BN 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 AN but generally lower than the age of onset for binge-eating disorder. The prevalence of BN in children younger than 14 years appears to be less than 5%. BN has also been reported in the elderly.[20]
Despite the major public health burden of anorexia nervosa (AN), bulimia nervosa (BN), and binge-eating disorder (BED), there is lack of evidence on the differences in the health-related quality of life (HRQoL) and economic impact of different eating disorders (EDs).
A systematic review of 69 studies in the published literature on the HRQoL and economic burdens found that 17 types of HRQoL instruments were applied, including the Medical Outcome Study Short Forms (ie, Short Form 36 [SF-36] and Short Form 12 [SF-12]) alone or in combination with others.[21] Patients with AN, BN, and BED were shown to have significantly lower HRQoL than the general population. For example, the BN patients had lower scores on the role emotional, social functioning, mental health, vitality, and general health scales than the non-ED subjects, and the BED patients had lower scores on the role emotional, mental health, and vitality scales than the non-ED subjects. In terms of economic burden, AN (78%), BN (88%), and BED (73%) were associated with increased health service use (for any treatment, lifetime) compared with individuals without an ED (44%). The health service use in AN was reported to be equal to or higher than in BN or BED in many studies, and the biggest difference in healthcare utilization was higher hospitalization for AN compared to BN patients was largest, along with a longer length of hospital stay for AN (15.0–52.7 days) than for BN (9.0–45.7 days).
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 daughter’s 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 patient’s 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 and self-reproach,[22] though it is unclear whether shame is a risk factor for the development of AN and BN or a consequence of these difficulties; while guilt may be present, its role is unclear. 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
The differential diagnosis of BN includes depression, anxiety and age-appropriate developmental problems (eg, lack of esteem). These issues are common co-occurrences.
A biopsychosocial treatment plan will be necessary to provide her the care she needs.
Collaboration with primary care providers is often necessary for short-term and sometimes long-term.
History
BN 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, histories of childhood or adolescent trauma, 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. BN 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 high-calorie 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 BN frequently engage in physical activity cyclically, in a fashion similar to that of the binging 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.[23] 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. Up to 40% of patients misuse laxatives, thinking that their use will help them lose weight. In fact, laxative misuse results in additional dehydration and often electrolyte abnormalities as well. Screening for laxative use should be a routine topic of assessment.
Patients with BN 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 BN; significant proportion of remaining patients have irregular periods. Many more will have menstrual irregularity and scanty 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[24] , 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:
Do you make yourself S ick because you feel uncomfortably full?
Do you worry you have lost C ontrol over how much you eat?
Have you recently lost more than O ne stone (about 14 lbs or 6.35 kg) in a 3-month period?
Do you believe yourself to be F at when others say you are too thin?
Would you say that F ood dominates your life?
The Eating Disorder Screen for Primary Care (ESP) questionnaire is an alternative screening tool.[25] It contains the following 5 questions:
Are you satisfied with your eating patterns?
Do you ever eat in secret?
Does your weight affect the way you feel about yourself?
Have family members suffered from an eating disorder?
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.[26] (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 BN and should be investigated.
Generally, patients with BN 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.[27]
For individuals still living with their parents, careful assessment of the family’s dynamics should be undertaken.
