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(p. 289) Defining Eating Disorders 

(p. 289) Defining Eating Disorders
Chapter:
(p. 289) Defining Eating Disorders
Author(s):

Evelyn Attia

, Anne E. Becker

, Cynthia M. Bulik

, Alison E. Field

, Neville H. Golden

, Richard E. Kreipe

, Daniel Le Grange

, James E. Mitchell

, Kathleen M. Pike

, Robyn Sysko

, C. Barr Taylor

, and B. Timothy Walsh

DOI:
10.1093/med-psych/9780199928163.003.0013
Page of

date: 16 August 2018

(p. 290) Overview

The wide range of human food preferences and of human practices surrounding food preparation and consumption make the definition of an “eating disorder” challenging. This challenge is amplified during adolescence by the dramatic changes in energy requirements required to support normal growth and development. For example, between ages 9 and 19, the estimated caloric requirements for girls increases by almost 50% and, for boys, by 80% (Wadsworth, 2003). Adolescence therefore provides a fertile environment for the development of disordered eating; however, surprisingly little attention has been devoted to precisely how to define an eating disorder. The most widely used definitions are those provided by the fifth edition of the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders (DSM-5; APA, 2013), which are described in detail below. In this and previous versions of the DSM, the presence of excess body fat alone (i.e., being overweight or obese) is classified as a general medical problem, not a mental disorder (Marcus & Wildes, 2009).

Further, although most eating disorders begin in adolescence, a limited amount of research has focused on this age range. This part of the volume will review what is known and unknown about defining eating disorders, their treatment, and their prevention. This chapter includes a discussion of the etiology of eating disorders; the DSM-5 diagnostic criteria for feeding and eating disorders, and how well the criteria apply to adolescents; the demographics and prevalence of eating disorders among adolescents; issues of comorbidity, outcome, and diagnostic migration for adolescents with eating disorders; and the medical complications of eating disorders. Chapter 14 describes psychological and pharmacological treatments for adolescents with eating disorders, and studies of relapse prevention using psychological or pharmacological interventions. Chapter 15 addresses the risk factors for the development of eating disorders, culture and eating disorders, and prevention. Chapter 16 suggests promising directions for future study.

Etiology of Eating Disorders

A variety of biological, environmental, and psychosocial factors are associated with the development of an eating disorder, suggesting that such factors may play a causative role in their evolution. However, as is discussed in detail in Chapter 15, there is no conclusive evidence that any characteristic or event is specifically associated with the development of anorexia nervosa (AN), bulimia nervosa (BN), or binge-eating disorder (BED). AN and BN primarily affect women and usually begin around the time of, or soon after, puberty, suggesting that developmental factors during adolescence play a crucial role in their onset. However, it is not clear whether the biological changes that accompany adolescence, psychological changes, and/or an interaction between the two types of phenomena account for the occurrence of eating disorders. BED is less common in adolescence, but aberrant behaviors (e.g., loss of control over eating) may be observed prior to the onset of a full threshold diagnosis, and can be influenced by risk factors occurring during this developmental period. As discussed more extensively in Chapter 15, there is growing evidence of genetic and cultural influences playing an important role in eating disorders, but precisely how genetic or cultural factors may contribute to an individual’s vulnerability to develop an eating disorder is poorly understood. There is little question that psychological distress is common within the families of adolescents with serious eating disorders, but it is not clear to what degree such disturbances precede rather than follow the development of the eating disorder. In short, despite extensive information about the clinical characteristics of eating disorders and much theoretical discussion, solid knowledge of the etiology of eating disorders is elusive.

In addition, it is likely that different factors contribute to the onset and to the maintenance of eating disorders. If risk and maintenance factors are distinct, prevention efforts and treatment interventions need to be directed at different targets and, potentially, separate populations. However, there is currently insufficient (p. 291) evidence to differentiate with confidence those factors that increase the risk of developing an eating disorder from those that perpetuate a disorder once it has begun. The lack of knowledge about such issues clearly limits the development of more effective prevention and treatment interventions.

Diagnostic Criteria for Feeding and Eating Disorders

The most widely used diagnostic classification system for feeding and eating disorders is presented in the DSM-5 (APA, 2013). This manual describes individuals with feeding and eating disorders as exhibiting persistent disturbances in behavior leading to changes in the consumption or absorption of food that produce significant impairments in health or psychosocial functioning. The DSM-5 diagnoses for feeding and eating disorders were revised and expanded and include pica, rumination disorder, avoidant/restrictive food intake disorder, AN, BN, and BED. The DSM-5 categories are intended to be mutually exclusive, allowing an individual to receive only one diagnosis in a given episode, with the exception of pica, which can be assigned in the presence of any other feeding or eating disorder.

Anorexia Nervosa

The DSM-5 criteria for AN are listed in Box 13.1.

Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Copyright 2013. American Psychiatric Association.

The first criterion (A) is a significantly low body weight for the individual (e.g., not within normal limits or expectations) brought about by a restriction of calorie intake relative to factors such as age, sex, development, physical activity, and overall health. Low weight can result from acute weight loss, but with younger patients, longitudinal information about height and weight may be the best metric to identify whether the individual has failed to follow his or her expected growth trajectory. Although a specific cutoff is not provided for this criterion in the DSM, clinicians are directed to BMI-for-age percentile calculators (e.g., Center for Disease Control and Prevention; http://apps.nccd.cdc.gov/dn-pabmi/) with the guidance that a body weight associated with a BMI-for-age below the fifth percentile suggests a low body weight.

The B criterion (fear of weight gain/becoming fat, behavior interfering with weight gain) for AN can be assigned if the clinician notes behaviors that suggest an intense fear of gaining weight or becoming fat, as this diagnostic feature may not be acknowledged, especially among younger patients (Becker, Thomas, & Pike, 2009).

Body shape and weight distortions are the focus of Criterion C, and a variety of manifestations of this disturbance are possible among patients with AN. Adolescents may not have developed the complex reasoning skills required for endorsing some of the cognitive aspects of this criterion (e.g., expressing the role of body shape and weight in influencing self-worth; Bravender et al., 2010); however, the clinician may consider behaviors suggesting a failure to recognize the seriousness of low weight (e.g., lack of interest in receiving treatment because the adolescent does not believe he or she has a problem).

DSM-5 suggests that individuals with AN be further described as belonging to one of two mutually exclusive subtypes, the restricting type (AN-R) and the binge-eating/purging type (AN-B/P). Subtype is determined by the presence or absence of persistent binge eating and/or purging behavior over the 3 months prior to assigning a diagnosis, as crossover between categories during the longitudinal course of AN occurs frequently (Peat, Mitchell, Hoek, & Wonderlich, 2009). New provisions for partial remission, the absence of low body weight while continuing to meet criteria B and C, full remission, and current severity (mild, moderate, severe, extreme) on the basis of BMI are also provided in DSM-5.

Bulimia Nervosa

The DSM-5 diagnostic criteria for BN are listed in Box 13.2.

Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Copyright 2013. American Psychiatric Association.

Criterion A provides a definition of a binge eating episode in terms of amount (“definitely larger than most people would eat”), timeframe (“in a discrete period of time”), and (p. 292) psychological state (“a sense of a lack of control”). Clinical judgment is required to determine whether an eating episode meets the definition of a binge episode.

Criterion B describes recurrent and inappropriate behaviors, including some easily characterized (self-induced vomiting) and others that are less straightforward, like the “misuse” of laxatives and diuretics or what constitutes excessive exercise.

The frequency criterion (Criterion C) for BN was decreased for DSM-5 and requires that episodes of binge eating and inappropriate compensatory behaviors occur on average at least once weekly for 3 months.

Criterion D attempts to capture an important psychopathological parameter (self-evaluation based on body shape and weight), which is also required for a diagnosis of AN. Younger patients (p. 293) may deny this symptom and clinicians may have difficulty distinguishing between “undue influence” and the normative overconcern with shape and weight among female adolescents.

Specifiers for partial remission of BN and current severity, determined on the basis of the frequency of inappropriate compensatory behaviors and functional impairment, are also provided.

Binge-Eating Disorder

Criteria for the diagnosis of BED are provided in Box 13.3. Binge-eating disorder was officially recognized in DSM-5 on the basis of data accumulated after the inclusion of this category as a provisional diagnosis in the prior version of the DSM.

Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Copyright 2013. American Psychiatric Association.

