Pediatric Bulimia

Bulimia nervosa is an eating disorder characterized by binge eating and purging. It usually begins in adolescence or young adulthood, and is far more common in females than in males.

Diagnostic criteria (DSM-5)

Criteria for the diagnosis of bulimia include preoccupation with eating and overeating large amounts of food in short periods, also described as binge eating. This behavior is then followed by inappropriate behavior to avoid weight gain, most notably, self-induced vomiting. Other methods of avoiding weight gain include laxative/diuretic abuse and excessive exercise. Bulimia nervosa is a disease with a highly focused patient population; it is predominantly found in women and is virtually nonexistent in nonindustrialized countries.[1, 3, 4, 5, 6, 7, 8, 9]

Bulimia nervosa is a disease that most likely emerges from a complex integration of many factors. These factors may be psychological, cultural, environmental, and societal. Many proposed associated factors are involved in the development of bulimia. These factors can include chemical imbalances in neurotransmitters, such as serotonin or pancreatic polypeptides (eg, pancreatic peptide YY [PYY]). Psychological and psychiatric problems are also thought to contribute to the development of bulimia. Another contributing factor is family problems. Participation in extracurricular activities that emphasize body shape and image has also been linked to the development of bulimia.

The binge and purge cycle characteristic of bulimia affects multiple organ systems. The GI system can be affected by the overeating associated with binge episodes. This overeating can stretch the stomach or delay gastric emptying. Purging can induce esophagitis or esophageal rupture due to vomiting. Pancreatitis can also occur. Electrolyte abnormalities can include hypokalemia and hypochloremia. Cardiovascular abnormalities can lead to arrhythmias, arrest, cardiac rupture, or pneumomediastinum. The pulmonary system can be damaged by aspiration of gastric contents upon vomiting. Renal function impairment is also possible.[4, 6, 10, 11, 12, 13]

Frequency

United States

The lifetime prevalence of bulimia nervosa among women is 1%–3%, and a comparable percentage of women have less severe variants of the disorder. Lifetime prevalence among men is 0.1%.[3, 13]

Although no concrete data are available, bulimia is a disease that is highly culturally dependent. It is found solely in societies in which a high cultural value is placed on slimness and is virtually nonexistent in nonindustrialized countries.

Mortality/Morbidity

Death is a relatively uncommon outcome for bulimia. Approximately 0-3% of women with the disease eventually die from complications of the disease; however, these numbers may be underestimated owing to low ascertainment rates and short follow-up periods.

The leading cause of death among patients with eating disorders is suicide, which is more common in patients with bulimia nervosa than in those with anorexia nervosa (AN). Factors most strongly associated with suicide attempt or suicidal ideation in patients with eating disorders include concurrent drug use, alcohol use, and tobacco use.[14] Suicide risk should be carefully monitored in patients with eating disorders who also have these risk factors.

One third of patients who present for treatment of bulimia nervosa have past histories of anorexia nervosa.

Bulimia has many complications (see Complications).[3, 10, 14]

Race

Bulimia has traditionally been thought of as a disease that predominantly affects whites. The low incidence of eating disorders among nonwhites has been attributed to differences among ethnic groups in ideal body image. Studies have shown that black women are less likely to develop eating disorders and tend to express more satisfaction with their bodies than white women of similar weight; however, other studies suggest that the incidence of bulimia among minority groups is higher than previously thought. Studies suggest that patients from higher socioeconomic groups are more likely to seek treatment, making the incidence within these groups appear to be higher.

Some population studies suggest an equal incidence of bulimia in blacks and whites. Overall, strong circumstantial evidence suggests that cultural factors play large roles in eating disorder development. Most cases of bulimia nervosa originate in industrialized countries. In general, industrialized countries are places where food is plentiful and a preoccupation with thinness in women is present.[5, 11]

Sex

Bulimia primarily occurs in young women. Males comprise only 2-8% of all bulimia cases; however, this number is thought to be on the rise.[15]

Age

Bulimia is most common in adolescents and young adults. Median age of onset is 18 years.[4, 9]

Obtaining a thorough history is essential in any patient in whom bulimia is suggested. Patients with bulimia often deny and make attempts to minimize the problem; however, thorough and careful questioning may reveal clues that the patient has bulimia. Often, patients have a history of dieting attempts and may admit to feeling fat even when they appear thin.

