INTRODUCTION

Eating disorders are complex psychiatric illnesses characterized by pathological eating, related behaviors, and disturbances in body image that cause significant distress and impairment in those affected. The statistics associated with eating disorders can be overwhelming and heartbreaking. In the United States, approximately 30 million individuals are affected by an eating disorder in their lifetime, and while it is commonly thought to be a disease primarily in females, one-third of those who suffer from an eating disorder are male.¹ Ninety-five percent of those with eating disorders are between the ages of 12 to 25 with anorexia nervosa being the third most common chronic illness among adolescents. While not yet having developed a full-blown disorder, 50% of girls between the ages of 11 and 13 see themselves as overweight, and 80% of 13-year-olds have attempted to lose weight.² However, it is not just a disease of adolescents, 13% of women over the age of 50 have eating disorder symptoms.¹ An estimated 1 in 200 American women suffer from anorexia nervosa and approximately 2-3 per 100 American women suffer from bulimia nervosa. Eating disorders have the highest mortality rate of any mental illness and carry the highest mortality rate of any psychiatric disorder due to high suicide rates, particularly in anorexia nervosa. A study by the National Association of Anorexia Nervosa and Associated Disorders reported that 5 – 10% of anorexics die within 10 years after contracting the disease; 18-20% of anorexics will be dead after 20 years and only 30 – 40% will ever fully recover. Among women in the United States, the prevalence of eating disorders is similar across all major racial/ethnic groups.²

Eating disorders can have severe medical complications as well as psychiatric comorbidities, including cardiovascular, pulmonary, gastrointestinal and electrolyte complications requiring medical intervention. Prevention and early identification are critical as these disorders can become chronic and have serious psychiatric, psychosocial and medical consequences. Unfortunately, over 70% of those who suffer from an eating disorder will never seek treatment due to stigma.¹ Because of the complexity and breadth of clinical presentations and extent of co-occurring psychopathology the assessment and treatment of eating disorders is quite complex requiring a multidisciplinary approach and referral to a specialist is typically required. The physical, cognitive, emotional and social effects of starvation serve to maintain the illness in those who become significantly underweight making treatment even more difficult.³ This continuing education lesson will familiarize the pharmacist and technician with the different types of eating disorders as well as equip them to recognize the common clinical presentations and eating disorder behaviors. The psychiatric and physical comorbidities will be discussed in those suffering from the various eating disorders. 

MULTIDIMENSIONAL MODEL OF EATING DISORDERS

A comprehensive multidimensional model best illustrates the role various factors play in the origin of clinically significant eating disturbances. Psychological, biological, and sociocultural stressors contribute to the development of the disorder. This multidimensional model regards illnesses such as eating disorders to be multifactorial and determined by biochemical alterations on the molecular level as well as psychological and social influences. To adequately understand eating disorders one must take into account genetic susceptibilities and pathophysiologic processes as well as unique life circumstances, stressors, and psychological aspects by which patients construct their reality.⁴ Much is still unknown about the causes of eating disorders, but the dynamic interplay of multiple factors is evident in the development and maintenance of these complex disorders.

Sociocultural factors 

Sociocultural factors figure prominently in the etiology of eating disorders. Sociocultural (e.g., media, family, peer and partner) pressures for thinness have long been implicated in the development and maintenance of disordered eating behavior among women. It is speculated that pressure for thinness directly influences women’s tendencies to experience higher levels of internalization of the thin-ideal stereotype and body image disturbances. When women are surrounded by pressures to lose weight from significant others (or from media) who associate thinness with well-being and success they are likely to internalize this thin-ideal image. The more women feel pressured to be thin, the more they experience body image disturbances.⁵ As women are socialized to equate their self-worth with their body image they may likely foster the conclusion that one’s appearance is unsatisfactory, and as a result, have lower self-esteem which can make them more vulnerable to develop an eating disorder.⁶ This idealization of thinness and subsequent body dissatisfaction contributes to dieting behavior often beginning in early adolescence and is frequently a precursor to the development of an eating disorder. The adoption of these Western ideals of beauty and accompanying dieting behavior is contributing to an increased prevalence of eating disorders, both in the United States and globally.⁷

Psychological factors

Psychological factors associated with eating disorders includes personality features such as obsessive-compulsive traits, cognitive rigidity, emotional sensitivity and impulsivity. Other common traits seen in individuals suffering from an eating disorder include elevated perfectionism, neuroticism, negative urgency (the tendency to act rashly when distressed), avoidance motivation, sensitivity to social rewards, low extraversion, and high self-directedness. Since perfectionism and obsessive-compulsive traits share several overlapping features, such as rigidity, a need for control, and orderliness, it is not surprising that obsessive-compulsive personality disorders often co-occur with eating disorders. ⁸ Determining personality traits in the treatment of eating disorders may not only help to better understand their etiology and maintenance, but also develop more effective ways of matching specific treatment to patients.