The definition of binge eating for individuals with BED (Criterion A) is identical to that used for BN, with the requirement that at least three additional features associated with these episodes (Criterion B; e.g., eating until uncomfortably full, eating alone because of embarrassment) be endorsed. Further, the individual must report “marked distress” related to binge-eating episodes (Criterion C) that occur at least once weekly over a 3-month period (Criterion D). To receive a diagnosis of BED, the recurrent use of inappropriate compensatory behavior must be denied (Criterion E). Definitions for partial remission, full remission, and current severity (mild, moderate, severe, extreme) derived from binge-eating frequency are also provided in DSM-5.

(p. 294) Although the onset of BED typically occurs in late adolescence or young adulthood (Hudson, Hiripi, Pope, & Kessler, 2007), little is known about the presentation of BED in this age group. However, loss of control over eating (with and without the consumption of an objectively large amount of food) is known to be an important clinical characteristic among youth (e.g., Decaluwé, Braet, & Fairburn, 2003; Tanofsky-Kraff et al., 2009). Relationships have been noted between broadly defined forms of binge eating, weight gain, increased body fat, depressive and anxiety symptoms, low self-esteem, and other eating pathology (Decaluwé & Braet, 2003; Isnard et al., 2003; Sonneville et al., 2013; Wildes et al., 2010). It is possible that episodes of loss-of-control eating may develop into full-syndrome BED (Tanofsky-Kraff et al., 2011), but additional studies are needed to better characterize the course of patients with this diagnosis.

(p. 295) Pica

Pica is characterized by the developmentally inappropriate, persistent consumption of substances that are nonnutritive and nonfood (e.g., paper, clay) over at least a 1-month period, and to a degree that merits clinical intervention. Such eating cannot be culturally sanctioned or developmentally normal. If the individual has another diagnosis, such as intellectual developmental disorder, pica should only be assigned if it is severe enough to warrant clinical attention independent of the other co-occurring condition.

Rumination Disorder

Rumination disorder is diagnosed when an individual frequently and repeatedly over a period of at least 1 month regurgitates food following eating. The regurgitation must not simply be due to a gastrointestinal/medical illness, and as with pica, rumination disorder should be assigned as a co-occurring diagnosis for an individual with another mental disorder only if the feeding disturbance is severe enough to require additional intervention. Preliminary data suggest that rumination disorder occurs infrequently among older children and adolescents presenting for an evaluation to an adolescent medicine physician (Ornstein et al., 2013).

Avoidant/Restrictive Food Intake Disorder

Unlike pica and rumination disorder, which were not substantially changed between DSM-IV and DSM-5, the DSM-IV diagnosis “feeding disorder of infancy or early childhood” was rearticulated and renamed “avoidant/restrictive food intake disorder.” Individuals with avoidant/restrictive food intake disorder consistently fail to achieve nutritional or energy needs and display at least one clinically significant symptom, such as notable weight loss/failure to gain weight, a nutritional deficiency, a need for food supplementation, or impaired psychosocial functioning. The feeding disturbance is not attributable to cultural or religious practices or problems obtaining food, is not associated with the shape or weight concerns characteristic of AN and BN, and is not merely a symptom of another co-occurring mental or physical disorder. Among the presentations subsumed within the avoidant/restrictive food intake disorder category are (1) food avoidance emotional disorder, or emotional distress leading to insufficient calorie consumption; (2) an aversion or avoidance of foods because of their appearance, smell, taste, or texture; and (3) food avoidance due to a specific fear, or functional dysphagia or fear of swallowing (Bryant-Waugh et al., 2010). Differentiating avoidant/restrictive food intake disorder from AN requires a careful assessment of the rationale for food restriction to determine the most appropriate diagnosis, which may be especially challenging among adolescents, whose level of insight may be limited.

Emerging evidence since the publication of DSM-5 suggests that avoidant/restrictive food intake disorder has significant clinical utility. Five percent to 20% of youngsters presenting to adolescent medicine physicians with eating problems may meet the criteria for avoidant/restrictive food intake disorder (Norris & Katzman, 2015; Ornstein et al., 2013). Individuals with avoidant/restrictive food intake disorder appear to be younger than those presenting with AN, have been ill longer, and are more likely to be male. Body weights are intermediate between those with AN and those with BN (Fisher et al., 2014).

Other Specified Feeding and Eating Disorder, Unspecified Feeding or Eating Disorder

The DSM-5 categories of other specified and unspecified feeding or eating disorder are provided to permit identification of subsyndromal feeding or eating symptoms that nonetheless lead to notable distress or impairment in functioning (e.g., social, occupational, other important areas of functioning; APA, 2013). The other specified feeding or eating disorder category is distinguished from the unspecified feeding or eating disorder category by the provision of five descriptions: for atypical AN, subthreshold BN (p. 296) and BED (of low frequency and/or limited duration), purging disorder, and night eating syndrome. The final category, unspecified feeding or eating disorder, is assigned to individuals with an eating disorder that does not meet the criteria for any of the officially recognized disorders and does not match one of these descriptions. Adolescents assigned an “other” eating disorder may not have a less severe illness, as exemplified by serious medical conditions or comorbidities (e.g., a prolonged QTc interval) observed in this heterogeneous diagnostic group (Peebles et al., 2010).

Summary

The DSM-5 criteria for feeding and eating disorders were published in 2013. Although relatively limited information is available at this time to evaluate the utility of these new categories, emerging data from adults and adolescents (Norris & Katzman, 2015; Ornstein et al., 2013; Stice, Marti, & Rohde, 2013; Sysko et al., 2012; Thomas et al., 2015) suggest that the revised categories improve on the DSM-IV scheme, which failed to capture many adolescents and adults with clinically significant eating problems. Although pica, rumination disorder, and avoidant/restrictive food intake disorder are likely particularly relevant to adolescents, limited information is available about these disorders. Thus, these conditions are not further considered in the sections that follow.

Demographics and Prevalence of Eating Disorders

Relatively few large population-based studies conducted during the past two decades are available to provide estimates of the prevalence of eating disorders. Since only a minority of individuals with a mental illness, including eating disorders, seek treatment (Demyttenaere et al., 2004; Merikangas et al., 2011; Preti et al., 2009; Swanson, Crow, Le Grange, Swendsen, & Merikangas, 2011), prevalence estimates from clinical samples are likely biased. Healthcare system databases also provide estimates of the age-specific prevalence and incidence of eating disorders (Currin, Schmidt, Treasure, & Jick, 2005; Nicholls, Lynn, & Viner, 2011; Pinhas, Morris, Crosby, & Katzman, 2011; van Son, van Hoeken, Bartelds, van Furth, & Hoek, 2006a, 2006b). Although many of these studies are large and carefully conducted and make important contributions to the literature on eating disorders, it is unclear whether the results are generalizable since many cases of eating disorders are not detected by the healthcare system (Keski-Rahkonen et al., 2007). Therefore, the literature cited in the sections that follow focuses on population-based samples, including nationally or locally representative ones (e.g., Hudson et al., 2007; Kessler et al., 2013; Swanson et al., 2011), cross-sectional convenience samples (e.g., Preti et al., 2009), and birth or population-based cohort studies (e.g., Field et al., 2012; Machado, Goncalves, & Hoek, 2013).

The typical onset of eating disorders is during preadolescence or adolescence, but most epidemiological samples are too small to study eating disorders meeting full diagnostic criteria. Thus, the majority of studies of children and adolescents instead focus on weight concerns, unhealthy weight-control behaviors, and/or bulimic behaviors. However, age of onset of AN, BN, and BED is primarily derived from studies asking adults to recall retrospective information about symptoms at younger ages and symptoms in the past year, data that are subsequently used to generate age-specific or lifetime prevalence. The accuracy of such information is unknown, and the results should therefore be interpreted cautiously.

Anorexia Nervosa

In DSM-IV, the nosological system used for eating disorders until very recently, only AN and BN were specifically recognized as eating disorders, and the diagnostic criteria were very stringent. Thus, extremely large samples were needed to accurately assess current prevalence. For example, Machado et al. (2013) reported a point prevalence of 0.6% among adolescent and young adult females, and estimates from other large population-based samples of female youth report an even lower prevalence of 0% (p. 297) to 0.3% (see Box 13.1), suggesting that samples of at least 300 to 500 adolescent females are needed to identify one current case of AN among adolescents, and even larger samples to assess the prevalence among males or adults. Therefore, studies with more than 1,000 females and as many or more males are desirable. Unfortunately, a relatively small number of studies with samples of approximately 500 or more females is available (Table 13.1).