Patients often state that their self-esteem is linked closely to their body weight or shape. The patient may have a history of using diet pills, laxatives, ipecac, or thyroid medication to lose weight. Patients may become vegetarians or eat only select low-calorie foods. Diabetic patients may withhold insulin.

Patients who admit to purging behavior often describe a history of uncontrolled eating binges at least once weekly (DSM-5). During these binges, large amounts of food are consumed in private. Some patients plan ahead for binges by secretly hoarding food. They can also drive from one fast food restaurant to another so that those at home are not aware of the behavior. There is a large component of shame and guilt that accompanies both binging and purging behavior. Patients may describe feeling a loss of control when the binge begins, then a period of frenzied and rapid eating. The binge is followed by inappropriate compensatory behavior, usually self-induced vomiting. Excessive laxative use may occur too. Diabetics have been known to misuse their insulin as a dangerous way to purge calories.

The diagnosis of bulimia is not conditional on physical findings. Physical findings may not be present in all patients. Patients may have some findings, all findings, or none at all. The sections that follow describe the physical findings that are associated with bulimia.[3, 4, 5, 7, 10, 16, 17]

General findings include the following:

• Normal body weight, but may be increased or decreased

• Often frequent fluctuations in weight

• Loss of subcutaneous fat

Vital signs:

• Temperature - Hypothermia

• Blood pressure - Hypotension

Head, ears, eyes, nose, and throat:

• Dental erosion - Decalcification of dental surfaces exposed to vomitus (Amalgams and fillings are relatively resistant to acid and often project above the surface of the teeth. It is important to note that the surfaces of the teeth most often exposed to vomitus are facing the posterior oropharynx; therefore, a mirror may be necessary to fully evaluate dentition.)

• Palatal trauma

• Painless enlargement of parotid glands

• Esophageal tears

Cardiovascular findings may include bradycardia.

Patients may present with frequent complaints of diffuse pain upon palpation of the abdomen.

Extremities:

• Metacarpal phalangeal bruises, calluses, scarring, abrasions (Russell sign)

• Edema possible if patient abuses laxatives or diuretics

• Proximal muscle weakness if patient abuses ipecac

• Waddling gait if patient abuses ipecac

Rectal prolapse may be present.

Bulimia nervosa (BN) is a complex disease that most likely emerges from an integration of physiological, psychological, and environmental factors. Currently, no defined single cause of bulimia nervosa is recognized. Several factors are believed to play a strong role in the development of bulimia.[3, 5, 11, 16, 18, 19]

Chemical

A few hypotheses suggest specific chemical abnormalities in the body are associated with bulimia.

Serotonin is a neurotransmitter with broad functions within the body. Among these functions, serotonin is involved in the development of satiety. Increased levels of serotonin are associated with decreased food intake. Serotonin is believed to increase postprandial satiety rather than directly decrease appetite.

One hypothesis of the development of bulimia involves abnormalities in serotonergic function. Some patients with bulimia have been found to have low serotonin levels. Because serotonin is involved in the development of satiety, these disturbances may contribute to the persistence of binge eating.

A potential hypothesis is that an impaired serotonergic response may contribute to the blunted satiety and prolonged periods of rapid food ingestion present in bulimia nervosa. Dieting has also been associated with altered serotonin function, more markedly in women than in men. Dieting is often a precursor to the development of bulimia; however, not all women who diet develop bulimia. This hypothesis is not thought to provide a sufficient sole explanation for the development of bulimia.