Biological factors

Biological factors are highly contributory to the development and maintenance of eating disorders. Data suggest that genetic factors contribute to approximately 56% of the risk of developing an eating disorder. A female with a mother or sister with anorexia nervosa is approximately 12 times more likely to develop anorexia nervosa and four times more likely to develop bulimia nervosa than other individuals without a family history of these disorders. As well as hereditary factors, research suggests that several different neurotransmitters are involved in eating disorders and dysfunction of serotonin, dopamine and norepinephrine has been identified. Serotonin is partially responsible for the regulation of appetite, creating a sense of satiation, and regulating emotions and judgment. Bulimics have been shown to have decreased binding of serotonin to receptors in the brain and as a result studies suggest that the hypothalamus of bulimics may not trigger a normal satiation response. The successful treatment of bulimia nervosa with fluoxetine is additional evidence that abnormal levels of serotonin may play a key role in the development of bulimia nervosa.⁹

The regulation of appetite is a complex process that involves the integration of neurotransmitters, neuropeptides, hormones and metabolic signals. While most of the research has been done in animal studies, there has been speculation and various small studies documenting the abnormal neurotransmitters and metabolic processing in eating disorder subjects. Cholecystokinin octapeptide (CCK-8) is a digestive hormone that is released after food consumption to promote digestion and induce satiety. Those experiencing anorexia nervosa have a higher level of this hormone and there is now strong evidence that endogenous CCK-8 can be a powerful suppressor of food intake in those suffering from anorexia nervosa.^10,11 Gastrin is one of the major hormones released by the gastric mucosa after eating and has been demonstrated to be closely related to the secretion and motility of the digestive tract. Patients with anorexia nervosa have shown a decreased gastrin level which results in impaired gastric motility and ensuing symptoms that further discourage eating.¹² Biological factors may play a significant role in the development and maintenance of eating disorders and could be a potential target for future drug treatments.

CLASSIFICATION OF EATING DISORDERS

The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) is the 2013 publication of the American Psychiatric Association (APA) classification and assessment tool. The eating disorders listed in the DSM-5 include Anorexia Nervosa, Bulimia Nervosa, Binge Eating Disorder, Avoidant/Restrictive Food Intake Disorder and Other Specified Feeding and Eating Disorders. The last category identifies disorders having symptoms characteristic of a feeding and eating disorder that cause clinically significant distress or impairment in social, occupational, or other important areas of functioning, but do not meet the full criteria for any of the disorders in the other diagnostic classes. Examples include Atypical Anorexia Nervosa, Bulimia Nervosa or Binge Eating Disorder of low frequency and/or limited duration, Purging Disorder or Night Eating Syndrome. Other disorders discussed in the DSM-5 include pica, Rumination Disorder, Body Dysmorphic Disorder and Orthorexia Nervosa.¹³ This continuing education lesson will focus on Anorexia Nervosa and Atypical Anorexia Nervosa, Bulimia Nervosa, Binge Eating Disorder and Avoidant/Restrictive Food Intake Disorder. Table 1 lists the defining characteristics of the other eating disorders as outlined in the DSM-5.

Case 1

Karen, a 14-year-old female high school freshman, presented to her pediatrician at her mother’s insistence with vague complaints of abdominal pain and bloating, particularly after meals. She complained of infrequent constipation and two missed periods over the last six months. She was 64 inches tall and weighed 102 pounds (BMI of 17.5) which was a 9-pound weight loss since her annual examination approximately eight months ago. In private, Karen’s mother told the pediatrician that she has been less socially engaged and noted that Karen started jogging outside every day and was concerned that her daughter may have lost weight recently. This would not ordinarily concern her, but Karen was also skipping meals and had become “picky” regarding food choices. She was concerned that Karen was establishing unhealthy eating and exercise habits.