Table 13.1 Prevalence Estimates from Population-Based Epidemiological Studies

AN

BN

BED

Authors

Sample Size

Sampling

Age

Country

Assessment

DSM

Point

Lifetime

Point

Lifetime

Point

Lifetime

Ackard et al.

4,746

Cohort study

Adolescents

USA

Self-report questionnaire

DSM-IV

0.0% M,

0.04% F

0.2% M,

0.3% F

0.3% M

1.9% F

Swanson et al.

10,123

Nationally representative

Adolescents

USA

Composite International Diagnostic Interview (CIDI)

DSM-IV

0.2%

(0.1% M,

0.2% F)

0.3%

(0.3% M,

0.3% F)

0.6%

(0.3% M,

0.9% F)

0.9%

(0.5% M,

1.3% F)

0.9%

(0.4% M

1.4% F)

1.6%

(0.8% M,

2.3% F)

McKnight Investigators

1,103 females

Prospective cohort study

Preadolescents

USA

McKnight Eating Disorder Examination (EDE)

DSM-IV

0.0% F

0.4% F

Machado et al.

3,048 females

Convenience sample

Adolescents and young adults

Portugal

2-stage design: Eating Disorder Examination Questionnaire (EDE-Q) followed by EDE

DSM-IV

0.6% F

0.5% F

Stice et al.

496 females

Prospective cohort study

Adolescents and young adults

USA

EDD Interview

DSM-IV

0.6% F

1.6% F

1.0% F

Wittchen et al.

3,021

Convenience sample?

Adolescents and young adults

Germany

M-CIDI

DSM-IV

0.0% M, 0.3% F

0.1% M, 1.0% F

0.0% M, 0.7% F

0.0% M, 1.7% F

Keski-Rahkonen et al.

2,881

Cohort study of twins

Adolescents and young adults

Finland

2-stage design: Structured Clinical Interview for DSM-IV (SCID)

DSM-IV

2.2% F

2.3%

Hudson et al.

9,282

Nationally representative

Adults

USA

CIDI

DSM-IV

00

0

0.6%

(0.3% M,

0.9% F)

0.3%

(0.1% M,

0.5% F)

1.0%

(0.5% M,

1.5% F)

1.2%

(0.8% M,

1.6% F)

2.8%

(2.0% M,

3.5% F)

Preti et al.

21,425

Probability sample

Adults

6 European countries

CIDI

DSM-IV

0%

(0.0% M,

0.0% F)

0.5%

(0.0% M,

0.9% F)

0.2%

(0.0% M,

0.3% F)

0.5%

(0.1% M,

0.9% F)

0.3%

(0.1% M,

0.6% F)

1.1%

(0.3% M,

1.9% F)

Micali et al.

5,256 females

Birth cohort study

Adults

Netherlands

DSM-IV

0.3% F

2.1% F

Kessler et al.

24,124

Nationally representative

Adults

14 countries around the world

CIDI

DSM-IV

0.4%

1.0%

0.8%

1.9%

Bulik et al.

31,406

Twin registry

Adults

Sweden

SCID Screen Patient Questionnaire

DSM-IV

1.2% F

0.3% M

Trace et al.

13,295 females

Twin study

Adults

Sweden

SCID Screen Patient Questionnaire

DSM-IV

1.2% F

0.2% F

Wade et al.

1,002 females

Cohort study of twins

Adults

Australia

EDE

DSM-IV

1.9% F

2.9%

2.9%

Swanson et al.

10,123

Nationally representative

Adolescents

USA

CIDI

DSM-5

0.2%

(0.1% M,

0.2% F)

1.1%

(0.4% M,

1.8% F)

2.0%

(1.4% M,

2.6% F)

4.1%

(3.4% M,

4.6% F)

Machado et al.

3,048 females

Convenience sample

Adolescents and young adults

Portugal

2-stage design: EDEQ followed by EDE

DSM-5

0.7% F

0.6% F

0.6% F

Field et al.

8,594 females

Prospective cohort study

Adolescents and young adults

USA

Self-report questionnaire

DSM-5

0.8% F

1.8% F

Stice et al.

496 females

Prospective cohort study

Adolescents and young adults

USA

EDD Interview

DSM-5

0.8% F

2.6% F

3.0% F

Trace et al.

13,295 females

Twin study

Adults

Sweden

SCID Screen Patient Questionnaire

DSM-5

1.6% F

0.4% F

Bulik et al.

41,157 females

Birth cohort study

Adults

Norway

Self-report questionnaire

DSM-5

0.1% F

0.7%

3.5%

Most large epidemiological studies have used rigorous assessment tools, such as the Composite International Diagnostic Interview, the Eating Disorder Examination, or the Structured Clinical Interview for DSM-IV. With these measures, the point prevalence of AN ranges between 0.04% and 0.6% among adolescent females (Ackard, Fulkerson, & Neumark-Sztainer, 2007; Machado et al., 2013; Swanson et al., 2011; Wittchen, Nelson, & Lachner, 1998), between 0% and 0.1% among adolescent males (Ackard et al., 2007; Swanson et al., 2011; Wittchen et al., 1998), and between 0% and 0.1% among adults (Bulik et al., 2007; Hudson et al., 2007; Preti et al., 2009; see Table 13.1).

In the National Survey Replication Survey sample of 9,282 adults, median age of recalled onset of AN was 18 years, with an interquartile range of 16 to 22 years (Hudson et al., 2007). Among the 21,425 adults in the European Study of the Epidemiology of Mental Disorders project, all cases of anorexia developed before 20 years of age (Preti et al., 2009). Lifetime rates appear to decrease as age increases among adults, which has been interpreted as a cohort effect with eating disorders becoming more prevalent in recent decades. However, this may also reflect greater awareness of eating disorders among younger individuals.

The low incidence of AN has made it challenging to conduct prospective studies of individuals with subthreshold variants who may be at risk for the development of full-syndrome AN (see also Chapter 15). The dearth of empirical data evaluating subthreshold versions of AN is particularly important in adolescence, as most cases of AN develop during this period. The identification of clinically significant cases of subthreshold AN prior to meeting full criteria is complicated by the weight trajectories of children and adolescents, as they may have lost weight, or failed to make adequate gains, but are not yet at a low weight. Unlike cancers, which are staged into in situ (completely local and not entirely cancerous) and stages I through IV depending on the size and spread of the tumor, the diagnostic criteria for AN identify an already severe eating disorder. Numerous investigators have attempted to study less severe AN (atypical, broad AN, etc.) but without employing standard definitions, making comparisons across studies very difficult.

Finally, in DSM-5, amenorrhea is not required for a diagnosis of AN, and in combination with a more flexible weight standard, prevalence estimates may increase (Keski-Rahkonen et al., 2007; Wade, Bergin, Tiggemann, Bulik, & Fairburn, 2006).

Bulimia Nervosa

In the DSM-IV and DSM-5 diagnostic schemes, a hierarchy prevents the concurrent diagnosis of BN if an individual meets the criteria for AN. The following sections therefore focus on studies employing DSM-IV or DSM-5 criteria so estimates of BN can be compared across studies. Using data from 24,124 adults in the World Health Organization World Mental Health Surveys, the highest prevalence of BN was noted in Brazil (0.9%) and the lowest in Romania (0%; Kessler et al., 2013). Similar studies have not been conducted with adolescents, but it is reasonable to assume that the same patterns exist among younger individuals.

Studies have consistently found that BN is more common among females than males (see Table 13.1). Among 10,123 adolescents in the National Comorbidity Survey Replication Adolescent Supplement, a nationally representative sample, current BN prevalence was higher (0.3% of males and 0.9% of females) but lifetime rates were similar (0.5% males and 1.3% of females; Swanson et al., 2011) to the adults in the National Comorbidity Survey Replication, which suggests that there is either a secular trend in rising rates or poor recall of past history of BN. There is some evidence to suggest that (p. 298) (p. 299) (p. 300) past recall of binge eating and purging results in underestimation (Field, Colditz, Herzog, & Heatherton, 1996), but it is difficult to draw conclusions about secular trends since there are not large-scale studies that have been done repeatedly over time. However, Hudson et al. (2007) did note a cohort effect in the National Comorbidity Replication Sample.