Another suggested pathophysiology involves increased levels of peptides involved in mediating appetite. Increased levels of a pancreatic polypeptide PYY, a peptide known to increase appetite, have been found in some patients with bulimia after a period of eating stability. This would suggest that these patients have a higher level of appetite, even when given a normal diet.

Psychiatric

Premorbid psychiatric disorders are often associated with development of bulimia. These can include affective disorders, anxiety disorders, and substance abuse.

Many patients with bulimia have concomitant depression and/or bipolar disorder.

Psychological and environmental

The strongest risk factor in the development of bulimia is history of dieting. Many patients report that their eating binges began in the context of or immediately following a diet. Many patients continue to restrict their caloric intake even when not binge eating.

Strong circumstantial evidence suggests that cultural factors play a large role in eating disorder development. Most cases of bulimia nervosa originate in industrialized countries where food is plentiful and a preoccupation with thinness in women is present.

Obesity is another risk factor for bulimia.

Family

Family conflict and instability are also associated with the development of bulimia.

A history of sexual abuse has been associated in some literature as a risk factor for development of bulimia.

A family history of eating disorder increases a child's risk of developing an eating disorder to 2-20 times that of the general population.

Interests and activities

Certain athletes and groups are thought to be more prone to development of bulimia. Specifically, these include ballet dancers, models, cheerleaders, runners, gymnasts, weight lifters, body builders, jockeys, divers, wrestlers, figure skaters, and field hockey players. Persons in these particular sports and activities often place a high value upon thinness or maintaining a particular weight.

The bodies of participants in these activities are often on display in front of crowds or judged in terms of body shape and weight. These high-pressure situations and preoccupation with weight can place teens at risk for eating disorders.

Bulimia nervosa (BN) requires a clinical diagnosis. No single laboratory test can be diagnostic. The laboratory tests listed below may be helpful in assessing the medical complications that arise from bulimia nervosa.

Routine laboratory tests[7, 4, 8, 9, 20]

• CBC count: Malnutrition can cause neutropenia and, rarely, anemia or thrombocytopenia.

• Biochemistry panel: If dehydration or electrolyte imbalances are suspected, electrolytes, calcium, magnesium, phosphorous, glucose, creatinine, and BUN levels may be obtained to measure liver, kidney, and pancreatic functioning. Common findings include the following:

  • Dehydration

  • Hypokalemia - Secondary to purging, or use of diuretic or laxatives

  • Hypochloremia - Secondary to purging and laxative or diuretic use

  • Hypocalcemia

  • Hypomagnesemia - Due to diarrhea resulting from laxative use

  • Hypophosphatemia

  • Hyponatremia - Secondary to use of diuretics

  • Metabolic acidosis - Secondary to laxative use

  • Metabolic alkalosis - Secondary to purging

  • Increased BUN levels

• Endocrine studies in patients with bulimia nervosa may exhibit the following abnormal findings:

  • Decreased follicle-stimulating hormone (FSH), leuteinizing hormone (LH), and estradiol levels

  • Prolactin levels: Studies have documented both increased and decreased basal serum prolactin in association with bulimia nervosa.

  • Increased cortisol levels; positive dexamethasone suppression test result

• Thyroid and parathyroid panels

  • Hypothyroidism can occur as a mechanism of energy conservation.

  • Decreased free triiodothyronine (FT3) and free thyroxine (FT4) levels may be observed.

• Gastrointestinal laboratory tests may reveal the following:

  • Increased amylase secondary to vomiting

  • Esophagitis, pancreatitis, or delayed gastric emptying

  • Liver function test results usually normal

Situational laboratory tests[8, 21, 9]

• A drug screen may be indicated for patients with possible drug use. Attention should be paid to adolescent confidentiality anytime drug testing involves an adolescent patient.[22]

• Ipecac use can cause emetine cardiomyopathy, hepatic toxicity, or peripheral myopathy. Hypokalemia can also result, and the following laboratory studies may be indicated for patients suspected of using ipecac:

  • Stool and urine analyses for emetine (a byproduct of ipecac)

  • Cardiac assessment - Muscle enzyme values, lipid levels, magnesium, zinc, electromyography

  • Electrocardiography (Findings may include cardiac arrhythmias, a prolonged QT interval, ipecac cardiomyopathy.)