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 BN, 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 BN 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 BN. Some studies suggest increased secretory diurnal amplitudes in cortisol and adrenocorticotropic hormone (ACTH) in BN 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 BN. Similar to findings in anorexia nervosa, patients with BN 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 BN.[28] About half of women with BN 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.[28, 29]
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[30, 31] , autoantibodies against neuropeptides[32] , various chromosome regions[33] , brain-derived neurotrophic factor[34] , and peptides leptin and ghrelin.[35] In a few instances, cerebral hemispheric lesions may be involved in pathogenesis.[36] Regional cerebral blood flow abnormalities have been noted in adolescents.[37] 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 BN.[10] 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.[38] Major depressive disorder (MDD) is particularly common (approximately 50%) in this regard. Whether the association is causative (primary), secondary to the BN itself, or represents a common set of risk factors for BN and MDD is still unclear. Depressive symptoms can occur during pregnancy and postpartum in women with BN.[39] Bipolar II disorder also appears to be more common in patients with BN 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 BN (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.[40]
Substance use disorders: Some evidence suggests a relationship between disorders of substance abuse and dependence and BN, including alcohol dependence[41] , nicotine dependence[42] , and drug dependence[43] . For example, with regard to smoking in healthy controls, there were significantly more smokers among people with bulimia (lifetime OR = 2.165) and BED (lifetime OR = 1.792), but not for those with anorexia (lifetime OR = 0.927). Studies on caffeine intake are mixed.[44] Alcohol abuse or dependence has a lifetime comorbidity with BN 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 BN, 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 BN.[45]
Attention deficit hyperactivity disorder (ADHD): ADHD may be associated with bulimia.[46] In one study of more than 2,000 female inpatients treated for BN, 9% were also diagnosed with ADHD. The average rate of ADHD in the general population of young women is approximately 3.4%.[47] Lifetime comorbidity with ADHD and BN 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.[48] Some reports suggest a strong association, while others detect no increased association. Borderline personality disorder is found frequently.[49] These patients usually have histories of trauma and abuse and may represent a distinct subgroup. Pathologic narcissism[50] and identity impairment[51] may be present. Features of obsessive compulsive personality disorder (OCPD), particularly perfectionism, may be increased among patients with BN.
Suicidal behavior
BN is associated with increased risk of suicide attempts and suicidal ideations.[52] In one study, all-cause mortality rate for BN was 3.9%, higher than other reported studies in the past.[53] However, the standardized mortality ratio with respect to suicide was 6.51, a much higher than expected rate.
Although patients with bulimiia nervosa (BN) are often unremarkable in general appearance and frequently have no signs of illness on physical examination, several characteristic findings may occur.
Physical findings may include the following:
Bilateral parotid enlargement, largely consequent to noninflammatory stimulation of the salivary glands, may be seen.[54] See parotid gland swelling in following image.
View Image
Parotid hypertrophy. Reprinted with permission from Mandel, L and Siamak, A. Diagnosing bulimia nervosa with parotid gland swelling. J Am Dent Assoc 2....
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.[55]
View Image
Dental caries. Reprinted with permission from Wolcott, RB, Yager, J, Gordon, G. Dental sequelae to the binge-purge syndrome (bulimia): report of cases....
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.[56]
View Image
Russell sign. Reprinted with permission from Glorio R, et al. Prevalence of cutaneous manifestations in 200 patients with eating disorders. Int J Derm....
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.[57]
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 BN 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.[57]
A community-based household survey involving 52,095 adults in 19 countries found, after adjustment for pertinent comorbidities, that the rate of BN among the 2580 identified cases of adult-onset diabetes mellitus was twice that of non-diabetic individuals.[58]
A typical Mental Status Examination for a patient with BN is detailed below. (The formal Folstein Mini-Mental Status Examination [MMSE] is usually unnecessary in the evaluation of patients with BN 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 BN.
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, 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.
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 (AN) and bulimia nervosa (BN).
Norepinephrine: Lower levels of serum neurotransmitter are typically thought to be associated with AN.
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 BN and binge eating. This 7 repeat allele is thought to possibly be involved with weight gain in patients with BN.
Hormonal
Although many reported abnormalities in BN 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 BN have normal NP-Y and PYY levels, which do increase after successful treatment. Patients with AN, on the other hand, have elevated levels of NP-Y and lower levels of PYY (therefore, less orexigenic peptide action). Furthermore, people with BN 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 NB. There have been proposed genetic links at chromosomes 1, 3, and 10p related to BN. 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 BN.
Suppression of cholecystokinin and ghrelin after meals may be decreased in individuals suffering from BN. This may suggest a predisposing factor that could lead to impaired sense of satiety and influence eating disorder behavior.[62]
Developmental factors
Developmental factors include childhood anxiety, (eg, difficulties separating from caretakers).[63] 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 BN 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 AN and BN.
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.[64]
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.