Another methodological concern is the challenge of assessing criteria for BN among adolescent males. The definition of binge eating requires the consumption of an abnormally large amount of food, larger than others would eat in a similar circumstance, and a sense of loss of control during the episode of eating. Adolescent males, especially if physically active, require prodigious caloric consumption to support normal growth and development (Shomaker et al., 2010), making the assessment of an “unusually large” amount of food difficult. In addition, adolescent males may be reluctant to admit that their eating sometimes feels out of control.

Binge-Eating Disorder

Although BED was not formally recognized until the publication of DSM-5, numerous studies have investigated the prevalence and correlates of this disorder using the DSM-IV definition in both adolescent and adult samples. The prevalence of BED is higher than AN and BN combined, with a range in population-based samples from 0.6% to 4.6% among adolescent and young adult females (Ackard et al., 2007; Field et al., 2012; Machado et al., 2013; Stice et al., 2013; Swanson et al., 2011). Since DSM-5 BED includes a lower binge-eating frequency cutoff than the provisional criteria for BED in DSM-IV and reduces the required timeframe (>3 months) for diagnosis, rates of BED will be higher in studies using the most recent criteria, although it is not clear by how much (Hudson, Coit, Lalonde, & Pope, 2012; Trace et al., 2012).

Apart from Brazil, studies in U.S. populations report higher prevalence rates (Ackard et al., 2007; Field et al., 2012; Hudson et al., 2007; Swanson et al., 2011) than other countries (Kessler et al., 2013; Machado et al., 2013; Preti et al., 2009). Few differences in prevalence estimates are noted in studies using clinical interviews (Hudson et al., 2007; Swanson et al., 2011) and self-report questionnaires (Ackard et al., 2007; Field et al., 2012). As with other eating disorders, a cohort effect appears to occur with BED such that samples with large numbers of older adults report lower prevalence rates. For example, Hudson et al. (2007) found a lifetime rate for BED of 4.2% among 18- to 29-year-old women but a much lower (2.4%) rate among women older than 60 years.

Other Specified Eating Disorders

In both clinical samples and research studies, the majority of adolescents with an eating disorder do not have either AN or BN and were classified as (1) not having an eating disorder, (2) having an eating disorder not otherwise specified, or (3) having BED, a specific variant of eating disorder not otherwise specified, the residual category of DSM-IV. In DSM-IV, eating disorder not otherwise specified captured a wide range of eating pathology, making comparisons across studies difficult. Moreover, although the boundary between full-criteria disorders and an eating disorder not otherwise specified is clear, there has been no discussion about the lower bound for inclusion in the eating disorder not otherwise specified category, further complicating an understanding of the prevalence of clinically significant eating pathology.

Although not recognized by the DSM-IV, and only listed as a specific example of other specified feeding and eating disorder in DSM-5, a nontrivial number of youths engage in frequent purging but do not binge eat. Whether they have a “purging disorder” or are a non-binge-eating variant of BN is not yet completely understood. Purging disorder has not been as thoroughly studied as other eating disorders; however, a growing number of large population-based epidemiological samples are beginning to include this category. Among the 9,000 girls in the Growing Up Today Study, 4.1% developed purging disorder during adolescence or young adulthood (Field et al., 2012). A slightly lower (p. 301) rate (3.4%) was observed by Stice et al. (2013) in a smaller sample followed for 8 years.

Population-Based Studies of Eating Disorder Symptoms and Behaviors

All of the recognized eating disorders require frequently engaging in bulimic behaviors and/or a low weight resulting from use of extreme weight-control behaviors over an extended period of time. Many researchers, particularly epidemiologists and others interested in prevention, have examined less frequent or extreme weight-control behaviors and binge eating, which might be particularly relevant for adolescents if these symptoms represent an early stage of an eating disorder or are associated with harmful outcomes regardless of whether they progress to a full-threshold eating disorder.

Cross-sectional studies of disordered eating among adolescents and young adults and a growing number of prospective investigations have provided information about other forms of eating disorder psychopathology. Neumark-Sztainer et al. (2012) reported that among 2,793 adolescents in Project Eating Among Teens, 9.6% of females and 6.3% of males had engaged in binge eating at least once during the past year. Lower rates of binge eating were observed among 10,334 young adults in the Longitudinal Study of Adolescent Health. In a nationally representative sample, Striegel-Moore et al. (2011) found that among Caucasians, 1.3% of females and 0.4% of males reported binge eating, but rates were much higher among American Indians and Native Americans (3.8% and 0.8%, respectively). Large ethnic differences in purging were also observed among the more than 10,900 adolescents assessed in the Youth Risk Behavior Surveillance System, with Chao et al. (2008) reporting purging in the past 30 days among 6.7% of whites and 6.8% of Hispanics, but in only 4% of blacks. For boys, rates were highest among Hispanics (3.9%) and lowest among whites (2.3%). Even larger disparities were observed among 16,978 children from 47 Massachusetts middle schools participating in the Healthy Choices overweight prevention study (Austin et al., 2011). In females, the prevalence of use of vomiting, laxatives, or diet pills to control weight was lower among whites (2.7%) than blacks (6.7%), Hispanics (6.6%), Pacific Islanders (24.2%), or American Indians (23.3%), and a similar pattern was observed among boys. Fewer studies have assessed the incidence of bulimic behaviors, but among 12,534 adolescents in the Growing Up Today Study, during 7 years of follow-up, 4.3% of females and 2.3% of males started to binge eat at least weekly and 5.3% of females and 0.8% of males started to purge at least weekly, but few adolescents engaged in weekly binge eating and purging (Field et al., 2008).

Summary

A growing number of studies have been published on eating disorders and disordered eating among adolescents and young adults. Comparisons between studies can be challenging because of sample characteristics (i.e., size and sampling methodology) and lack of standard definitions for the most common behaviors and disorders (e.g., eating disorder not otherwise specified) among adolescents. For example, some studies include only presentations that miss the duration criterion for BN or BED, while others include all disordered eating not captured by a full-threshold eating disorder diagnosis (Box 13.4). Comparisons between studies of disordered eating are equally (p. 302) challenging. Some studies focus only on frequent binge eating and purging; others examine any use of a large variety of weight-control behaviors (diet pills, laxatives, vomiting, etc.), or include dieting in the same category as vomiting and laxatives. Despite these methodological challenges, more females than males try to control their weight, engage in weight-control behaviors including purging, and binge eat. Eating disorders are also more common among females, but the gender difference in rates of BED may appear to be much smaller in future studies using DSM-5 criteria.

Comorbidity, Outcome, and Diagnostic Migration

In addition to examining the diagnostic categories and data on the prevalence of eating disorders, it is important to know what other forms of psychopathology individuals with eating disorders are prone to develop, and to describe what is likely to occur over time to individuals with eating disorders in terms of stability of diagnoses and outcome. Knowledge of comorbidity, outcome, and migration among diagnostic categories is important to match patients to interventions and to assessing the overall effectiveness of treatments. A number of studies have addressed comorbidity, course, and outcome of adult patients with eating disorders, but studies of adolescents are limited. The available literature suggests that the comorbidities commonly seen in adults with eating disorders are also seen in adolescents with such problems, with elevated rates of affective disorders, anxiety disorders, and substance abuse compared to control groups (Castro-Fornieles et al., 2010; Herpertz-Dahlmann, 2009; Kirkcaldy, Siefen, Kandel, & Merrick, 2007; Swanson et al., 2011; Touchette et al., 2011).