ECG should be considered in the following conditions:

• Hypokalemia: This condition can cause cardiac conduction defects that may lead to heart arrhythmias or seizures.[9]

• Severe purging behaviors or suspected ipecac use

• Symptoms and signs of arrhythmias

Gastric motility studies should be considered in the following conditions:

• Prolonged history of bulimia

• History of constipation (often due to chronic use of laxatives)

• Recent weight loss: Consider other causes of vomiting such as superior mesenteric artery (SMA) syndrome

• Other unexplained abdominal pain

Inpatient care is warranted if the patient is suicidal, has abnormal ECG findings or electrolyte levels, is dehydrated, or has had no response to outpatient therapy. Intensive outpatient treatment is currently being evaluated as an alternative to inpatient care.[23, 24, 25]

Inpatient care should include the following:

• Supervised meals

• Supervised bathroom privileges

• No access to bathroom for 2 hours after eating

• Monitoring of weight and physical activity. If underweight, patients will often attempt to artificially increase their weight by drinking water, not emptying their bladder or hiding weighted objects in their clothing prior to known weighing periods.

• Assessment of nutritional state

• Identifications of precipitants to binge and purge

• Frequent assessment of electrolytes

• Individual psychotherapy[26]

• Frequent doctor visits

See Further Outpatient Care for outpatient management.[4, 5, 6, 7, 9]

Future directions

In addition to medications and therapy, there has been some preliminary work investigating effects of brain stimulation and neuromodulation in adults with bulimia. Further research is needed to see if transcranial magnetic stimulation will become an effective modality in treating bulimia and other eating disorders.[27, 28]

Surgical care is indicated only in cases in which gastric or esophageal ruptures are suspected.[4, 5, 7, 8]

Cognitive behavior therapy (CBT) has been shown to improve outcomes in patients with bulimia. Referral to a mental health provider with experience in CBT is recommended.

Dental consultation is appropriate to help avoid progression of enamel erosion due to frequent vomiting.

Nutrition consultation can be very helpful in guiding patients toward normal eating patterns and healthy food choices.

Emphasis in diet instruction is on eating balanced meals, achieving a normal eating pattern, and consuming adequate calories.

Another goal is to reintroduce feared foods that patients previously binged on in small amounts, allowing patients to enjoy these foods without overeating.

Patient and family should be counseled to monitor excess activity. Practitioners should stress the importance of playful, pleasurable activities to reduce stress.

Canadian practice guidelines

Canadian practice guidelines for treating children and adolescents with eating disorders were published in 2020.[29] Recommendations include the following:

• Family-based treatment (FBT) is strongly recommended for children and adolescents with anorexia nervosa or bulimia nervosa.

• Multi-family therapy (MFT) is a reasonable treatment option for children and adolescents with anorexia nervosa.

• Cognitive-behavioral therapy (CBT) is a reasonable treatment option for children and adolescents with anorexia nervosa or bulimia nervosa.

• Adolescent-focused therapy (AFP) is a reasonable treatment option for children and adolescents with anorexia nervosa.

• Yoga, in addition to standard treatments, is a reasonable treatment option for medically stable children and adolescents with anorexia nervosa, bulimia nervosa, and other specified feeding and eating disorders.

• Olanzapine or aripiprazole may be reasonable treatment options for certain populations of children and adolescents with anorexia nervosa if monitored carefully.

• It is strongly recommended that the least intensive treatment environment be provided, especially for those children and adolescents with anorexia nervosa requiring a first admission to hospital and/or with a duration of illness less than 3 years.