Imaging studies are rarely routinely indicated or ordered for uncomplicated or typical cases of bulimia nervosa (BN). Nonetheless, there has been growing interest in the use of neuroimaging techniques to explore the structural and functional brain changes that take place in those with eating disorders, though the majority of research has focused on patients with anorexia nervosa (AN). A systematic review of 32 papers found a small number of consistent findings in individuals in the acute phase of illness with BN or binge-eating disorder (BED) including: volume reduction and increases across a range of areas; hypoactivity in the frontostriatal circuits; and aberrant responses in the insula, amygdala, middle frontal gyrus and occipital cortex to a range of different stimuli or tasks; a link between illness severity in BN and neural changes; and diminished attentional capacity and early learning.[65] Additional research is suggested related to the findings of reduced cortical volumes and diminished activity in regions associated with self-regulation (e.g. frontostriatal circuits) and in exploring responses to disorder-related stimuli in those with BN or BED.
Because of the potential for arrhythmias and cardiomyopathy as possible complications, an electrocardiogram 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.[6]
DEXA
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.
Neuropsychological
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.[66, 67]
Most individuals with eating disorders do not receive treatment for their ED. The "treatment gap" may involve individuals' attitudes about accessing various types of treatment, as well as perceived barriers to seeking treatment.[68] A study of people diagnosed or undiagnosed with eating disorders showed that undiagnosed individuals have more positive attitudes towards novel Internet- and smartphone-delivered treatments than diagnosed individuals. The strongest barriers to seeking treatment were fear of losing control, fear of change, and finding motivation to change. When adjusting for past experiences of treatment, ED symptoms were positively associated with the strength of most treatment barriers.
Specifically, the most prominent perceived barriers to help-seeking were stigma and shame, denial of and failure to perceive the severity of the illness, and practical barriers (eg, cost of treatment); some cite lack of encouragement from others to seek help and lack of knowledge about help resources.[69] Therefore, programs targeting prevention and early intervention for EDs should focus on reducing stigma and shame, educating individuals about the severity of eating disorders, and increasing knowledge around help-seeking pathways for eating disorders. Mental health literacy, overall, may offer pathways into treatment. Not surprisingly, common themes reported by participants describe the process of recovery from anorexia nervosa (AN) include dealing with a fragmented sense of self, a turning point where insight and commitment to recovery is developed, and, in recovery, a reclamation of self through meaningful relationships, rebuilding identity, and self-acceptance.[70]
A range of psychotherapies and pharmacotherapies are efficacious for bulimia nervosa (BN),[22] as are a range of nutrition-based and self-help interventions. A meta-analysis of 79 RCTs included 19 different interventions, with primary outcome measures of abstinence from binge eating episodes, compensatory behaviors, and reduction of symptom severity; reduction of self-reported eating pathology and depression served as secondary outcome variables. Retrieved RCTs were meta-analyzed using fixed and random effects models. Overall, slightly reduced effects were obtained for self-help and moderate effects for pharmacotherapy. Similarly, psychotherapy yielded large-to-very-large effects in regard to secondary outcome variables, while moderate-to-large effects were observed for self-help, pharmacotherapy, and combined therapies. Follow-up analyses revealed the sustainability of psychotherapies in terms of large effects in primary outcome criteria, while these effects were moderate for self-help, pharmacotherapy, and combined therapies. The authors concluded that CBT can be recommended as the best intervention for the initial treatment of BN.
Regarding binge eating disorder (BED), a meta-analysis of 45 studies found only moderate support for the efficacy of CBT and CBT guided self-help, and modest support for interpersonal psychotherapy (IPT), selective serotonin reuptake inhibitors (SSRI), and lisdexamfetamine in the treatment of adults with BED in terms of cessation of or reduction in the frequency of binge eating.[11]
Initial care for bulimia nervosa (BN) 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.[8]
Interdisciplinary approach
BN 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:[71]
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.