Comorbidity

Comorbidity of Anorexia Nervosa

Overall, the lifetime rates of psychiatric comorbidity among patients with eating disorders are substantial (Halmi et al., 1991, Spindler & Milos, 2007; Villarejo et al., 2012; von Lojewski, Boyd, Abraham, & Russell, 2012). Affective disorders, anxiety disorders, substance use disorders, and personality disorders are all commonly associated with AN. The affective disorder that most commonly co-occurs with AN is major depressive disorder, with a lifetime comorbidity of 50% to 70% (Herzog, Nussbaum, & Marmor, 1996; von Lojewski et al., 2012). Lifetime rates of anxiety disorders are seen in between 50% and 70% of these patients (Dellava, Kendler, & Neale, 2011; Godart, Flament, Perdereau, & Jeammet, 2002; Swinbourne & Touyz, 2007; Strober, Freeman, Lampert, & Diamond, 2007); common comorbid anxiety diagnoses are social phobia (40%–55%) and obsessive-compulsive disorder (OCD; 5%–69%; Godart et al., 2002; Halmi et al., 1991). Of particular note, AN seems to commonly develop following childhood anxiety disorders (Bulik et al., 1997; Raney et al., 2008; Swinbourne et al., 2012). Also of note, there is a clear association between OCD and AN, and similarities between the two conditions have often been cited (Altman & Shankman, 2009). Lifetime prevalence of substance use disorders ranges between 12% and 21% (Bulik, Sullivan, McKee, Weltzin & Kaye, 1994; Herzog, Keller, Sacks, Yeh, & Lavori, 1992; Root, Pisetsky, et al., 2010; Stock, Goldberg, Corbett & Katzman, 2002), and patients with the binge/purge subtype are more likely than those with restrictor subtype to manifest such problems (Herzog, Keller, Sacks, Yeh & Lavori, 1992; Root, Pinheiro, et al., 2010). Current prevalence rates are also notable, with over 70% meeting criteria for a current psychiatric disorder when presenting for treatment (Braun, Sunday & Halmi, 1994; Herpertz-Dahlmann, Müller, Herpertz, Heussen, Hebebrand & Remschmidt, 2001; Herzog et al., 1992; Wonderlich & Mitchell, 1997).

The developmental sequence of AN in relation to other comorbid conditions varies significantly. Affective disorders may begin before or after the onset of AN, or the disorders can begin concurrently (Braun et al., 1994). Anxiety disorders, in particular social phobia and OCD, frequently predate the onset of AN (Anderluh, Tchanturia, Rabe-Hesketh & Treasure, 2003; Braun et al., 1994; Bulik, Sullivan & Joyce, 1997; (p. 303) Swinbourne & Touyz, 2007), whereas substance use disorders often develop after the onset of AN (Braun et al., 1994).

Comorbidity of Bulimia Nervosa

Approximately 70% to 85% of patients with BN report a lifetime history of another psychiatric disorder, and the rates of current disorders at time of presentation are also elevated (Fichter & Quadflieg, 1997; Halmi et al., 2002; Herzog et al., 1992; Mitchell, Specker, & de Zwaan, 1991; Wonderlich & Mitchell, 1997). Affective disorders, anxiety disorders, substance use disorders, and personality disorders are commonly associated with BN, with major depressive disorder the most common mood disorder among patients with BN. In community samples, approximately one third meet lifetime criteria, a rate that increases to 65% in inpatient and outpatient samples. In clinical samples, the lifetime rates of comorbidity with at least one anxiety disorder range from 3% to 65% (Herzog et al., 1992; Swinbourne & Touyz, 2007), with social phobia, OCD, panic disorder, and posttraumatic stress disorder (PTSD) commonly observed (Brewerton et al., 1995; Mitchell, Mazzeo, Schlesinger, Brewerton & Smith, 2012; von Ranson, Kaye, Weltzin, Rao & Matsunaga, 1999). Some literature also suggests that eating disorders, in particular BN, may also be associated with attention-deficit/hyperactivity disorder (ADHD; Nazar et al., 2008; Yates, Lund, Johnson, Mitchell, & McKee, 2009).

The lifetime prevalence of substance use disorders is approximately 25% (Bulik et al., 1994); alcohol is most frequently cited, followed by cocaine and marijuana. A meta-analysis suggested that substance abuse problems primarily cluster among those with binge-eating behaviors, such as those with BN, BED, and the binge/purge subtype of AN (Gadalla & Piran, 2007). Patients with BN and substance use disorders commonly exhibit impulsivity in multiple domains, including suicide attempts, self-injurious acts, and stealing. Some reports describe an increased prevalence of bipolar affective disorders among those with eating disorders, particularly those with BN (Brietzke, Moreira, Toniolo & Lafer, 2011; Fornaro et al., 2010, Lunde, Fasmer, Akiskal, Akiskal & Oedegaard, 2009; McElroy et al., 2011).

As in AN, the sequence of development of BN and comorbid conditions varies, as onset of the comorbid disorder can occur prior to, at the same time as, or following the development of BN (Braun et al., 1994). As with AN, anxiety disorders commonly predate the onset of BN, whereas substance use disorders more often develop after the onset of BN (Braun et al., 1994; Bulik et al., 1997; Swinbourne & Touyz, 2007).

Comorbidity of Binge-Eating Disorder

Although the literature on BED and comorbidity remains limited, there again appears to be an increased rate of various forms of other psychopathology, although this issue has yet to be adequately addressed in adolescent populations (Grilo, White, Barnes & Masheb, 2012; Grilo, White, & Masheb, 2009).

Outcomes

Outcome of Anorexia Nervosa

One of the problems in examining the outcome of eating disorders is that widely varying criteria for recovery have been employed (Noordenbos, 2011; Williams, Watts, & Wade, 2012). However, the available data suggest that approximately 40% to 70% of adolescents with AN recover, 20% to 30% are improved but continue to have residual symptoms, and 10% to 20% develop a chronic form of illness (Herpertz-Dahlmann et al., 2001; Morgan, Purgold, & Welbourne, 1983; Steinhausen, 1997, 2002, 2009). Most adolescents with AN continue to recover over time; for example, Strober, Freeman, and Morrell (1997) reported a 1% probability of adolescents reaching full recovery at 3 years, which increased to 72% after 10 years. Patients experiencing persistent symptoms typically display abnormalities in weight, eating behaviors, menstrual function, comorbid psychopathology, and difficulties with psychosocial functioning (Herpertz-Dahlmann et al., 2001; Steinhausen, 2009; Strober et al., (p. 304) 1997; Wentz, Gillberg, Gillberg, & Rastam, 2001). Relapse is common after weight gain in hospitalized patients, with up to one third of adolescent AN patients relapsing soon after discharge (see also Chapter 14; Herzog, Nussbaum, & Marmor, 1996; Strober et al., 1997).

AN has one of the highest mortality rates among psychiatric disorders. Approximately 5.6% of patients diagnosed with AN die per decade of illness, and long-term follow-up studies consistently find increased rates of death from both medical complications and suicide (Crow et al., 2009; Franko et al., 2013; Keel & Brown, 2010; Papadopoulos, Ekborn, Brandt, & Ekselius, 2009; Sullivan, 1995). Although the combined mortality rate for AN among adolescents and adults is over 5% (Steinhausen, 2002), the mortality rate during adolescence is believed to be low.

Some studies have found lower weight at presentation, longer duration of illness, and severe comorbid alcohol use to be associated with higher risk of mortality. Few variables are consistently associated with outcome in adolescents with AN, but the most positive outcomes are seen in patients between the ages of 12 and 18 with a short duration of illness. Poor outcome in adolescent patients is associated with extremely low weight at presentation and, in some studies, with vomiting.

Outcome of Bulimia Nervosa

Most adolescents and adults with BN improve over time, with recovery rates ranging from 35% to 75% at 5 or more years of follow-up (Fairburn, Cooper, Doll, Norman, & O’Connor, 2000; Fichter & Quadfleig, 1997; Keel & Brown, 2010; Steinhausen & Weber, 2009). However, approximately one third of individuals with BN relapse (Keel & Brown, 2010; Keel & Mitchell, 1997; Keel, Mitchell, Miller, David, & Crow, 1999), often within 1 to 2 years of recovery. Although approximately 40% to 60% of patients with BN eventually recover, the remaining individuals continue to be symptomatic, often with substantial impact on physical and psychosocial functioning (Steinhausen & Weber, 2009). While there have been some hints of an elevated mortality associated with BN (e.g., Crow et al., 2009), recent data indicate that BN without a history of AN is not associated with a significant increased risk of premature death (Franko et al., 2013). Few prognostic factors have been consistently reported across studies, but low self-esteem, longer duration of illness prior to presentation, higher frequency or severity of binge eating, substance abuse history, and a history of obesity have been associated with poorer outcome (Bulik, Sullivan, Joyce, Carter & McIntosh, 1998; Keel et al., 1999; Keel & Brown, 2010; Steinhausen & Weber, 2009).