The medications most commonly used to treat bulimia are antidepressants, typically selective serotonin reuptake inhibitors (SSRIs) or tricyclic antidepressants (TCAs). A Cochrane Database Review showed that patients with bulimia nervosa (BN) who were treated with antidepressants were more likely to interrupt their treatment prematurely due to adverse events and patients treated with TCAs dropped out of treatment more frequently than patients treated with placebo.[30] Of note, the opposite was found in those treated with fluoxetine, suggesting that it may be a more acceptable treatment as it is typically better tolerated. In some cases, CBT may be a more acceptable first-line treatment than medication, especially in patients concerned about medication side effects[31] or in those without comorbid anxiety or depression.

Other classes of medications, including mood stabilizers (eg, lithium), antiemetics, antipsychotics, serotonin/norepinephrine reuptake inhibitors (SNRIs), anticonvulsants, and trazodone, have been investigated for the treatment of eating disorders.[32, 33, 13, 30]

In 2011, the World Federation of Societies of Biological Psychiatry (WFSB) compiled an extensive review regarding pharmacological treatment of eating disorders.[34] Their report provides guidelines regarding the use of TCAs, SSRIs, MAOIs, mood stabilizers, and naltrexone, among others. In brief, the most robust evidence is for the use of fluoxetine in treating bulimia. It has been well studied and received a recommendation grade of 1, meaning that it has a good risk-to-benefit ratio and has undergone a number of randomized controlled trials. These same guidelines assign a moderate risk-to-benefit ratio to TCAs and topiramate.

Topiramate has been assigned grade A evidence based on 2 randomized controlled studies, which showed improvement over placebo. The use of topiramate in children and adolescents has not been well established and the use of topiramate in adults carries a moderate risk-to-benefit ratio, given a number of potential use-limiting adverse effects, including sedation, cognitive impairment, and dizziness. There have been case reports but no randomized trials investigating carbamazepine and oxcarbazepine.

Class Summary

SSRI medications are thought to help ameliorate depressive symptoms associated with bulimia and to help patients achieve a healthier body image.

SSRIs are greatly preferred over the other classes of antidepressants. Because the adverse effect profile of SSRIs is less prominent, improved compliance is promoted. SSRIs do not have the cardiac arrhythmia risk associated with TCAs. Arrhythmia risk is especially pertinent in overdose, and suicide risk must always be considered when treating a child or adolescent with mood disorder.

Physicians are advised to be aware of the following information and use appropriate caution when considering treatment with SSRIs in the pediatric population.

In December 2003, the UK Medicines and Healthcare Products Regulatory Agency (MHRA) issued an advisory that most SSRIs are not suitable for use by persons younger than 18 years for treatment of "depressive illness." After review, this agency decided that the risks to pediatric patients outweigh the benefits of treatment with SSRIs, except fluoxetine (Prozac), which appears to have a positive risk-benefit ratio in the treatment of depressive illness in patients younger than 18 years.

In October 2003, the US Food and Drug Administration (FDA) issued a public health advisory regarding reports of suicidality in pediatric patients being treated with antidepressant medications for major depressive disorder. This advisory reported suicidality (both ideation and attempts) in clinical trials of various antidepressant drugs in pediatric patients. The FDA has asked that additional studies be performed because suicidality occurred in both treated and untreated patients with major depression and, thus, could not be definitively linked to drug treatment.

However, a study of more than 65,000 children and adults treated for depression from 1992-2002 by the Group Health Cooperative in Seattle found that suicide risk declines, not rises, with the use of antidepressants. This is the largest study to date to address this issue. Another study published in the Journal of the American Medical Association in 2004 showed that a combination of CBT plus SSRI treatment (fluoxetine) significantly decreases suicidal thinking in patients with depression, and the reduction is far greater than with placebo or therapy alone.[35]

Currently, evidence does not associate obsessive compulsive disorder (OCD) and other anxiety disorders treated with SSRIs with an increased risk of suicide.