When presented with her mother’s concerns and the information by her pediatrician, Karen insisted that there was nothing to worry about and denied voluntary attempts to lose weight. She did admit that she was concerned about the amount of food her mother was serving at dinner and that she had started to avoid “fattening” foods and desserts, insisting that it was for health reasons. She reluctantly added that she was concerned that her hips were too large for her body frame and was hoping that continued exercise might minimize this defect. She was unconcerned about her irregular periods even though the pediatrician explained that it was unhealthy and likely due to her recent changes in weight, exercise and eating habits.

Anorexia Nervosa and Atypical Anorexia Nervosa (AN)

Symptoms/Characteristics

Anorexia Nervosa is characterized by persistent dietary restriction leading to a significantly low body weight (in context of what is minimally expected for age, sex, developmental trajectory, and physical health), distorted perception of body image, and an intense fear of gaining weight or becoming fat. The prevalence of AN is greater than previously suggested, since prior diagnostic criteria were more restrictive and individuals with AN often prefer to conceal their illness. The DSM-5 defines two subtypes of AN: binge-eating/purging type and restricting type. The binge-eating/purging subtype is characterized by recurrent episodes of binge-eating or purging (i.e., self-induced vomiting and/or abuse of diuretics, laxatives, enemas, or cathartics). The restricting subtype is characterized by dieting, fasting or excessive exercising without associated binge-eating or purging. Individuals who meet the above criteria but who have a BMI within average or above average range despite significant weight loss are classified as having atypical AN. Atypical AN is not as readily identified, although its psychological and medical presentation is comparable if not more severe than typical AN. The DSM-5 classifies the severity of AN according to BMI (Table 2).¹³

Although the cause of AN is unknown, most experts favor a psychiatric origin. Comorbidity with depression, anxiety, or obsessive-compulsive disorder is common, leading to an obsession with food and perfectionist tendencies and other behavior. Some theories allude to the patient’s attempt to gain control of one’s body to defy parental control while still others postulate that a patient's unwillingness to inhabit an “adult body” may represent a rejection of adult responsibilities and the implications of adult interpersonal relationships.¹⁴ Whatever the etiology, it is multifaceted and not one hypothesis can explain each individualized case.

Patients suffering from AN may exhibit severe emaciation and complain of cold intolerance as well as various gastrointestinal complaints. Bradycardia, hypotension, and hypothermia may be present in severe cases. Upon examination a patient will present with various other physical signs/symptoms related to complications of decreased body fat (Table 3). The need to remain on oral contraceptives to maintain menses or a cessation of menstruation is a common finding. Laboratory values are variable depending on the severity of the disorder but may include anemia, leukopenia, electrolyte abnormalities, and elevations of blood urea nitrogen (BUN) and serum creatinine.¹⁴ In addition to these symptoms and abnormal lab results there are several warning signs that signify the onset of this eating disorder that a pharmacist or technician can screen for as listed in Table 3.

Treatment

The goal of treatment is restoration of normal body weight and improvement in psychological difficulties. Hospitalization may be necessary but, in a patient, who is otherwise stable, outpatient management that includes family members (if the patient is an adolescent) is considered best practice. Family-based treatment (FBT) has the strongest evidence for the treatment of adolescents with AN, and preliminary data suggest that this approach can be extended successfully to treat adolescents with atypical AN. FBT assumes that AN is not under the control of the adolescent, and therefore it empowers parents to directly manage eating disorder behaviors (e.g., dietary restriction, excessive exercise, binge eating and purging). An important component of family therapy is psychoeducation about eating disorders. Families are taught that eating disorder behaviors reflect emotional and social consequences of the disorder, rather than manifestations of other problems or their child’s personality. This stance is very helpful in reducing any guilt or blame related to the development of the eating disorder in the family, as well as reducing criticism, which is common in the context of caregivers making extraordinary efforts to help their child recover in the face of the adolescent demonstrating great resistance or behavioral challenges. As health is restored, greater adolescent autonomy is negotiated so that the adolescent can manage eating behaviors in a developmentally appropriate way and return to their normal activities in a healthy manner.¹⁶