Diagnostic Migration

Few studies address diagnostic migration, or the movement from one eating disorder subtype or eating disorder to another within the adolescent eating disorder population. While some patients migrate from BN to AN (Kassett, Gwirtsman, Kay, Brandt, & Jimerson, 1988), the most frequent change is from the restrictor subtype to the binge/purge subtype, reflecting the development of bulimic symptoms, and this migration may herald an increase in various other problems, such as suicidal ideation (Foulon et al., 2007). Some individuals gain weight in association with the binge eating, leading to a change in diagnostic status from either subtype to BN (Peat et al., 2009). In one study, more than 50% of restrictor AN patients, both adolescents and adults, developed BN symptomatology (Eddy et al., 2002), and only a small fraction of patients with the restrictor subtype remained in that diagnostic subtype. The remaining patients with the restrictive subtype who did not develop binge eating or purging were partially or fully recovered. It is unknown what factors lead to the development of binge/purge symptoms among patients with the restrictor subtype, and the precise time course of this development; however, overall diagnostic crossover should be regarded as a common phenomenon (Castellini et al., 2011).

Summary

The occurrence of other psychiatric disorders is very common in association with AN, BN, and (p. 305) BED, and this comorbidity complicates both diagnosis and treatment. Many treatment studies of eating disorders exclude patients with serious comorbid disorders, such as substance use disorders, resulting in few available data regarding the appropriate treatments for such high-comorbidity patients. Although information about the course and outcome of eating disorders in adolescents is limited, adolescents with AN appear to have a better prognosis when they receive treatment early in the course of the illness. Diagnostic migration appears to be common from the restrictor subtype to the binge/purge subtype to BN. Little is known about the course and outcome of BN among adolescents; among adults, full recovery is common, but BN can be a chronic condition. Excess mortality has been clearly demonstrated for those with AN.

Medical Complications of Eating Disorders

Eating disorders are associated with significant medical morbidity and significant mortality. Most complications result from physiological adaptations to the effects of malnutrition, or occur as a result of unhealthy weight-control behaviors. Many, but not all, of the complications are reversible with nutritional rehabilitation and symptomatic improvement. However, in an adolescent whose growth and development are not yet complete, the medical consequences of eating disorders can be long-lasting and potentially irreversible. Particularly worrisome complications for adolescents include growth retardation, pubertal delay or arrest, impaired acquisition of peak bone mass, and structural brain changes. During normal pubertal development, body weight doubles and maturation of various organs occurs, with increases in the size of the heart, brain, lungs, liver, and kidneys. Approximately 17% to 18% of final adult height is achieved (Abbassi, 1998), and between 40% and 60% of peak bone mass is accrued (Golden & Shenker, 1992; Katzman, Bachrach, Carter, & Marcus, 1991).

The medical complications of AN and BN are listed in Table 13.2. Individuals with symptoms of both disorders (e.g., patients with AN and episodes of binge eating and/or purging) are at risk for complications of both AN and BN. Adolescents with symptoms of eating disorders that do not meet the full criteria for AN or BN are also at risk for medical complications (Peebles, Hardy, Wilson & Lock, 2010). Most complications occur with equal frequency in adults and adolescents, but in contrast to adults, a young adolescent with incompletely formed stores of body fat and other substrates can suffer significant medical compromise after a relatively small degree of weight loss.

Table 13.2 Signs and Symptoms of Eating Disorders in Adolescence1

Factor

AN2

BN

Weight

Markedly decreased

Usually normal

Menstruation

Absent

Usually normal

Skin/Extremities

Growth of fine downy hair (lanugo)

Calluses on back of hand

Cold blue hands and feet (acrocyanosis)

Swelling of feet (edema)

Cardiovascular

Low heart rate (bradycardia)

Hypotension

Orthostasis

Gastrointestinal

Elevated liver enzymes

Parotid and salivary gland enlargement

Delayed gastric emptying

Constipation

Dental erosion

Esophagitis

Barrett’s esophagus

Hematopoietic

Normochromic, normocyctic anemia

Leukopenia

Thrombocytopenia

Low erythrocyte sedimentation rate

Fluid/Electrolytes

Increased blood urea nitrogen

Hypokalemia

Increased creatinine

Hypochloremia

Hyponatremia

Alkalosis

Hypophosphatemia

Hypomagnesemia

Endocrine

Hypoglycemia

Low estrogen or testosterone

Low luteinizing hormone

Low follicle-stimulating hormone

Low-normal thyroxine, low T3

Normal thyroid-stimulating hormone

Increased cortisol

Delayed puberty

Growth retardation

Skeletal

Reduced bone mineral density

Increased bone fragility

1 Partially adapted from Walsh, B. T., & Attia, E. (2011). Eating disorders. In: D. L. Longo, A. S. Fauci, D. L. Kasper, S. L. Hauser, J. L. Jameson, & J. Loscalzo (Eds.), Harrison’s principles of internal medicine (18th ed.). New York: McGraw Hill.

2 Individuals with AN who engage in binge eating and/or purging may also develop signs and symptoms of BN.

Medical Complications of Anorexia Nervosa

The most notable medical complications of AN result from malnutrition. Subcutaneous tissue and muscle mass are lost, and patients display sunken cheeks and prominence of bony protuberances. Body temperature is usually low and patients often wear multiple layers of clothing to keep warm. The hands and feet may be cold and blue (acrocyanosis); the skin may be pale, dry, and yellow. Fine downy hair (lanugo) may be present over the arms, back, and abdomen. Scalp hair is dry, listless, and brittle, and there may be evidence of hair loss. Resting pulse and blood pressure are both low, and dizziness and fainting may occur upon standing as a result of orthostatic changes in pulse and blood pressure. There may be generalized muscle weakness.

Life-threatening complications of AN include electrolyte disturbances and cardiac arrhythmias. Patients may present with dehydration and abnormal serum levels of sodium, potassium, chloride, phosphorus, magnesium, carbon dioxide, and blood urea nitrogen. Electrolyte disturbances are more likely in those who are vomiting or abusing laxatives or diuretics. Hyponatremia (low sodium levels) can occur in those who drink excessive amounts of water either to satisfy hunger urges or to falsely elevate body weight prior to a medical visit. Water intoxication with hyponatremia can cause seizures, coma, and death. Serum phosphorus levels may be normal on presentation but may drop upon refeeding, and hypophosphatemia may play a role in the development (p. 306) (p. 307) of cardiac arrhythmias and sudden unexpected death seen in the “refeeding syndrome” (Kohn, Golden, & Shenker, 1998). Hypomagnesemia is more likely to occur in those who are purging (Raj, Keane-Miller, & Golden, 2012).

Resting pulse rates among patients with AN may be as low as 30 to 40 beats per minute (Palla & Litt, 1988), and systolic and diastolic blood pressures are low. Within the first 4 days of hospitalization, 60% to 85% of patients demonstrate orthostatic pulse changes on standing (Shamim, Golden, Arden, Filiberto, & Shenker, 2003). Both cardiac structure and function are affected (Casiero & Frishman, 2006), left ventricular mass and cardiac output are reduced (Mont et al., 2003; Moodie & Salcedo, 1983), heart rate variability is increased (Kosche et al., 2010; Mont et al., 2003), and exercise capacity is diminished (Nudel, Gootman, Nussbaum & Shenker, 1984). Electrocardiographic abnormalities have been noted in up to 75% of hospitalized adolescent patients (Galetta et al., 2002; Palla & Litt, 1988). A prolonged QTc interval, one type of electrocardiographic abnormality, is particularly concerning because it appears to precede ventricular arrhythmias and sudden death in patients hospitalized with AN (Isner, Roberts, Heymsfield, & Yager, 1985). A mild to moderate pericardial effusion (fluid around the heart) that is clinically silent, has been reported in 60% to 70% of patients with AN (Ramacciotti, Coli, Biadi, & Dell’Osso, 2003; Silverman & Krongrad, 1983; Silvetti et al., 1998). Congestive heart failure does not usually occur in the starvation phase and is more likely to occur during refeeding (Powers, 1982).