Treatment should be comprehensive and generally requires an interdisciplinary approach with many of the components described below.[8]
Core nonpharmacologic interventions
Individual therapies
Two systemic reviews have evaluated psychotherapy, psychopharmacology, and other treatment interventions. The first focused on 21 studies in the United Kingdom and the outcome analyzed was full remission at the end of treatment.[72] The study included 12 treatments, including wait list, and found individual cognitive behavioral therapy (CBT) was most effective in achieving remission at the end of treatment compared with wait list (OR 3.89, 95% CrI 1.19–14.02), followed by guided cognitive behavioural self-help (OR 3.81, 95% CrI 1.51–10.90). The other meta-analysis of 79 randomized-controlled trials (RCTs) with 19 interventions revealed moderate-to-large intervention effects for psychotherapy, primarily CBT and substantial sustainability of psychotherapies compared to self-help, pharmacotherapy, and combined treatments.[22]
CBT is an evidence-based, effective treatment for bulimia nervosa (BN). 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.[71]
CBT is indicated as first-line treatment. Patients with other comorbid personality disorders, specifically borderline personality disorder, may not respond to conventional CBT to the same degree as those without these comorbidities. The more complex patients have better experiences with “enhanced” versions of CBT (specifically CBT-E) consisting of CBT augmented with techniques taken from interpersonal psychotherapy and other forms of psychotherapy.[73] CBT may help to reduce binge eating and purging behavior, but is generally not effective alone for producing weight loss.[74]
A systematic review of CBT-enhanced (CBT-E) RCTs and open trials for BN, binge eating disorder (BED), and transdiagnostic samples found seven effectiveness studies (five randomized and two open trials).[75] Substantial differences in posttreatment remission rates were found (range: 22.2–67.6%) due, in part, to differences in samples and operationalization of clinical significant change, though more studies on differential effects and working mechanisms are required to establish the specificity of CBT-E.
Interpersonal psychotherapy
Interpersonal psychotherapy (IPT) 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 BN. The efficacy of IPT is roughly similar to CBT in reducing binge eating, but it may be somewhat less effective in curbing purging.
A systematic review of 15 studies (RCTs and long-term, follow-up studies derived from the RCTs) revealed six main findings: 1) no significant differences between IPT and cognitive-behavioral therapy (CBT) were found when administered as monotherapy to patients with anorexia nervosa (AN); 2) when administered as monotherapy to patients with BN, IPT had lower outcomes than CBT and its enhanced version; 3) patients with BN who remitted with IPT showed a prolonged time spent in clinical remission, when followed up on the long term; 4) IPT and CBT, with different timings and methods, have both shown efficacy in the mid-term/long-term period in patients with BN; 5) CBT and its enhanced version produced rapid changes in the acute phase. IPT led to improvements occurring later, with slower changes that tended to maintain efficacy in the long term; and 6) abstinence from binge eating with group IPT for binge eating disorder is stable and maintained (or further improved) in the long term.[76] IPT is a reasonable, cost-effective alternative to CBT for the overall ED spectrum.
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.
For adolescents, a randomized controlled trial showed family-based treatment to be more effective for achieving abstinence than cognitive-behavioral therapy at the end of 6 months of treatment. However, little difference was seen between these two treatments at the end of one year.[77]
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 BN.
Couples therapy
Patients with marital discord may benefit from couples therapy. Although research concerning marital and cohabitation relationships in patients with BN is limited, many patients with BN 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.[78]
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.[79]
Virtual reality
Virtual reality (VR) is a technology with a variety of uses including clinical research, education/training, and assessment and treatment of several medical and psychological conditions. A colloquial definition is that it is a human–computer interface that allows the user to interact with and become immersed in a computer-generated environment, which produces the feeling of “being there.” A review of 19 studies on the use of VR in BN and BED found nine studies on assessment and 10 on treatment.[80] Though the research is at an early stage, the use of VR in the assessment of those conditions showed some promise in identifying: 1) how those patients experienced their body image; and 2) environments or specific kinds of foods that may trigger binge–purging cycle. Some studies using VR-based environments associated to CBT showed their potential utility in improving motivation for change, self-esteem, body image disturbances, and in reducing binge eating and purging behavior.
