Eating Disorders

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Chapter 26 Eating Disorders

Eating disorders (EDs) are characterized by body dissatisfaction related to overvaluation of a thin body ideal associated with dysfunctional patterns of cognition and weight control behaviors that results in significant biologic, psychologic, and social complications. Although largely affecting white, adolescent girls, EDs also affect boys and cross all racial, ethnic, and cultural boundaries. Early intervention in EDs improves outcome.

Definitions

Anorexia nervosa (AN) involves significant overestimation of body size and shape, with a relentless pursuit of thinness that typically combines excessive dieting and compulsive exercising in the restrictive subtype; in the binge-purge subtype, patients might intermittently overeat and then attempt to rid themselves of calories by vomiting or taking laxatives, still with a strong drive for thinness (Table 26-1). Bulimia nervosa (BN) is characterized by episodes of eating large amounts of food in a brief period, followed by compensatory vomiting, laxative use, and exercise or fasting to rid the body of the effects of overeating in an effort to avoid obesity (Table 26-2).

Table 26-2 DIAGNOSTIC CRITERIA FOR 307.51 BULIMIA NERVOSA

Specify Type:

From American Psychiatric Association: Diagnostic and statistical manual of mental disorders, ed 4, Washington, DC, 1994, American Psychiatric Association.

The majority of children and adolescents with EDs do not fulfill all of the criteria for either of these syndromes in the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) classification system but fall instead into the category of eating disorder, not otherwise specified (ED-NOS) (Table 26-3). ED-NOS includes a wide variety of subthreshold clinical presentations. Binge eating disorder (BED), in which binge eating is not followed regularly by any compensatory behaviors, is included in ED-NOS in DSM-IV and shares many features with obesity (Chapter 44). ED-NOS, often called “disordered eating,” can worsen into full syndrome EDs.

Epidemiology

The classic features of AN include a white, early to middle adolescent girl of above-average intelligence and socioeconomic status, who is a conflict-avoidant, risk-aversive, perfectionist struggling with disturbances of anxiety and/or mood. BN tends to emerge in later adolescence, sometimes evolving from AN, and is typified by impulsivity and features of borderline personality disorder that are associated with depression and mood swings. The 0.5-1% and 3-5% incidence rates among younger and older adolescent girls for AN and BN, respectively, probably reflect ascertainment bias in sampling and underdiagnosis in cases not fitting the typical profile. The same may be true of the significant gender disparity, in which female patients account for about 90% of patients with diagnosed EDs. Ten percent or more of some adolescent female populations have ED-NOS.

No single factor causes the development of an ED; sociocultural studies indicate a complex interplay of culture, ethnicity, gender, peers, and family. The gender dimorphism is presumably related to girls having a stronger relationship between body image and self-evaluation, as well as the influence of the Western culture’s thin body ideal on the development of EDs. Race and ethnicity appear to moderate the association between risk factors and disordered eating, with African-American and Caribbean girls reporting lower body dissatisfaction and less dieting than Hispanic and non-Hispanic white girls. Because peer acceptance is central to healthy adolescent growth and development, especially in early adolescence when AN tends to have its initial prevalence peak, the potential influence of peers on EDs is significant, as are the relationships among peers, body image, and eating. Teasing by peers or by family members (especially male) may be a contributing factor for overweight girls.

Family influence in the development of EDs is even more complex because of the interplay of environmental and genetic factors; shared elements of the family environment and immutable genetic factors account for significant (about equal) variance in disordered eating. There are associations between parents’ and children’s eating behaviors; dieting and physical activity levels suggest parental reinforcement of body-related societal messages. The influence of inherited genetic factors on the emergence of EDs during adolescence is also significant, but not in a direct fashion. Rather, the risk for developing an ED appears to be mediated through a genetic predisposition to anxiety (Chapter 23), depression (Chapter 24), or obsessive-compulsive traits that may be modulated through the internal milieu of puberty. There is little evidence that parents “cause” an ED in their child or adolescent; the importance of parents in treatment and recovery cannot be overestimated.

Pathology and Pathogenesis

The emergence of EDs coinciding with the processes of adolescence (e.g., puberty, identity, autonomy, cognition) indicates the central role of development. A history of sexual trauma is not significantly more common in EDs than in the population at large, but when present it makes recovery more difficult and is more common in BN. EDs may be viewed as a final common pathway, with a number of predisposing factors that increase the risk of developing an ED, precipitating factors often related to developmental processes of adolescence triggering the emergence of the ED, and perpetuating factors that cause an ED to persist. EDs often begin with dieting but gradually progress to unhealthy habits that lessen the negative impact of associated psychosocial problems to which the affected person is vulnerable because of premorbid biologic and psychologic characteristics, family interactions, and social climate.

When persistent, the biologic effects of starvation and malnutrition (e.g., true loss of appetite, hypothermia, gastric atony, amenorrhea, sleep disturbance, fatigue, weakness, and depression) combined with the psychologic rewards of increased sense of mastery and reduced emotional reactivity, actually maintain and reward pathologic ED behaviors. This positive reinforcement of behaviors and consequences, generally viewed by parents and others as negative, helps to explain why affected persons characteristically deny that a problem exists and resist treatment. Though noxious, purging can be reinforcing due to reduction in anxiety triggered by overeating; purging also can result in short-term, but reinforcing, improvement in mood that is related to changes in neurotransmitters. In addition to an imbalance in neurotransmitters, most notably serotonin and dopamine, there are also alterations in functional anatomy that support the concept of EDs as brain disorders. The cause-and-effect relationship in central nervous system (CNS) alterations in EDs is not clear, nor is their reversibility.

Clinical Manifestations

A central feature of EDs is the overestimation of body size, shape or parts (e.g., abdomen, thighs) leading to weight-control practices intended to reduce weight (AN) or prevent weight gain (BN). Associated practices include severe restriction of caloric intake and behaviors intended to reduce the effect of calories ingested, such as compulsive exercising or purging by inducing vomiting or taking laxatives. Eating and weight loss habits commonly found in EDs can result in a wide range of energy intake and output, the balance of which leads to a wide range in weight from extreme loss of weight in AN to fluctuation around a normal to moderately high weight in BN. Reported eating and weight-control habits (Table 26-4) thus inform the initial primary care approach.

Although weight-control patterns guide the initial pediatric approach, an assessment of commonly reported symptoms and findings on physical examination is essential to identify targets for intervention. When reported symptoms of excessive weight loss (feeling tired and cold; lacking energy; orthostasis; difficulty concentrating) are explicitly linked by the clinician to their associated physical signs (hypothermia with acrocyanosis and slow capillary refill, loss of muscle mass, bradycardia with orthostasis), it becomes more difficult for the patient to deny that a problem exists. Furthermore, awareness that bothersome symptoms can be eliminated by healthier eating and activity patterns can increase a patient’s motivation to engage in treatment. Tables 26-5 and 26-6

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