Bloating and constipation are frequent complaints of patients with AN and reflect delayed gastric emptying and decreased intestinal motility. Liver enzyme levels are elevated in 4% to 38% of patients (Mickley, Greenfeld, Quinlan, Roloff, & Zwas, 1996; Palla & Litt, 1988; Sherman, Leslie, Goldberg, Rybczynski, & St. Louis, 1994). Liver enzyme elevations are usually mild, most frequently are present before refeeding has been initiated, and usually respond to nutritional rehabilitation (Narayanan, Gaudiani, Harris, & Mehler, 2010; Rautou et al., 2008). On occasion, they can be aggravated by refeeding. Acute liver failure can occur but is rare (De Caprio et al., 2006; Furuta et al., 1999). Cholesterol levels may be high but most frequently are normal (Arden, Weiselberg, Nussbaum, Shenker, & Jacobson, 1990; Boland, Beguin, Zech, Desager, & Lambert, 2001; Mehler, Lezotte, & Eckel, 1998). Serum carotene levels may be elevated in 13% to 62% of cases and may lead to a yellowish discoloration of the skin (Boland et al., 2001; Sherman et al., 1994). The cause of the high serum carotene levels is not clear but is thought to be a combination of increased dietary intake of pigmented vegetables such as carrots and derangements of hepatic conversion of beta-carotene to vitamin A. In contrast to other forms of malnutrition, serum albumin levels are usually normal. Rapid weight loss is associated with gallstone formation. With malnutrition, metabolic rate slows as an adaptive response to starvation. In AN, measured resting energy expenditure may be 65% to 70% of predicted values (Schebendach et al., 1995), and consequently, caloric requirements are lower in the malnourished state. With nutritional rehabilitation, metabolic recovery occurs over a 4- to 6-week period and caloric requirements increase dramatically (Schebendach, Golden, Jacobson, Hertz, & Shenker, 1997).

Suppression of the bone marrow occurs frequently in AN, resulting in low white blood cell, red blood cell, and platelet counts (Misra et al., 2004). Leukopenia (low white blood cell count) has been reported in one third to two thirds of patients with AN and is thought to be secondary to bone marrow suppression (Palla & Litt, 1988; Sharp & Freeman, 1993). Despite the low white blood cell count, there does not appear to be an increased risk of infection. Once a bacterial infection is present, however, low complement levels may prolong the course of the infection. All hematological abnormalities are reversed with nutritional rehabilitation.

The major neurological complications of eating disorders are seizures and structural brain changes, found on computed tomography and magnetic resonance imaging scans (Enzmann & Lane, 1977; Golden et al., 1996; Katzman et al., 1996; Nussbaum, Shenker, Marc, & Klein, 1980). Muscle weakness and a peripheral (p. 308) neuropathy can also occur. Neuropsychological testing notes impairments of attention, concentration, and memory, with deficits in visuospatial ability (Kingston, Szmukler, Andrewes, Tress, & Desmond, 1996). While the ventricular enlargement and white matter changes revert to normal after weight restoration (Golden et al., 1996; Katzman, Zipursky, Lambe, & Mikulis, 1997), the gray matter volume deficits and regional blood flow disturbances may persist, suggesting that these changes may predate the illness (Golden et al., 1996; Gordon, Lask, Bryant-Waugh, Christie, & Timimi, 1997; Katzman et al., 1997). Similarly, some, but not all, of the cognitive deficits improve with weight restoration (Kingston et al., 1996).

Adolescents who develop AN prior to the completion of growth can exhibit growth retardation and short stature. Patients are shorter than expected (Nussbaum, Baird, Sonnenblick, Cowan, & Shenker, 1985), and growth stunting may even be the presenting feature (Modan-Moses et al., 2003; Root & Powers, 1983). Growth retardation is more likely to occur in adolescent boys because boys grow, on average, for 2 years longer than girls. In girls, growth is almost complete by menarche, which occurs at an average age of 12.4 years in the United States (Chumlea et al., 2003). Catch-up growth can occur with nutritional rehabilitation; even with intervention, however, these adolescents may not reach their genetic height potential (Lantzouni, Frank, Golden, & Shenker, 2002).

Hypothalamic dysfunction is evidenced by amenorrhea (loss of menses) as well as disturbances in satiety, difficulties with temperature regulation, and ability to concentrate urine (Mecklenberg et al., 1976). There is activation of the hypothalamic–pituitary–adrenal axis with elevated levels of serum cortisol. Clinically, patients with AN have symptoms that look very much like those seen in hypothyroidism (dry yellow skin, low heart rate, low metabolic rate, amenorrhea, and constipation). Disturbances in thyroid function tests resolve with improved nutrition and should not be treated with thyroid hormone replacement.

Pubertal delay is frequently found among patients who develop AN prior to the completion of puberty (Palla & Litt, 1988; Russell, 1985). Amenorrhea occurs as a result of suppression of the hypothalamic–pituitary–ovarian axis secondary to an energy deficit associated with poor nutritional intake and excessive exercise. Levels of pituitary and ovarian hormones controlling menstruation are all low, and the uterus and ovaries shrink (Golden & Shenker, 1992). In most instances, amenorrhea is associated with weight loss, but in approximately 20% of cases, loss of menses may precede significant weight loss (Golden et al., 1997). Weight gain is usually accompanied by restoration of normal hypothalamic–pituitary–ovarian function and resumption of spontaneous menses, but in many cases, amenorrhea may be prolonged.

Provided weight is restored and menses are regular, the ability to conceive should be normal. Persistence of low body weight and weight-control behaviors, however, may be associated with infertility (Bates, Bates, & Whitworth, 1982). Women with a past history of AN have similar pregnancy rates and are no more likely to have received treatment for infertility than healthy controls, but they are more likely to have a miscarriage, presumably because of continuation of inappropriate weight-control behaviors during pregnancy (Bulik et al., 1999). Although the majority of women with eating disorders have positive pregnancy outcomes, some studies have demonstrated an increased risk of birth by cesarean section (Bulik et al., 2009; Franko et al., 2001) and higher rates of preterm delivery and low birth weight (Micali, Simonoff & Treasure, 2007; Sollid, Wisborg, Hjort, Secher, 2004).

Osteoporosis is a serious long-term medical complication of AN (Golden, 2010). Bone formation is impaired and bone resorption is increased, resulting in net reduction in bone mineral density (BMD) and increased fracture risk. Compared to controls, fracture risk is estimated to be increased twofold to threefold in women who have previously had AN (Lucas, Melton, Crowson & O’Fallon, 1999; Vestergaard et al., 2002). BMD reduction may occur after a relatively short duration of illness, and those who develop AN prior to menarche have lower BMD than those who develop it after menarche (p. 309) (Bachrach, Guido, Katzman, Litt, & Marcus, 1990; Golden et al., 2002; Grinspoon et al., 2000). Contributing factors include poor nutrition, low body weight, estrogen deficiency, excessive exercise, and high levels of cortisol in the bloodstream. In women, the degree of BMD reduction in AN is more severe than that seen in women with other conditions associated with amenorrhea and a low estrogen state, suggesting that, in addition to estrogen deficiency, nutritional factors play an important role (Grinspoon et al., 1999). Low BMD is also found in males with AN and is associated with low testosterone levels (Andersen, Watson, & Schlechte, 2000; Mehler, Sabel, Watson, & Anderson, 2008; Misra, Katzman, et al., 2008).

Adolescence is a critical time for bone mass acquisition: approximately 60% of peak bone mass is accrued during the adolescent years, and there is very little net gain in bone mass after 2 years following menarche (Bonjour, Theintz, Buchs, Slosman, & Rizzoli, 1991; Golden & Shenker, 1992; Katzman et al., 1991; Theintz et al., 1992). Whether or not a young woman will develop osteoporosis in later life depends not only on the rate of bone loss in adulthood, but also on the amount of bone present at skeletal maturity, often referred to as “peak bone mass.” Multiple studies have shown that peak bone mass is achieved toward the end of the second decade of life (Bonjour et al., 1991; Faulkner et al., 1996; Katzman et al., 1991; Southard et al., 1991). A woman who develops AN during adolescence will not reach peak bone mass, placing her at increased risk of developing fractures, and since she has a lower peak bone mass, the increased fracture risk may persist for years after recovery from AN. More than 90% of adolescents and young adults with AN have reduced BMD at one or more skeletal sites (Grinspoon et al., 2000). Both intermediate (Bachrach, Katzman, Litt, Guido, & Marcus, 1991; Golden et al., 2002; Rigotti, Neer, Skates, Herzog, & Nussbaum, 1991; Soyka et al., 2002) and long-term studies (Hartman et al., 2000; Herzog, Minne, et al., 1993; Ward, Brown & Treasure, 1997) have demonstrated that BMD reduction is persistent and may be irreversible despite full recovery from the eating disorder. In women recovered from AN for an average of 21 years, hip BMD remained lower than in controls, and a relatively high percentage of patients reported a history of pathological bone fractures (Hartman et al., 2000). Weight gain is associated with some BMD improvement, but levels do not return to normal (Bachrach et al., 1991; Golden et al., 2005; Misra, Prabhakaran, et al., 2008).

