23: Eating Disorders

The eating disorders, including anorexia nervosa and bulimia nervosa, continue to receive appreciable clinical and research attention, paralleling an increase in their prevalence over the past few decades. Disturbances in eating behavior are, of course, not new. Historical documentation of anorexia nervosa dates back to the early Christian saints. Binging and purging, although distinct from our current concept of bulimia nervosa, took place in the lives of ancient Romans.

The eating disorders are best viewed as clinical syndromes rather than specific diseases, as they do not result from a single cause or follow a single course. As psychiatric syndromes, they are defined largely by a constellation of behaviors and attitudes that persist over time and have characteristic complications contributing to physical and psychosocial dysfunction. Because of the complexity and breadth of contributing factors, as well as the extent of comorbid psychopathology, knowledge of the behavioral characteristics of the eating disorders can lead to improved recognition and implementation of effective treatment strategies. In light of the complicated interplay of psychiatric, psychosocial, and medical consequences, treatment beyond initial medical stabilization generally requires referral to specialists. Importantly, though, the primary care physician is in a position to identify at-risk behaviors that may contribute to the development of eating disorders, particularly in adolescent and young adult females.

A comprehensive multidimensional model best illustrates the role various factors play in the genesis of clinically significant eating disturbances. In this schema, also referred to as a stress–diathesis model, psychological, biological, and sociocultural stressors contribute to the development of the syndrome (see Chapter 34).

Psychological factors include personality features, such as the anorectic’s obsessive-compulsive qualities, constrained affect, and sense of ineffectiveness, and the bulimic’s impulsivity. They also include the influence of developmental stressors and family dynamics. Body dissatisfaction, combined with other psychological, behavioral (in particular, dieting), or biological vulnerabilities, appears to be an important contributor and may identify those at greater risk.

Biological factors are most often due to the adverse effects of starvation, malnutrition, and purging behaviors, including vomiting and the misuse of laxatives and diuretics. Restrictive dieting and subsequent malnourishment may contribute to the development or exacerbation of comorbid psychiatric conditions, such as anxiety and depression. In addition, a preexisting biological vulnerability is supported by neurophysiologic investigations showing dysfunction of serotonin, dopamine, and norepinephrine neuromodulator systems; a small number of patients with anorexia develop amenorrhea preceding significant weight loss suggestive of hypothalamic dysregulation. The additional contribution of components of the peripheral satiety network is being elucidated. Genetic findings are suggestive and support evidence of substantial hereditability, but require further investigation given the complexity of these conditions.

Sociocultural factors figure prominently in the etiology of the eating disorders. The idealization of thinness contributes to dieting behavior, often beginning in early adolescence. Of note, dieting is almost always present as a precipitant to the development of an eating disorder. Adoption of Western ideals of beauty and accompanying dieting behavior is contributing to an increased prevalence of eating disorders in ethnically diverse populations both in the United States and globally. Other precipitants include periods of illness leading to weight loss; in vulnerable individuals, this may be followed by willful dieting.

Conceptual models aid in understanding the etiology and possible sustaining factors involved in the genesis and persistence of eating disorder behavior. Important models include those derived from learning theory and neurophysiologic abnormality or dysfunction.

Cognitive behavioral theory, which is derived from learning theory, states that cognition influences behavior in a predictable manner. Cues, both internal and external, can provoke behavioral outcomes through activation of cognitive sets. A change in negative cognition, therefore, influences a change from dysfunctional to healthy behavior. Thoughts that overvalue weight, food, and diet, especially the idealization of thinness, lead to the perpetuation of compromising responses, such as heroic dietary measures and abuses of substances believed effective for weight reduction. The coupling of such cognitions and behaviors affects self-esteem and may severely impair an individual’s psychological state. Cognitive behavioral therapy has been effective in achieving symptom reduction and improvement in both medical and psychological status.

The search for specific biological markers that may help identify patients with eating disorders has focused increasingly on neurotransmitters and other neuromodulators. Research findings suggest that dysfunction in various neurotransmitter systems, including serotonin, dopamine, and norepinephrine, as well as opioids and cholecystokinin (CCK), might play a role in the development and maintenance of the eating disorders. Rationale for the examination of these hormones and other substances derives from our understanding of the pathways modulating appetitive behavior, including hypothalamic regulation and the known connection between the gastrointestinal tract and the central nervous system. The complexity of these disorders, including the stress of eating disorder behavior on physiology, however, makes it unlikely that a neurophysiologic hypothesis alone can explain the etiology and maintenance of these complex syndromes.