While the most useful approach for children and adolescents is FBT, cognitive behavior therapy (CBT) is usually recommended as the first line treatment approach among adults and a potential secondary option for working with younger cases. Cognitive behavior therapy focuses on changing erroneous and rigid cognitive distortions that prompt and maintain maladaptive behaviors that arise out of negative experiences associated with eating, food, or body image. Cognitive behavior therapy helps the patient to establish more effective behavioral alternatives and may also be helpful in dealing with the central psychological features of AN, such as disturbances in body image.³

Pharmacological therapy can play an adjunctive role in the management of both primary eating symptoms and their co-occurring psychiatric features, including anxiety and depression. Such treatments should focus on target symptoms or behaviors. No single medication is consistently effective in managing the primary psychiatric disturbances of AN. Antidepressants are generally ineffective in the context of AN, particularly while individuals remain underweight. A variety of medications including tricyclic antidepressants, selective serotonin reuptake inhibitors (SSRIs), and lithium carbonate are effective in some cases however, clinical trial results have been disappointing. There is some research to suggest that low doses of atypical antipsychotics may possibly enhance weight gain, with particular benefit for patients who are severely obsessional or agitated although they are not advised as a stand-alone treatment. Multiple randomized trials suggest that the atypical antipsychotic, olanzapine, modestly enhances weight gain; however, it has not received FDA approval for use in patients with AN. Anxiolytics, especially benzodiazepines, should generally not be given due to lack of evidence to support their efficacy and risk of addiction.¹⁷ To date, there is no convincing evidence for the positive effect of pharmacotherapy regarding the core symptoms of AN.¹⁸

Treatment often succeeds in temporarily restoring weight, but AN individuals are at an exceedingly high risk for early relapse, and upwards of 50% relapse within the first year after successful hospital treatment.¹⁹ About 2 - 6% of patients die of the complications of the disorder or commit suicide. The remainder continue to experience difficulties with underweight, eating behaviors, and associated psychiatric conditions. Following stabilization and resolution of the acute crisis, including achievement of weight restoration, patients often require longer-term psychotherapeutic interventions. ¹⁵ Clearly, while weight restoration remains the most proximal goal of treatment in offsetting the medical effects of starvation, it should not be expected that weight gain alone will ultimately lead to psychological symptom remission. If the mechanisms that drive behavioral symptoms are targeted and ameliorated through treatment interventions this may alleviate the need for longer-term psychotherapeutic interventions and reduce the morbidity and mortality associated with AN.

Medical Complications

More than half of the deaths in AN are attributable to medical complications.²⁸ All major organ systems can be affected by the progressive malnutrition that characterizes AN. Emaciation and associated electrolyte disturbances can contribute to significant cardiac abnormalities, particularly for those who purge. Changes in the structure and function of the heart, autonomic parameters, and cardiac repolarization are common in those suffering from AN. Sudden cardiac death is often the cause of premature death in these patients and may be related to multiple factors including QTc prolongation, electrolyte abnormalities, and the presence of torsade de pointes. As a direct result of weight loss and malnutrition, gastrointestinal complications are common especially as weight loss becomes more severe. Gastrointestinal transit times slows and if the patient is symptomatic, metoclopramide or a macrolide antibiotic can be given until some weight is reestablished. Diarrhea is also common early in the refeeding process due to small bowel atrophy and a reduction in the absorption area. Patients may present with lab abnormalities signifying liver disease as demonstrated by elevated aminotransferase levels. Prior to refeeding, elevated aminotransferase levels are likely due to apoptosis, programmed death of hepatocytes due to starvation. If levels start to abnormally elevate with refeeding it is more likely due to steatohepatitis, accumulation of fat in the liver due to the alteration in the composition of the diet related to improved nutrition. Many endocrine abnormalities occur in patients with AN including low estrogen levels in females and low testosterone levels in males due to reversion to the prepubertal state in the hypothalamic pituitary axis. Menstruation in women will generally resume when approximately 95% of ideal body weight is achieved although it can take up to nine months to occur. Notably, pregnancy can still occur with amenorrhea but is dangerous for both the fetus and the patient.²⁰

