Eating Disorders: Evaluation and Management

Overview

Eating disorders comprise several phenomenologically-related conditions that are characterized by a disturbance in patterns of eating, often in concert with body image disturbance. Each of the eating disorder diagnoses is associated with substantial distress and psychosocial impairment. Moreover, because the behaviors can result in serious medical complications, these illnesses can have a catastrophic impact on physiological health, as well as on psychological function.

Classification

Current Diagnostic and Statistical Manual of Mental Disorders , Fifth Edition (DSM-5) diagnostic categories for eating disorders include anorexia nervosa (AN), bulimia nervosa (BN), binge-eating disorder (BED), and other specified feeding or eating disorder (OSFED). AN is further divided into two sub-types (restricting and binge-eating/purging). DSM-5 specifiers for AN, BN, and BED allow for descriptive indicators of relative severity (mild, moderate, severe, or extreme) and symptomatic improvement (partial vs. full remission). Severity is dictated primarily by body mass index (BMI) for AN, frequency of binge eating and purging for BN, and frequency of binge-eating for BED. OSFED (previously termed “eating disorder, not otherwise specified” in DSM-IV ) allows for specification of sub threshold or atypical symptom presentations. A change from prior versions of DSM, DSM-5 combines both feeding and eating disorders into a single section. Feeding disorders in DSM-5 include pica (persistent ingestion of non-nutritive, non-food substances), rumination disorder (regular regurgitation of previously ingested food), and avoidant/restrictive food intake disorder (limited food intake leading to nutritional deficiency, in the absence of shape and weight concerns). Because research on the etiology, clinical features, and treatment of feeding disorders is ongoing, this chapter will focus specifically on eating disorders (i.e., AN, BN, BED, and OSFED), which are better understood.

Epidemiology

The incidence of eating disorders ascertained by case registries probably underestimates the true incidence for several reasons. Data from the National Comorbidity Survey Replication (NCS-R) indicated that fewer than half of individuals with an eating disorder access any kind of health care service for their illness. Many of those affected are known to avoid or to postpone clinical care for the condition. In addition, both BN and BED may manifest without clinical signs, making them difficult, if not impossible, to recognize in a clinical setting without patient disclosure of symptoms, which may not be forthcoming. Furthermore, whereas AN may manifest with a variety of clinical signs, including emaciation, many patients effectively conceal their symptoms; up to 50% of cases of eating disorders may be missed in clinical settings. The lifetime prevalence of AN has been estimated at 0.9% for adult females, 0.3% for adult males, and 0.3% among adolescent males and females. BN is more common than is AN, with a reported lifetime prevalence in adult women of 1.5% and adult men of 0.5%, and 0.9% in adolescent males and females. BED appears to be the most common eating disorder, with a lifetime prevalence ranging from 2.0% for adult males to 3.5% for adult females and 1.6% in adolescents. In addition, sub threshold presentations (captured by OSFED) are at least twice as common as AN, BN, and BED combined. The prevalence of eating disorders appears to vary by gender, ethnicity, and the type of population studied. Although eating disorders historically have been reported as more common in females than males, males may be under-identified. Eating disorders also occur in culturally, ethnically, and socioeconomically diverse populations. It is thus important for clinicians to remain vigilant for possible eating disorder symptoms regardless of patient demographics.

Course, Co-Morbidity, and Mortality Rate

AN can onset from childhood to adulthood, but it most commonly begins in post-pubertal adolescence. Likewise, the most common time of onset for BN is in post-pubertal (usually late) adolescence. Both BN and BED can onset in later decades.

Greater than half of those with AN and BN will achieve recovery over long-term follow-up, and more will have symptomatic improvement short of full recovery; approximately 20-33% will have a chronic course. Notwithstanding the data and conventional wisdom that AN, in particular, often follows a chronic course, the NCS-R study reported that AN had a significantly shorter course than either BN or BED. These data suggest that there may be more variation in the course of AN than previously thought, possibly due to the fact that some individuals experience remission before seeking care. Outcomes for BED are somewhat more favorable with the majority achieving symptom remission over time but still up to one third remaining more chronically ill. Moreover, there is also considerable diagnostic migration across eating disorder categories, typically reflecting crossover from a primarily restrictive to a bingeing and/or purging presentation over time. Eating disorders are associated with high medical co-morbidity (as nutritional derangement and purging behaviors frequently lead to serious medical complications); they are also associated with a high degree of psychiatric co-morbidity. The NCS-R study found that a majority of respondents with each of the full threshold eating disorders (AN, BN, and BED) had a lifetime history of another psychiatric disorder. Of these, 94.5% of respondents with BN had a lifetime history of a co-morbid mental illness. The mortality risk associated with eating disorders is also elevated. The risk of mortality may be increased by co-morbid factors, such as substance abuse, and by a longer duration of illness. The high mortality rate is accounted for by both serious medical complications of the behaviors, and by a suicide rate that is 18 times that expected in AN, in particular.

Etiological Factors

Although the etiology of eating disorders is likely multi-factorial, causal factors are uncertain. Possible sociocultural, biological, and psychological risk factors all have been identified, despite methodological limitations that characterize many studies. In addition to female gender and ethnicity, weight concerns and negative self-evaluation have the strongest empirical support as risk factors for eating disorders. In particular, risk factors for obesity appear to be associated with BED, and risk factors for dieting appear to be associated with BN. Risk for an eating disorder may also be elevated by generic risk factors for mental illness.

Sociocultural factors are strongly suggested by population studies that have demonstrated that transnational migration, modernization, and Westernization are associated with an elevated risk for disordered eating among vulnerable sub-populations. Other social environmental factors (such as peer influence, teasing, bullying, and mass media exposure) have been linked with an elevated risk of body image disturbance or disordered eating.

Numerous psychological factors have been identified as either risk factors or retrospective correlates of eating disorders. Among these is exposure to health problems (including digestive problems) in early childhood, exposure to sexual abuse and adverse life events, higher levels of neuroticism, low self-esteem, and anxiety disorders. Furthermore, a cognitive style characterized by weak set-shifting (i.e., difficulty switching between tasks) and poor central coherence (i.e., hyper-focus on minor details to the detriment of grasping the bigger picture) is common in AN and may increase risk for the disorder.

Genetic influences on eating disorders have also been studied. Although family and twin studies support a substantial genetic contribution to the risk for eating disorders and molecular genetic studies hold promise, our understanding of the genetic transmission of risk for eating disorders remains limited. Evolving studies in the area are focusing on the genetic underpinnings of symptoms associated with the eating disorders (rather than diagnoses), as well as gene–environment interactions. Emerging evidence from neuroimaging research suggests that, compared to healthy controls, individuals with AN experience an over-activation of neural circuitry in the fear network when presented with food stimuli. In contrast, individuals with BN may binge eat, in part, due to hypoactivation of reward circuitry and impairments in neural networks that contribute to impulse control.

Diagnostic Features

Considerable phenomenological overlap and diagnostic migration across AN, BN, BED, and OSFED has contributed to a “transdiagnostic” view of eating disorders that highlights similarities in both symptoms and maintaining mechanisms. However, by definition, a diagnosis of one eating disorder is mutually exclusive with another at any particular point in time.