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[81] , 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.[82]
One study provided some support for guided imagery compared to journaling. However, long-term maintenance of treatment effects is unknown.[83]
Recent research has shown Web-based CBT to improve psychopathology, decrease body dissatisfaction, and benefit other problems related to eating disorders. Overall, technology-based interventions (using computers, the Internet, and mobile resources) have been efficacious both in preventing and treating eating disorders.[84, 85]
Food and Drug Administration (FDA) approved treatments
Fluoxetine (Prozac): Initial dose 20 mg/d with advance over 1–2 weeks to 60 mg/d in the morning as tolerated. 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 – particularly selective serotonin reuptake inhibitors (SSRIs) – are the mainstay of pharmacotherapy for bulimia nervosa (BN).[8] 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 SSRIs.[86, 8] As mentioned above, only fluoxetine (Prozac) is approved by the FDA for the treatment of BN. 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[87] and citalopram[88] have also shown benefit. However, recent current FDA guidance advises that citalopram not be prescribed in doses more than 40 mg/d, which may be suboptimal for many patients. The exact mechanisms underlying the efficacy of antidepressants in BN 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 BN because of a higher risk of seizures in patients with eating disorders associated with this medication.[8]
Tricyclic antidepressants (TCAs)[89] and monoamine oxidase inhibitors (MAOIs) have been shown to be effective in small randomized controlled trials in patients with BN, but due to higher risks of adverse effects and toxicity in overdose they are not recommended as initial treatments.[8]
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.[90]
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.[8, 91] 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.[92]
Lithium: Lithium has not been demonstrated to be effective for BN per se. In patients with co-occurring bipolar disorder and BN, 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.[8, 93]
Miscellaneous
In small studies, ondansetron[94] , baclofen[95] , and an antiandrogenic oral contraceptive[96] have been shown to have some use as alternative pharmacotherapeutic options in the management of BN. 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 on Antidepressant Use in Children, Adolescents, and Adults by the Food and Drug Administration.
Case reports indicate that methylphenidate may be helpful for patients with BN and concurrent ADHD.[8]
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.
Combination treatment
Patients with BN often benefit more from combinations of psychotherapy and pharmacotherapy than from either treatment alone, particularly in the presence of a comorbid depressive disorder, which is seen in the majority of cases. For uncomplicated bulimia nervosa, CBT alone is superior to pharmacotherapy alone.[97]
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.[8] 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.[83]
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.[8] 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 an 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.[98]
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.[99]
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.[100, 101, 102]
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[103] (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 (Mallory-Weiss syndrome) develop or in case of esophageal rupture, which can precipitate acute mediastinitis. (See images below). For more information, see Medscape Reference articles Mallory-Weiss Syndrome and Esophageal Rupture.
View Image
This chest radiograph demonstrates pneumomediastinum, which can occur in association with esophageal rupture from forceful vomiting.
View Image
Water-soluble contrast esophagram from a patient with esophageal perforation after esophageal dilation shows contrast leak (arrowheads) and normal eso....
View Image
Mallory-Weiss tear. Typical longitudinal mucosal tear with overlying fibrinous exudate extending from the distal esophagus to the gastric cardia. Cour....
These conditions are surgical emergencies and, although uncommon, are occasional causes of mortality related to bulimia nervosa.
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 long-term treatment of these patients.[104]
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.
Most authorities agree that patients with bulimia nervosa (BN) who have benefited from CBT are likely to benefit from a program of relapse prevention as well, lasting usually 1–2 years. Since simply telling patients with bulimia nervosa who have achieved abstinence following a course of CBT to return for additional sessions if they fear relapse has been ineffective for preventing relapse, planned visits or regularly scheduled phone calls might be used.[105]
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.[106]
Studies suggest that patients with bulimia nervosa (BN) have increased rates of major depressive disorder, 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. Patients with BN who are depressed and who have concurrent alcohol dependence are at exceptionally high risk of suicide, particularly those who overexercise. Studies have shows that in people with eating disorders, excessive exercise appears to be linked to an increased prevalence of acquired capability for suicide (ACS) and suicide attempts.[107, 108]
Medical complications
The all-cause mortality rate for BN per se is slightly lower than for anorexia nervosa (AN) (3.9% vs 4.0%, respectively).[53] Medical complications do arise and should be assessed carefully.
While the results of formal gastric emptying studies in patients with BN 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 BN.