Description

Anorexia nervosa is a relatively rare disorder affecting less than 1% of young women and a much smaller percentage of young men. Its most striking behavioral manifestation is the willful restriction of caloric intake secondary to an irrational fear of becoming fat, frequently in concert with a grossly distorted view of one’s self as overweight, even in the presence of severe emaciation. Patients often exhibit a phobic response to food, particularly to fatty and other calorically dense items. They develop an obsessive preoccupation with food, eating, dieting, weight, and body shape, and frequently exhibit ritualistic behaviors involving choosing, preparing, and ingesting meals (e.g., cutting food into very small pieces or chewing each bite a specific number of times).

Early in the course of the illness, patients begin to restrict many food items, as is typical of most dieters. As the disorder progresses, though, the anorectic’s menu becomes grossly constricted and he/she demonstrates greater rigidity. Minor variations in meal content can produce tremendous anxiety. Unlike the average dieter, the anorectic continues his/her pursuit of thinness to the extreme and becomes dependent on the daily registration of weight loss. This fuels even more restrictive dieting. Extreme dieting is often complicated by other weight-reducing behaviors. Exercise is frequently compulsive, and hyperactivity in underweight patients is a curious but often-encountered concomitant. Weakness, muscle aches, sleep disturbances, and gastrointestinal complaints, including constipation and postprandial bloating, are common physical findings. Amenorrhea, reflecting endocrine dysfunction secondary to malnourishment, is generally present.

Some anorectics engage in bulimic behaviors, including binging and purging. This binge–purge subtype of anorexia nervosa contrasts with the purely restricting subtype described earlier. Often, purging behavior, such as self-induced vomiting or the misuse of laxatives and diuretics, is seen in the absence of binging. The coupling of purging with self-starvation compounds the medical consequences of the disorder. Furthermore, anorectics, particularly adolescents, generally minimize their symptoms and the negative consequences of their disorder and are thus rarely motivated for treatment. The characteristics of the illness, both medical and psychological, are intensified with weight loss, further frustrating attempts at engaging the patient in a meaningful therapeutic process. Family and friends become increasingly anxious, angry, and at times alienated, as their loved one regresses. Superficial compliance, as is sometimes seen, belies a profound resistance. Anorectic patients can be challenging to treat as they cling tenaciously to their beliefs and behaviors.

Psychosocial dysfunction is common in patients with anorexia. Although educational performance may not be affected in adolescent patients, social relations become increasingly constricted, and sexual interest is generally diminished or absent.

Differential Diagnosis

The pathognomonic features of anorexia nervosa, namely the intense fear of becoming fat coupled with the relentless pursuit of thinness, are generally absent in other medical and psychiatric conditions. The term anorexia, which itself refers to absence of appetite, is a misnomer in the case of the syndrome of anorexia nervosa. True anorexia, such as that encountered in many medical conditions or diseases, would be accompanied by other signs or symptoms of those illnesses (as in gastrointestinal disease or many cancers).

Lack of appetite or decreased intake, with or without subsequent weight loss, is encountered in a number of psychiatric disorders. These include depression, hysterical conversion, other psychosomatic disorders, schizophrenia, and certain delusional disorders, but each of these is associated with a cluster of other substantiating symptomatology. Some patients with obsessive-compulsive disorder (OCD) may exhibit what appears to be bizarre behavior around food, eating, or meal preparation, but, on further exploration, their behavior is in response to obsessional ideation, for example, the fear of contamination. Such patients, in contrast to those with anorexia nervosa, generally admit their discomfort with the need to perform such compelling and often excessive or senseless acts.

In summary, although comorbid psychopathology may be encountered in patients with anorexia nervosa, including symptoms of depression or OCD, the hallmark of anorexia nervosa (the morbid fear of becoming fat and the relentless pursuit of thinness) is absent in other psychiatric syndromes. In none of these syndromes does the goal of weight loss drive the behavior.

Medical Complications & Treatment

Treatment of anorexia nervosa is initially directed at correcting the acute medical complications and is followed by supportive nutritional rehabilitation. Most medical consequences resolve with nutritional rehabilitation and the discontinuation of purging behaviors. Exceptions include persistent osteopenic changes in those who have experienced extended periods of malnourishment and suppression of growth in severe cases of adolescent anorexia.