Fluoxetine (Prozac)

Antidepressant medication that selectively inhibits presynaptic serotonin reuptake with minimal or no effect in the reuptake of norepinephrine or dopamine. Higher doses than those used to treat depression are typically needed in the treatment of bulimia nervosa.

Class Summary

TCAs are thought to help ameliorate depressive symptoms associated with bulimia and to help patients achieve a healthier body image.

Desipramine (Norpramin)

TCAs are only considered when safer antidepressants, such as SSRIs, are not effective. May increase synaptic concentration of norepinephrine in CNS by inhibiting reuptake by presynaptic neuronal membrane. May have effects in the desensitization of adenyl cyclase, down regulation of beta-adrenergic receptors, and down regulation of serotonin receptors. However, TCAs are generally not considered in the treatment of bulimia in children and are rarely considered in the treatment of bulimia in adolescents.

Class Summary

Some studies recommend short-term use of antiemetics at the onset of a patient's treatment. Antiemetics are thought to reduce a patient's stimuli to vomit and help patients through the few weeks it takes for antidepressants to become fully effective.[36] The WFSB assigns andansetron grade B evidence but recommends limiting its use secondary to adverse effects.

Ondansetron (Zofran)

Selective 5-HT3-receptor antagonist that blocks serotonin both peripherally and centrally.

The 2 standard approaches to outpatient care are counseling and medication; these are not mutually exclusive. A combination of these methods has been found to be most effective in patients with bulimia nervosa (BN).

The most studied form of outpatient care for patients with bulimia is CBT. A specific form of CBT has been created for patients with bulimia and is termed CBT-BN. CBT has been shown to have significantly better results in patients with bulimia nervosa than other forms of psychotherapy.

• This form of therapy is usually short-term (4-6 mo).

• CBT focuses on patients' preoccupation with body shape and weight, persistent dieting, and binge eating and purging.

• Patients are asked to monitor thoughts, feelings, and circumstances surrounding binge-purge episodes. Patients may be asked to keep a food diary and record feelings and urges to binge or purge along with foods the patient consumed during the day. By examining the cues that lead patients to binge, patients can learn to avoid these cues or to redirect their feelings when the cues emerge. These strategies can also help patients challenge their fears of loss of control.

• Patients are also instructed to cease dieting and begin regular eating. By quitting dieting and removing the feeling of being restricted in what one can eat, patients are less likely to binge on "forbidden foods."

• Patients are also asked to systematically challenge their assumptions linking weight to self-esteem.

• Therapy is focused on building trust and developing a treatment alliance.

• Patients are involved in setting the treatment goals.

• Some patients benefit from self-help groups. Family involvement in treatment is welcomed and encouraged.

• The goal of care is to focus on the overall well being of the patient.

• CBT is a highly effective treatment. A recent study of 78 adult women showed that over half achieved remission by the completion of CBT treatment. In addition to decreased frequency of binging and purging behaviors, subjects also showed improvement in mood and attitudes regarding feeding.[37] CBT is equally effective for both the purging type and nonpurging type of bulimia.[38]

Other staples of outpatient care include nutritional counseling and meal planning. Relaxation strategies are helpful for some, such as prolonged breathing and progressive muscle relaxation.

Other forms of therapy with unclear benefit include interpersonal psychotherapy, hypnobehavioral therapy, dialectical behavior therapy, and motivational enhancement therapy. These therapies have not been adequately studied in patients with bulimia nervosa.

Current research suggests that family therapy is as effective as CBT after 1 year of treatment; however, CBT shows improvement of symptoms within 6 months of initiation and improvement is seen as early as CBT session 3 in 50% of patients.[4, 21, 31, 39, 40, 41]

The second approach to treatment is the use of medications. The use of antidepressant medications, such as fluoxetine or a TCA, was initially based on an association between bulimia nervosa and mood disturbance. More than 12 double-blind placebo-controlled trials have shown that antidepressants help patients reduce binge frequency.

