The eating disorders, including anorexia nervosa and bulimia nervosa, are receiving more clinical and research attention than ever before, paralleling an increase in their prevalence over the past few decades. Such 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.
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.
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.
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 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 neuromodulators; a small number of patients with anorexia develop amenorrhea preceding significant weight loss.
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. 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-disordered 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 ...