In many cases of anorexia associated with significant weight loss (15–20% or more of ideal body weight) a structured inpatient facility is necessary to maintain an adequate level of medical surveillance and sustain a steady rate of weight gain. On admission to an inpatient treatment facility, laboratory screening should include tests for electrolytes, liver function, amylase (elevated in patients who purge), thyroid function, a complete blood count with differential, and a urinalysis. Common laboratory findings include leukopenia with a relative lymphocytosis, metabolic alkalosis with associated hypokalemia, hypochloremia, elevated serum bicarbonate levels, and, occasionally, metabolic acidosis in patients who abuse large amounts of stimulant-type laxatives. An electrocardiogram should also be obtained, since emaciation and associated electrolyte disturbances can contribute to significant cardiac abnormalities, especially in those who purge. Hypokalemia can lead to arrhythmia and the risk of cardiac arrest.

Acute medical conditions generally requiring immediate attention include electrolyte disturbances and dehydration, both of which are readily reversible. In most cases, initiating oral intake of fluids and food reverses minor disturbances in electrolytes and establishes adequate hydration. More severe cases, for example, patients with significant hypokalemia, may require intravenous hydration and parenteral replacement of depleted electrolytes, with daily electrolyte checks until the patient’s condition stabilizes. Care should be taken to avoid overhydration and the consequences of excess fluid retention in vulnerable individuals. Importantly, treatment must ensure prevention of purging behaviors in patients with this history, as persistence of purging will alter electrolyte and fluid balance.

In patients who are significantly underweight, use of a liquid supplement, initially as replacement for solid food, helps ensure necessary caloric intake. When given in divided feedings throughout the day, it may decrease the patient’s sense of postprandial discomfort and early satiety, both frequent consequences of extended caloric restriction and semistarvation. Further, this approach to refeeding decreases the inevitable manipulations around food choices. Replacement of solid food with a liquid supplement may also lessen the patient’s phobic avoidance of food and the subsequent anxiety around meal choices.

Psychotherapeutic Interventions

Given the lack of motivation and strong resistance to treatment exhibited by the majority of patients with anorexia, it is helpful to initiate behavioral strategies as soon as any acute medical condition is stabilized. Initial behavioral interventions, tied to daily weight gain in increments of no less than 0.25 lb or 0.1 kg, include obtaining visits from family or friends, lessening physical restrictions, and increasing involvement in activities on and off the unit. It is important that all contingencies be tied to daily weight gain, which is measured each morning at the same time and in like manner, as this is a quantifiable observation not open to argument or discussion. A milieu supportive of such interventions helps to motivate the patient and exerts pressure toward positive change.

As the patient reaches a target weight range and establishes some degree of commitment to treatment, solid food can replace the liquid supplement. The ability of the patient to maintain weight through normalization of intake marks a transition to less structured treatment, such as a partial hospitalization program or outpatient follow-up.

Other treatments applicable to both inpatient and outpatient settings include individual psychotherapy and family intervention. The initial focus in family therapy should be on psychoeducation and obtaining the support of family members. The dynamics that may be contributing to the patient’s eating disorder should be identified and, when possible, resolved. Such treatment often requires extensive contact beyond any acute interventions.

Individual psychotherapy is of limited value in the early stages of treatment, as the anorectic individual is generally unmotivated and, due to cognitive disturbances secondary to self-starvation, not capable of meaningful therapeutic work. Supportive therapy during this acute stage is often helpful in allaying anxiety and encouraging adherence to treatment. The more focused cognitive behavioral and interpersonal therapies are generally more effective when the patient has begun to gain weight and is beyond acute medical risk. Cognitive behavioral therapy focuses on the particular disturbing or distorted thoughts that contribute to the patient’s maladaptive behavior and helps the patient establish more effective behavioral alternatives. It may also be effective in dealing with the central psychological features of anorexia nervosa, such as disturbance in body image. Interpersonal therapy may also be helpful. It focuses on interpersonal conflicts rather than specific eating disturbances. Following stabilization and resolution of the acute crisis, including achievement of weight restoration, patients often require longer-term psychotherapeutic interventions.