Xerosis (dry skin) is a common finding in bulimia nervosa, which appears to be related to the chronic dehydration to which persons with BN 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.
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.[109] 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.[110]
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.[111]
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.[112] 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.[10] 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.[113]
Consistent predictors of outcome have not yet been identified. However, the severity of the purging sequelae, negative self-image,[114] childhood maltreatment,[115] childhood obesity/overeating,[116] individual/family eating patterns during childhood/early adolescence,[117] and ADHD[118] 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.[119]
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 patient’s consent, families should be involved in treatment. Such involvement may contribute to the likelihood of better outcomes.[8]
For excellent patient education resources, visit eMedicineHealth's Women's Health Center. Also, see eMedicineHealth's patient education article Bulimia.
For further information, see the following Web sites:
National Eating Disorders Association
Academy of Eating Disorders
Eating Disorders Coalition for Research, Policy, & Action
The Alliance for Eating Disorders Awareness
Eating Disorders Anonymous
Eating Disorders Information Network
The National Eating Disorders Screening Program
National Association of Anorexia Nervosa & Associated Disorders
Anorexia Nervosa & Related Eating Disorders
American Dietetic Association
Eating Disorders Online
US Department of Health and Human Services, National Institutes of Health, Health Information
American Pregnancy Association: Pregnancy and Eating Disorders
Something Fishy
Below is a list of workbooks and books for bulimia nervosa:
Sandoz E, Wilson K, Dufrene T: The Mindfulness and Acceptance Workbook for Bulimia: A Guide to Breaking Free from Bulimia using Acceptance and Commitment Therapy. Oakland, CA, New Harbinger Publications, Inc, 2011
Astrachan-Fletcher E, Maslar M: The Dialectical Behavior Therapy Skills Workbook for Bulimia: Using DBT to Break the Cycle and Regain Control of Your Life. Oakland, CA, New Harbinger Publications, Inc, 2009
Miller C: My Name Is Caroline, second edition. New York, Cogent Publishing, 2014
Miller C: Positively Caroline. New York, Cogent Publishing, 2013
Feigenbaum N: Maintaining Recovery From Eating Disorders: Avoiding Relapse and Recovering Life. London, UK, Jessica Kingsley Publishers, 2012
DeSole L: Eating Disorders and Mindfulness: Exploring Alternative Approaches to Treatment. New York, Routledge, 2014
Fairburn C: Overcoming Binge Eating, second edition. New York, Guilford, 2013
Schmidt U, Treasure J: Getting Better Bit(e) by Bit(e): second edition, A Survival Kit for Sufferers of Bulimia Nervosa and Binge Eating Disorder. East Sussex, UK, Psychology Press, 2015
Other books reported to be helpful by patients/families include the following:
Bulik CM, Taylor N: Runaway Eating: The 8-Point Plan to Conquer Adult Food and Weight Obsessions. New York, Rodale Books, 2005
Lock J, le Grange D: Help Your Teenager Beat an Eating Disorder. New York, Guilford, 2005
Walsh BT, Cameron VL: If Your Child Has an Eating Disorder: An Essential Resource for Parents. New York, Guilford, 2005
Donald M Hilty, MD, Associate Chief of Staff, Mental Health, Northern California VA Healthcare System; Vice-Chair of VA Mental Health Services
Disclosure: Nothing to disclose.
Coauthor(s)
Joel Yager, MD, Professor of Psychiatry, University of Colorado Health Sciences Center; Professor of Psychiatry Emeritus, University of California, Los Angeles, David Geffen School of Medicine; Professor of Psychiatry Emeritus, University of New Mexico School of Medicine
Disclosure: Nothing to disclose.
Specialty Editors
Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Chief Editor
David Bienenfeld, MD, Professor, Departments of Psychiatry and Geriatric Medicine, Wright State University, Boonshoft School of Medicine
Disclosure: Nothing to disclose.
Additional Contributors
Christine I Osterhout, MD, Resident Physician, Department of Psychiatry and Behavioral Sciences, University of California, Davis Health System
Disclosure: Nothing to disclose.