Bone loss is a serious and potentially irreversible consequence present with AN and many times the reduction in bone mineral density increases the likelihood of early development of osteopenia or osteoporosis even in adolescent patients. The loss of bone mineral density is multifactorial and likely due to elevated cortisol levels, decreased sex hormones, low body weight and growth hormone resistance. Other comorbidities including gastrointestinal malabsorption, hyperthyroidism, and renal or liver disease can be seen in patients with AN, which further increases the risk for low bone density. Weight restoration with resumption of spontaneous menses is the mainstay of therapy for patients with osteopenia including adequate calcium and Vitamin D intake. Most clinicians agree that cautiously aggressive treatment for osteoporosis is warranted. Evidence of efficacy in eating disorder patients has been demonstrated with transdermal estrogen plus oral progesterone, bisphosphonates (alendronate or risedronate), teriparatide and denosumab. There are no definitive guidelines when treating osteoporosis in males with eating disorders, however, treating with testosterone is reasonable if concomitant hypogonadism is detected.²¹ To help prevent the potentially debilitating consequences of low bone density and the unknown consequences of long-term osteoporotic medication use in this young population it is necessary to be vigilant about the effect of AN on bone mineral density.

Avoidant/Restrictive Food Intake Disorder (ARFID)

Symptoms/Characteristics

Avoidant/Restrictive Food Intake Disorder is the newest eating disorder described in the DSM-5. Like AN, ARFID is associated with restrictive eating patterns but the absence of body image concerns is the core feature that differentiates ARFID from AN. There are three types of this disorder specified in the DSM-5 including individuals with an aversion to the sensory characteristics of food (e.g., textures, smells, and visual appearance), those with a lack of interest in food or with limited appetite, and those who may fear negative consequences of eating, (e.g., vomiting, choking, gastrointestinal pain, or fullness), often related to a specific traumatic incident around eating. The degree of dietary restriction must be severe enough to lead to at least one of the following consequences: failure to attain growth milestones in height or weight or significant weight loss; nutritional deficiencies associated with exclusion of entire food groups; dependence on enteral feeding or nutritional supplementation; or marked interference in psychosocial functioning.¹³  Much less is known about what puts one at risk for developing ARFID but there are some common factors that have been observed. People with autism spectrum conditions, attention-deficit hyperactive disorder (ADHD) and other intellectual disabilities appear to be at an increased risk. Children who do not outgrow picky eating habits or those with a co-occurring anxiety disorder also appear to be at an increased risk to develop ARFID.¹⁵

Treatment

Both FBT and CBT are well-positioned to treat the features of food avoidance through use of exposure-based practices with prioritization of nourishment to reverse potential health consequences. Exposures are critical to encourage experiences that hinder previously held beliefs about food. For individuals with sensory sensitivities, exposures may involve engaging with food (touching, smelling, licking, examining visually), before even tasting a small quantity of the food. For the pediatric population, involvement of caregivers is indicated to interrupt familial patterns of accommodation (e.g., only buying preferred foods) to help the child eat a broader range of foods. For individuals who are experiencing significant physiological consequences of restrictive eating, treatment may require hospitalization and specialized feeding may be required, including nasogastric feeding, nutritional supplementation, and individualized nutritional plans that are closely monitored to reverse the physical consequences of ARFID. There are no evidence-based medication treatments for ARFID. Case reports have been published using cyproheptadine and mirtazapine to stimulate appetite and cause weight gain. However, these medications do not have FDA approval for use in this disorder.²²

Medical Complications

Avoidant/Restrictive Food Intake Disorder can lead to severe medical sequelae including amenorrhea, bradycardia, prolonged QT interval, and electrolyte abnormalities such as hypokalemia. Vitamin and mineral deficiencies may be seen in those with an extremely limited variety of nutrition (vitamin A, D, E, B12, K and folate) and can occur independent of weight status. Those avoiding eating due to fear of pain or other aversive consequences may limit intake to the point that gastric motility is impacted, thus resulting in increased discomfort and pain, further reinforcing avoidance behaviors. When and whether tube feeding is appropriate still requires active research although best practices indicate minimizing medical complications and prioritizing adequate nutritional intake.²²

Case 2

Elton, a 28-year-old male with no significant medical history, presented to the medical clinic with complaints of heartburn and regurgitation occurring several times a week, particularly following a large meal. He stated that he took the suggested dose of an over-the-counter laxative for constipation two-to-three times weekly. He appeared to have non-painful enlargement of the parotid glands as well. His BMI was in the normal range for his height. He reported running approximately 60 miles per week and weight training 3 days per week.