Pharmacotherapy

Pharmacological therapy can play an adjunctive role in the management of both primary eating symptoms and their comorbid psychiatric features, including anxiety and depression. Such treatments should focus on particular target symptoms or behaviors. No single medication is consistently effective in managing the primary psychiatric disturbances of anorexia nervosa. Antidepressants, especially the selective serotonin reuptake inhibitors (SSRIs), can alleviate depressive symptoms and, due to their ability to regulate obsessive-compulsive symptomatology, may help reduce the preoccupations and ritualistic behaviors encountered in most anorectics. Low doses of atypical antipsychotics may sometimes be employed in severely obsessional or agitated patients, but side effects, including movement disorders and metabolic aberrations, limit their utility. Anxiolytics, especially benzodiazepines, should generally not be given to anorectics, as they are prone to development of addiction.

Description

Bulimia nervosa affects approximately 2–3% of young women and 0.2% of young men, although bulimic behaviors may be encountered in many more patients. Bulimia nervosa is generally precipitated by periods of restrictive dieting. Bulimic individuals engage in regular episodes of binge eating, followed by compensatory behaviors to counteract the weight gain from ingested calories. Binge eating is characterized by the rapid consumption of large amounts of food over a short time, usually 1–2 hours. It is associated with a sense of being out of control and is often followed by feelings of guilt or shame and other dysphoric affective states, such as depression or anxiety. Some patients report alleviation of dysphoria or even emotional numbing during or immediately following the episode, although this is short lived. During a binge, a few thousand to as many as 15,000 kcal or more may be consumed. Sometimes trigger foods, often a fattening sweet such as chocolate, precipitate a binge, although the overall content of food consumed, by macroanalysis of nutritional content, varies. The bulimic individual generally binges in private; grossly overeating is humiliating. Embarrassment can lead to varying degrees of social avoidance or isolation.

Contributing further to avoidance behavior is the need to compensate for eating, frequently by purging. Most bulimic individuals induce vomiting during or after a binge, and some also use laxatives or diuretics. A minority of patients employs laxatives or diuretics alone. Nonpurging compensatory behaviors include compulsive exercising and restrictive dieting or fasting between binges.

Another characteristic of bulimia nervosa is patient dissatisfaction with body shape or weight. This may evolve into a significant degree of obsessional preoccupation, with self-evaluation overly influenced by these physical concerns. It can have a profound effect on self-esteem and is evidenced in part by comorbid depressive symptomatology in the majority of patients. Impulsive behavior is encountered in many individuals with bulimia nervosa and at times leads to substance abuse, sexual promiscuity, and theft.

Differential Diagnosis

Few medical or psychiatric disorders can be confused with bulimia nervosa. More frequently, signs of self-induced vomiting or use of diuretics or laxatives in a young woman who does not admit to binging or purging behaviors lead the primary care clinician to search for another primary medical diagnosis. Signs and symptoms associated with gastritis, esophagitis, dehydration, or electrolyte disturbances result in primary care or emergency room visits, postponing psychiatric consultation. If the patient is underweight, amenorrheic, and is binging and purging, he/she has anorexia nervosa of the binge–purge subtype rather than bulimia nervosa.

Medical Complications & Treatment

The majority of medical complications due to bulimia nervosa are consequences of purging behaviors. Self-induced vomiting can lead to gastritis, esophagitis, periodontal disease, and dental caries. Gastric dilatation and gastric or esophageal rupture are rare medical emergencies. Metabolic alkalosis with the development of clinically significant hypokalemia in patients who vomit is not unusual, and serum electrolytes show typical indices. When present, electrocardiographic changes are significant. Arrhythmias can lead to cardiac arrest if hypokalemia and related disturbances are not corrected. Use of diuretics cause similar disturbances. Metabolic acidosis can develop in patients who use a significant number of stimulant-type laxatives. Dehydration, sometimes requiring intravenous hydration, can accompany each of the aforementioned purging behaviors. More often associated with bulimic behaviors are general physical complaints such as fatigue and muscle aches. Long-term use of the emetic ipecac can lead to myopathies, including cardiomyopathy, the latter a rare cause of death in patients with bulimia.

Most patients with bulimia nervosa can be treated as outpatients or in more structured partial hospitalization programs. An individual with an acute medical condition, however, such as dehydration or symptomatic hypokalemia accompanied by electrocardiographic changes, requires hospitalization for medical stabilization. Patients who have failed outpatient treatment and continue to binge and purge frequently, and those with significant depression and associated suicidal ideation, may require inpatient treatment.