Gagandeep Randhawa, MBBS, Resident Physician, Department of Psychiatry, Kaweah Delta Medical Center, University of California, Irvine, School of Medicine
Disclosure: Nothing to disclose.
Lorin M Scher, MD, Associate Professor, Director, Emergency Psychiatric Services, Director, Integrated Behavioral Health Services, Director, Medical Student Education in Psychiatry, Medical Director, Government and Community Relations, University of California Davis Health System
Disclosure: Nothing to disclose.
Acknowledgements
Robert C Daly, MB, ChB, MPH Senior Fellow, Department of Behavioral Endocrinology, National Institute of Mental Health, National Institutes of Health
Disclosure: Nothing to disclose.
Raj K Kalapatapu, MD Fellow, Addiction Psychiatry, Columbia University College of Physicians and Surgeons
Raj K Kalapatapu is a member of the following medical societies: American Academy of Addiction Psychiatry, American Academy of Child and Adolescent Psychiatry, American Association for Geriatric Psychiatry, American Medical Association, and American Psychiatric Association.
Disclosure: Nothing to disclose.
Gabriel I Uwaifo, MD Associate Professor, Section of Endocrinology, Diabetes and Metabolism, Louisiana State University School of Medicine in New Orleans; Adjunct Professor, Joint Program on Diabetes, Endocrinology and Metabolism, Pennington Biomedical Research Center in Baton Rouge
Gabriel I Uwaifo, MD is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Physicians-American Society of Internal Medicine, American Diabetes Association, American Medical Association, American Society of Hypertension, and The Endocrine Society
Disclosure: Nothing to disclose.
Kelda Harris Walsh, MD Assistant Professor of Clinical Psychiatry, Section of Child and Adolescent Psychiatry, Department of Psychiatry, Indiana University School of Medicine; Chief, Obsessive-Compulsive/Tourette/Anxiety Disorders Clinic, Riley Hospital for Children
Disclosure: Nothing to disclose.
Acknowledgments
The authors would also like to acknowledge the contributions of Rebecca Davis, Librarian at the University of California (UC), Davis and Dr. Eric Rickin, Director for the Center for Overcoming Problem Eating (COPE) at the Western Psychiatric Institute and Clinic, University of Pittsburgh Medical Center. Finally, the authors thank the Department of Psychiatry and Behavioral Sciences at UC Davis.
References
American Psychiatric Association DSM-5. Diagnostic and Statistical Manual of Mental Disorders. 5th ed. 2013.
Mehler PS, Birmingham LC, Crow SJ, Jahraus JP. Medical Complications of Eating Disorders. Grilo CM, Mitchell JE. The Treatment of Eating Disorders: A Clinical Handbook. New York: The Guilford Press; 2010. 66.
Hudson, JI, Hirpi, E, Pope, HG, et al. The prevalence and correlates of eating disorders in National Comorbidity Survey Replication. Biol Psychiatry. 2—7;61:348-358.
Scherag,S, Hebebrand, J, Hinney, A. Eating disorders: the current status of molecular genetic research. Eur Child Adolesc Psychiatry. 2010. 19:211-226.
Kaye,W. Neurobiology of anorexia and bulimia nervosa. Physiology & Behavior 94. (2008). 121-135.
Bailer, UF, Kaye, WH. A review of neuropeptides and neuroendocrine dysregulation in anorexia nervosa and bulimia nervosa. CNS and Neurological Disorders. 2003. 2:53-59.
Self-help and guided self-help for eating disorders, Volume 4 [database online]. The Cochrane Database of Systematic Reviews: The Cochrane Library, The Cochrane Collaboration; 2002. Updated 2007.
Arbaizar, B, Gomez-Acebo, I, Llorca, J. Efficacy of Topiramate in bulimia nervosa an binge-eating disorder: a systematic review. General Hospital Psychiatry. 2008. 30:471-475.
Broft A, Berner LA, Walsh BT. Pharmacotherapy for Bulimia Nervosa. Grilo CM, Mitchell JE. The Treatment of Eating Disorders: A Clinical Handbook. New York: The Guilford Press; 2010. 388.
