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.