Psychotherapeutic Interventions

Helping patients recognize the negative consequences of their behavior and dispelling myths about the efficacy of many of their dietary maneuvers, especially the usefulness of laxatives, diuretics, and self-induced vomiting, may be enough to motivate them to decrease the frequency of bulimic behaviors. Similarly, self-monitoring intake with the use of food diaries and normalization of meal patterns can lead to short-term gains in control of bulimic symptoms. Time-limited psychotherapy, focused specifically on the disturbed eating patterns, can be conducted in an individual or group format and is often useful. More traditional exploratory psychotherapies, which are generally not time limited, do not predictably affect outcome but may play a role in the treatment of underlying or persistent difficulties following improvement or resolution of bulimia.

Cognitive behavioral therapy is an established treatment for bulimia nervosa and can lead to both acute reductions in symptoms of binging and purging and longer-term maintenance of gains. It targets the behavioral manifestations and challenges the cognitive distortions typically encountered in these patients. In cognitive behavioral therapy, identifying disordered behaviors is the first step toward productive intervention, because behavioral consequences follow specific cues. To intervene, one must recognize the various cues and respond to them deliberately rather than automatically. Cues affecting eating disorder patients are either internal or external. Internal cues include physiologic ones; most significantly hunger, as well as emotions and thoughts. External cues encompass a broad array of experiences from sensual, such as sight or smell, to situational. Cues lead to consequences that are either positive or negative; both can be reinforcing.

Following the identification of cues, associated responses can be addressed more specifically and in greater detail. Responses consist of thoughts, feelings, and behaviors. Helping the patient understand that thoughts and feelings affect behavioral responses to a cue is of great significance because both thoughts and feelings can be altered through cognitive behavioral techniques. For each cue identified, patients are taught to delineate the various response components and to evaluate the appropriateness of each. Although schematically simple, many eating-associated responses are automatic, and learning to identify the cues and various responses requires much practice.

During cognitive behavioral therapy patients are taught to recognize that behaviors follow cues and responses to cues can be broken down into thoughts, feelings, and behaviors. What patients think and feel about a cue dictate whether their response is adaptive or maladaptive. How they feel is influenced by how they think; therefore, the restructuring of thoughts is of primary importance. Eating disorder patients manifest certain patterns of distorted thinking; these patterns negatively influence feelings and fuel the maladaptive behaviors. These various styles of thinking are identified, and strategies to challenge and ultimately to alter the distortions are developed.

A simple example helps illustrate the applicability of cognitive behavioral therapy. A common cue that frequently leads to a bulimic response is the normal sense of fullness. Rather than recognizing satiety as a normal physiologic response, the eating disorder patient often misinterprets this cue, stating instead, “I feel fat.” This distorted thought, unchallenged, is associated with negative feelings and often leads to dysfunctional behaviors. Rather than the appropriate response to fullness, understanding that it is temporary and will pass, patients believe they must compensate for being “fat” and rid themselves of the meal through purging or compensate for the caloric intake through exercise. Such a response causes the cycle to reassert itself.

Pharmacotherapy

Pharmacological management may play a significant role in treatment and, unlike in anorexia, can more predictably affect outcome. Many antidepressants, including SSRIs, monoamine oxidase inhibitors (MAOIs), and tricyclic antidepressants (TCAs) are effective in treating bulimia. (Dietary proscriptions limit the usefulness of MAOIs, and lethality in overdose limits treatment with TCAs.) They reduce symptoms of depression and anxiety as well as the frequency of binging and purging. Bupropion is the only antidepressant that is contraindicated, as the metabolic imbalances precipitated by purging can make the patient more prone to seizures.

Eating disorders represent a broad spectrum of psychopathologic features. They are best understood in terms of multiple etiologic factors influencing the development of clinical syndromes. Understanding the complexity of these disorders, the behaviors associated with them, and their comorbid psychiatric features aids in their recognition and treatment. Focusing initially on control of these primary eating disorder behaviors helps reduce the likelihood of psychological morbidity. It also limits the medical complications that frequently develop in these conditions. Interventions to control behavior range from response prevention (for patients placed on special inpatient wards) to cognitive behavioral therapies for more motivated patients. Behavioral control may be augmented through pharmacological management as well as other psychotherapies (psychoeducational and interpersonal) that help reduce the role that sustaining factors play in the maintenance of these disorders.