Psychotherapy for bulimia nervosa and binging, Volume 1 [database online]. The Cochrane Database of Systematic Reviews: The Cochrane Library, The Cochrane Collaboration; 1998. Updated 2005.
Antidepressants versus psychological treatments and their combination for bulimia nervosa [database online]. The Cochrane Database of Systematic Reviews: The Cochrane Library, The Cochrane Collaboration; 1997. Updated 2005.
Haines, J, Neumark=Sztainer, D, Perry, CL, et al. V.I.K. (Very Important Kids): a school based program designed to reduce teasing and unhealthy weight-control behaviors. Health Education Research-Theory and Practic. 2006. 21(6):884-895.
Brauser D. Excessive Exercise Predicts Suicidal Behavior in Eating Disorders. Medscape Medical News. Apr 18 2013. Available at http://www.medscape.com/viewarticle/782742. Accessed: Apr 22 2013.
Fichter, MM, Quadflieg, N, Hedlund, S. Long term course of binge eating disorder and bulimia nervosa: relevance for nosology and diagnostic criteria. Int J Eat Disorders. 2008. 41:577-586.
Arikian, A, Keel, PK, Miler, KG. Parental psychopathology as a predictor of long-term outcome in bulimia nervosa patients. Eating Disorders. 2008. 16:30-39.
Von Holle, A, Pinheiro, AP, Thornton, LM, et al. Temporal patterns of recovery across eating disorder subtypes. Australia and New Zealand Journal of Psychiatry. 2008. 42:108-117.
Goebel-Fabbri, AE, Fikkan, J, Franko, DL, et al. Insulin restriction and associated morbidity and mortality in women with type 1 diabetes. Diabetes Care. 2008. 31:415-419.
Brooks M. Enhanced CBT Bests Psychoanalysis for Bulimia. Medscape Medical News. Available at http://www.medscape.com/viewarticle/815300. Accessed: December 8, 2013.
Wolcott, RB, Yager, J, Gordon, G. Dental sequelae to the binge-purge syndrome (bulimia): report of cases. JADA. 1984. 109:723-725.
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.
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. 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.
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.
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. 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.
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.
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.
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. 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.
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.
Anorexia Nervosa
AN and BN
Bulimia Nervosa
Restriction of energy intake relative to requirement, leading to significantly low body weight in the context of age, sex, developmental trajectory, and physical health
Recurrent episodes of binge eating: a) eating in a discrete period of time, within a 2-hour period, an amount that is definitely larger than what most would eat in that time period; b) a sense of lack of control over eating
Intense fear of gaining weight or of becoming fat, or persistent behavior that interferes with weight gain, even though at a significantly low weight
Recurrent inappropriate compensatory behaviors in order to prevent weight gain, such as self-induced vomiting; misuse of laxatives, diuretics, or other medications; fasting; or excessive exercise
Disturbance in which one's body weight or shape is experienced, undue influence of body weight or shape on self-evaluation, or persistent lack of recognition of the seriousness of the current low body weight
The binge eating and inappropriate compensatory behaviors both occur, on average, at least once a week for 3 months
Two types: Restrictive and Purge/Bing-Eating type
The disturbance does not occur exclusively during episodes of AN
Body Dysmorphic Disorder
BDD and BN
BN
Preoccupation with one or more perceived defects or flaws in physical appearance that are not observable or appear slight to others
Disturbance in which one's body weight or shape is experienced, undue influence of body weight or shape on self-evaluation
Recurrent episodes of binge eating: a) eating in a discrete period of time, within a 2-hour period, an amount that is definitely larger than what most would eat in that time period; b) a sense of lack of control over eating
At some point during the course of the disorder, the individual has performed repetitive behaviors or mental acts in response to the appearance concerns
The preoccupation causes significant distress or impairment in social, occupational, or other important areas of functioning
Recurrent inappropriate compensatory behaviors in order to prevent weight gain, such as self-induced vomiting; misuse of laxatives, diuretics, or other medications; fasting; or excessive exercise
The appearance preoccupation is not better explained by concerns with body fat or weight in an individual whose symptoms meet diagnostic criteria for an eating disorder
The binge eating and inappropriate compensatory behaviors both occur, on average, at least once a week for 3 months
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