A review of Evan’s laboratory values the next day revealed a serum potassium of 2.7 mEq/L. This laboratory abnormality, together with the enlarged parotids and his presenting complaints, suggested self-induced vomiting. During a telephone call to Evan that day, the clinician expressed concern and asked directly about engagement in purging or other eating disorder behaviors. Evan hesitantly admitted to having a 5-year history of bingeing and purging by self-induced vomiting that followed graduation from college, when he stopped running competitively. He agreed to return to the office for repeat electrolytes and to schedule an assessment at a nearby eating disorders clinic.

Bulimia Nervosa (BN)

Symptoms/Characteristics

Bulimia Nervosa is characterized by recurrent episodes of binge eating followed by recurrent and inappropriate compensatory behaviors to prevent weight gain including self-induced vomiting, misuse of laxatives, diuretics, or other medications, fasting, and/or excessive exercise. Like AN, a key feature of BN is the extreme dissatisfaction with body weight or shape. Although dietary restraint is common, the level of dietary restriction in combination with binge eating does not result in significant weight loss. Body weight may fluctuate but generally is within 20% of normal BMI. As opposed to AN, patients with BN have a higher incidence of obesity, greater use of cathartics and diuretics, more impulsive or antisocial behavior and menstruation is usually preserved.²³ Co-occurring psychiatric diagnoses in BN include mood and anxiety disorders, substance use disorders, and self-injury behaviors.¹⁵ While AN and BN have many similarities, Table 4 points out the characteristics of BN that will allow for the differentiation between the two disorders.

Treatment

In adolescents, clinically meaningful outcomes can be achieved when an approach that actively involves families is used in the treatment process (FBT). Families who cannot participate in treatment, would prefer individualized treatment, or when an adolescent is unwilling to involve caretakers, may find that CBT treatment is a beneficial alternative. Since no treatment tested to date demonstrates statistically superior outcomes after 12 months,CBT is an acceptable alternative for FBT.²⁴ Cognitive behavioral therapy is much more established as a treatment for adults with BN, having demonstrated greater effectiveness than nondirective supportive counseling, nutritional counseling, stress management, or antidepressant medication.²⁵

Pharmacological management may play a significant role in treatment of adults with BN and, unlike in AN, can more predictably affect outcome. Antidepressants (SSRIs) have the most evidence of efficacy in treating BN and can reduce symptoms of depression and anxiety as well as the frequency of bingeing and purging. Fluoxetine (target dose of 60 mg/day) is approved by the FDA for the treatment of BN in adults. The effect of fluoxetine in treating the symptoms of BN seem to be independent of its effects on mood and is thought to be related to the effects of the medication on satiety, thereby reducing binge eating. Bupropion is the only antidepressant that is contraindicated, as the metabolic imbalances precipitated by purging can make the patient more prone to seizures. ²⁵ Studies of pharmacotherapy for adolescents remain limited in their generalizability, and additional exploration of psychopharmacological interventions is warranted.²⁴ Antidepressants have not been shown to be as effective as CBT and are more effective when combined with therapy.²⁵ 

Medical Complications

Medical complications are numerous in BN and can be severe. The complications related to self-induced vomiting can be divided into local adverse effects and the electrolyte-acid base abnormalities that can ensue as this behavior becomes more extreme. Gastric acid reflux can lead to dysphagia and dyspepsia as a result of excessive vomiting as well as erosion of the dentin and enamel on the teeth due to repeated exposure to stomach acid. Repeated acid exposure can also result in damage to the larynx and changes in the voice. The most dangerous medical complications of self-induced vomiting are related to the acid-base and electrolyte changes. Potentially severe degrees of hypokalemia and metabolic alkalosis resulting in cardiac arrhythmias can develop in those who excessively purge are the likely reasons for the elevated mortality rate associated with BN. Cathartic and diuretic abuse can also add to these electrolyte abnormalities as well as dehydration. As a result of chronic use of laxatives, cathartic colon syndrome can result and may lead to permanent damage to the nerves that stimulate the colon.²⁵ Although most medical complication are treatable after effective medical interventions and psychotherapy, several may be associated with permanent harm. Therefore, there is an impelling need for early intervention to help achieve a successful treatment outcome.