Prevention efforts have centered on counseling to encourage rational attitudes about weight, moderation of overly high self-expectations, enhancement of self-esteem, and alleviation of stress and stimulating a healthy body image.

Prevention efforts can be pursued in primary care physicians' offices during health supervision visits.

Many complications to bulimia are possible, including the following:[14, 10, 13, 9]

• CNS - Seizures

• Cardiac - Cardiac arrhythmias secondary to hypokalemia; can lead to cardiac arrest, cardiac rupture, and cardiomyopathy secondary to ipecac abuse

• Pulmonary - Pulmonary aspiration of gastric contents, pneumomediastinum

• GI - Esophageal rupture, esophagitis, delayed gastric emptying, pancreatitis

• Musculoskeletal - Muscle weakness secondary to ipecac abuse and potassium irregularities, tetany

• Renal - Impaired renal function

• Psychiatric - Depression, suicide attempts, substance abuse

• Reproductive - Increased risk of induced abortion[42]

CBT has been shown to benefit patients. Evidence suggests persistent benefit 4 years after treatment; however, treatment benefit greatly depends on accessibility to CBT-trained therapists. Therapists with expertise in CBT may be difficult to find outside of established centers.

Medication therapy has also been shown to benefit patients; however, only a minority of patients achieve full remission on medication alone. Limited data suggest that a considerable rate of relapse is observed once medications are discontinued.

Studies have shown that patients who receive treatment (CBT or medication) demonstrate benefit. One study compared treated versus nontreated patients 6 months after initial presentation. Follow-up studies reported that 28-33% women without treatment were in remission, and follow-up studies of treated women reported 21–75% successful remissions.

• After one year, follow-up studies reported 28–33% of patients without treatment were in remission, and 5–83% of women in treatment were in remission.

• Follow-up studies reported a range of 13–69% of patients still in remission without ongoing treatment 2–4 years after initial remission. These data were compared to data pertaining to women who were still in treatment; these women had remission ranges of 46-50%. Over 5 years of follow-up, untreated women had maintained remission rates around 31–60%. This was compared to women who were still in treatment, who had an average remission rate of 54%. Women in treatment outcome studies had higher rates of remission than women in studies who did not receive treatment.

• Overall, 5–10 years following presentation, approximately 50% of all women with bulimia nervosa fully recover, and 20% still have full bulimia nervosa.

Given that eating disorders only have been defined and studied as diseases for 20 years, limited long-term data on prognosis exist. The imprecise, inconsistent, and often confusing data on remission rates and percentages available for patient follow-up are evidence that more research and follow-up are needed.

Lower weight (less than 75% of MBW mean body weight) and longer duration (more than 19 months) of symptoms were predictors of poorer outcomes in a 2011 study of 11 sites of 267 adolescents with eating disorders.[43, 44] There was a slight benefit to family therapy with the Maudsley Model; however, all adolescent medicine-based treatments were effective in helping adolescents to gain weight.

Overall, despite advances in medical care and therapy, the prognosis for patients with bulimia remains guarded. Even in the best of hands, both medications and therapy fail in 33–50% of patients. The relapse rate remains around 30%, and patient crossover to anorexia nervosa from bulimia nervosa ranges from 0–7%.

Studies have shown that patients with bulimia who have a previous diagnosis of anorexia nervosa are more likely to have a protracted illness or relapse into anorexia nervosa during follow up compared with patients with bulimia with no history of anorexia nervosa.[45]

Education of patients and families involves teaching the seriousness and consequences of bulimic behavior.

Information about complications and physiologic changes that can occur as a result of bulimia is important to convey to patients and families.

Information on proper nutrition and metabolic balance is also helpful.

For excellent patient education resources, see eMedicineHealth's patient education article Bulimia.

The National Eating Disorder Association is dedicated to providing education, resources, and support to those affected by eating disorders. Their Web site includes information for patients, families, and health care providers.[46]