Binge Eating Disorder (BED)

Symptoms/Characteristics

Binge eating disorder is characterized by recurrent binging episodes associated with at least three of the following behaviors: eating much more rapidly than normal; eating until feeling uncomfortably full; eating large amounts of food when not feeling physically hungry; eating alone because of feeling embarrassed by how much one is eating; and feeling disgusted with oneself, depressed or guilty afterward. Unlike BN, binge eating is not followed by recurrent compensatory behaviors. Binge eating disorder is distinguished from overeating in that it is associated with a sense of loss of control over eating, which is highly distressing and associated with other psychological problems.¹⁵ Binge eating disorder has been shown to co-occur with bipolar disorder, major depressive disorder, BN, most anxiety disorders and substance use disorders.²⁶ It is the most common eating disorder and affects approximately 3% of US adults in their lifetime.²⁷

Treatment

Current guidelines from the American Psychiatric Association (APA) and the National Institute for Health Care Excellence (NICE) both support the use of CBT and SSRIs but differ in their content and timing recommendations. The APA recommends CBT as the cornerstone for therapy and medication as an adjunctive to therapy. In contrast, NICE recommends CBT but also endorses medication monotherapy as sufficient in some patients.²⁷ Head-to-head trials are needed to determine inferiority of self-help with medication alone versus therapist led CBT. In most cases, pharmacotherapy is considered as adjunctive therapy. 

Certain pharmacological medications are indicated in the treatment of BED. Lisdexamfetamine is FDA approved to treat adult patients with moderate to severe BED. This controlled substance commonly used for ADHD, has shown clinically meaningful short-term reductions in binge eating frequency and the obsessive thoughts and compulsions related to binge eating. A recent meta-analysis concluded that the strongest evidence for treating adults with BED indicates CBT, lisdexamfetamine or an SSRI can be used to reduce the frequency of binge eating, increase the likelihood of abstinence, and improve other eating related psychological outcomes. Unlike lisdexamfetamine, SSRIs are not currently approved for BED. Less compelling evidence exists for use of topiramate and even though some studies have had successful outcomes it is currently not approved by the FDA for BED.²⁷

Medical Complications

Binge eating disorder is associated with both poor physical and psychological well-being. Many will suffer from relationship distress, impaired social functioning, and the psychiatric disorders listed above. Binge eating predisposes individuals to metabolic syndrome independent of weight gain, type 2 diabetes mellitus, earlier onset diabetes and worse diabetes related complications and outcomes related to non-adherence to dietary modifications. Obesity-associated comorbidity accounts for most of the medical complications and affects many organ systems.²⁷ The medical complications related to obesity include hypertension, osteoarthritis, hypercholesterolemia, heart disease, stroke, sleep apnea and many more. This disorder can be chronic and debilitating necessitating early intervention and successful treatment outcomes.

CONCLUSION

Eating disorders represent a broad spectrum of psychopathologic features and their development is influenced by an interplay of multiple factors. Specialized psychological treatment is indicated with the initial focus of treatment to normalize eating behavior and minimize medical consequences. Despite the need for specialized training and knowledge to medically manage eating disorders there are multiple ways a pharmacist and pharmacy technician can be involved. Pharmacists are well suited to help to manage the psychotropic medications associated with eating disorder treatment and other psychological co-morbidities the patient may be treated for while under care of a specialist. Both pharmacists and technicians can play a role in identifying warning signs associated with eating disorders and disordered eating. Monitoring non-prescription medications that may be enhancing eating disorder behaviors (e.g., laxatives, diuretics) can also take place in the pharmacy setting. Pharmacists and technicians are in a key position to detect the presence of an eating disorder, encourage the patient to seek treatment and assist with referrals.

If an eating disorder is suspected, creating a safe environment for the patient is important in prompting disclosure and discussing next steps. At this point the pharmacist should raise the issue in a kind, non-judgmental way and commend the patient if they are willing to discuss the disorder. It is important to avoid commenting on the patient’s health, appearance or any weight issues. If a patient is ready to find treatment there are some resources available to help with a referral. The National Eating Disorders Association offers access to a helpline, support groups, and treatment providers by location and can be accessed at https://www.nationaleatingdisorders.org/help-support. If the patient denies the eating disorder accepting the answer and continuing to be an open and non-judgmental source is of great value to anyone who is suffering from an eating disorder. Creating a safe harbor for patients in a supportive pharmacy environment may be the first step to encouraging a patient to get treatment.

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