Medical Complications of Bulimia Nervosa

Patients with BN can have large fluctuations in body weight, reflecting cycles of dehydration, electrolyte disturbances, and water retention associated with vomiting and abuse of laxatives and diuretics. Massive swelling of the hands and feet can occur among those who abruptly discontinue the use of laxatives or diuretics. Examination of the hands may reveal calluses or scars over the knuckles or skin of the dominant hand (Russell’s sign), caused by abrasions by the teeth during self-induced vomiting.

Hypokalemia, a reduced level of potassium in the blood, is the most frequently found significant electrolyte disturbance in patients who vomit or use laxatives or diuretics. Hypokalemia can be associated with life-threatening cardiac arrhythmias, and a low serum potassium level should be carefully corrected. Periods of caloric restriction result in episodes of bradycardia and vital sign instability, though not to the same degree as that seen in patients with AN.

Ipecac, a medication used to induce vomiting after accidental poisoning, is abused by some patients with BN. Ipecac contains the alkaloid emetine, which is toxic to both skeletal and cardiac muscle; excessive intake may cause muscle weakness, congestive heart failure, and cardiac arrest. Ipecac use is cumulative, and ipecac abuse can be a cause of sudden death among adolescents with BN (Schiff et al., 1986).

Enlargement of the parotid and salivary glands occurs in 10% to 30% of patients with BN and is thought to be secondary to binge eating and vomiting (Ogren, Huerter, Pearson, Antonson, & Moore, 1987). Erosion of the dental (p. 310) enamel is most evident on the lingual aspects of the anterior teeth and is caused by exposure to gastric acid while vomiting. Recurrent vomiting may also lead to gastroesophageal reflux, esophagitis, tears of the esophagus, and, less frequently, esophageal rupture. Small tears may be evidenced by bloodstained vomitus. Esophageal rupture is a catastrophic event and is usually fatal. Esophagitis is associated with epigastric or retrosternal chest pain and warrants treatment. Chronic exposure of the distal esophagus to acidic stomach contents can lead to precancerous changes in the mucosal lining of the esophagus, known as Barrett’s esophagus.

Patients with BN with a prior history of AN or amenorrhea may have reduced BMD, though not to the same degree as those with active AN (Naessen, Carlstrom, Glant, Jacobsson, & Hirschberg, 2006).

Treatment of Medical Complications

The goals of medical management of patients with eating disorders are threefold: acute medical stabilization, normalization of eating, and reversal of medical complications. In AN, weight restoration is an important early goal of treatment and is usually associated with improvements in mood and eating disorder symptoms.

Refeeding in Anorexia Nervosa

The greatest risk of cardiac decompensation and electrolyte disturbances occurs during the refeeding phase, in particular during the first 7 to 10 days of refeeding. It is during this time when the “refeeding syndrome,” a constellation of cardiac, neurological, and hematological complications, is most likely to occur. The refeeding syndrome can occur after intravenous, nasogastric, or oral refeeding. Hypophosphatemia is a hallmark of this syndrome and occurs in over one quarter of adolescents hospitalized with AN (Ornstein, Golden, Jacobson, & Shenker, 2003). Hypophosphatemia is more likely to occur in those who are severely malnourished (<70% of expected body weight) and may predispose patients to ventricular arrhythmias and sudden death.

The refeeding syndrome can be prevented by monitoring heart rate and serum electrolytes (especially phosphorus) during the first 7 to 10 days of treatment. Some authorities (American Dietetic Association, 2006; American Psychiatric Association, 2006; National Institute for Clinical Excellence, 2006) have recommended slow advancement in caloric intake as a measure to prevent the refeeding syndrome, but there is limited evidence to support this recommendation. Hypocaloric diets are associated with initial weight loss (Garber, Michihata, Hetnal, Shafer, & Moscicki, 2012; Solanto, Jacobson, Heller, Golden & Hertz, 1994) and prolonged hospitalization (Garber et al., 2012). Recent studies have demonstrated that more aggressive regimens, starting patients on 1,400 to 2,000 kcals/day, are safe on units where cardiac monitoring is performed to detect cardiac arrhythmias and electrolytes are frequently checked (Gentile, Pastorelli, Ciceri, Manna, & Collimedaglia, 2010; Golden, Keane-Miller, Sainani, & Kapphahn, 2013; Whitelaw, Gilbertson, Lam, & Sawyer, 2010). Because of the metabolic effects of carbohydrates on insulin secretion and cellular phosphorus uptake, the macronutrient composition of the diet, specifically the carbohydrate content, may be more important in the genesis of the refeeding syndrome than total number of calories prescribed (Kohn, Madden & Clarke, 2011).

The caloric requirements of children and adolescents with AN are usually higher than for adults, and may reach 3,000 to 4,500 kcals/day. The rate of weight gain should be 2 to 3 pounds per week for inpatient programs, 1 to 2 pounds per week for partial hospitalization programs (when such programs are stepdown programs from inpatient units), and 0.5 to 1 pound per week for outpatient management (Yager, Anderson, & Devlin, 2000).

Treatment of Osteoporosis in Anorexia Nervosa

Few controlled trials have evaluated the treatment of reduced bone mass in AN, fewer specifically focused on adolescents, and most studies enrolled only a modest number of subjects. (p. 311) Therefore, the preferred treatment of AN-related osteoporosis is unknown.

Calcium supplementation is known to improve bone mass in healthy adolescents (Cadogan, Eastell, Jones, & Barker, 1997; Johnston et al., 1992; Lloyd et al., 1993) and in postmenopausal women with osteoporosis (Reid, Ames, Evans, Gamble, & Sharpe, 1995), but no randomized controlled trials have documented the impact of calcium supplementation on BMD in AN. The Institute of Medicine (2011) recommends a dietary intake of 1,300 mg/day of calcium for healthy girls ages 9 to 18 years, and most authorities recommend calcium supplementation (1,000–1,200 mg/day of elemental calcium) for those patients with AN whose dietary intake contains less than the recommended amount.

Vitamin D, a fat-soluble vitamin that is often deficient in the diets of those with eating disorders, is necessary for absorption and utilization of calcium. Vitamin D supplementation increases bone mineral accretion in a dose-dependent manner in adolescent girls (Viljakainen et al., 2006). The American Academy of Pediatrics (2014) now recommends a daily intake of 600 IU vitamin D for adolescents to optimize bone health. Once again, no randomized controlled trials have studied the efficacy of vitamin D supplementation to increase BMD for adolescents with AN. Most authorities recommend supplementation with at least 600 IU vitamin D per day. Patients found to be deficient in vitamin D should be treated with vitamin D2 or D3, 50,000 IU weekly for 6 to 8 weeks, followed by a maintenance dose of 600 to 1,000 IU daily (American Academy of Pediatrics, 2014).

A number of studies have shown that body weight, and in particular lean body mass, is a significant determinant of BMD in healthy subjects (Glastre et al., 1990; Henderson, Price, Cole, Gutteridge, & Bhagat, 1995; Southard et al., 1991) and in those with AN (Bachrach et al., 1990; Goebel, Schweiger, Kruger, & Fichter, 1999; Golden et al., 2002; Gordon et al., 2002; Grinspoon et al., 1999; Soyka et al., 2002). While BMD increases with weight gain, even with weight restoration, reduced bone mass is not entirely reversible (Bachrach et al., 1991; Golden et al., 2002; Hartman et al., 2000; Rigotti et al., 1991). One study of adolescent girls with AN found that weight gain and resumption of menses was associated with arrest of the BMD decline, but lack of weight gain was associated with continued BMD decline. Girls who gained weight but did not resume menses had similar BMD to those who did not gain weight (Misra, Prabhakaran, et al., 2008).

Both weight-bearing and resistance exercise programs increase the spine BMD in children and young women (McKay et al., 2000; Snow-Harter, Bouxsein, Lewis, Carter, & Marcus, 1992), and, in AN, even 5 days of bed rest is accompanied by a reduction in markers of bone formation (DiVasta, Feldman, Quach, Balestrino, & Gordon, 2009). Exercise programs for patients with AN have not been studied. Excessive exercise, commonly used by patients with AN to control weight, could interfere with weight gain and produce amenorrhea. Therefore, any exercise should be undertaken cautiously.

Hormone replacement therapy is frequently prescribed to treat reduced BMD in adolescents with AN (Robinson, Bachrach, & Katzman, 2000) on the assumption that estrogen deficiency contributes to the bone loss. There is no evidence that oral contraceptives increase BMD in either adult (Klibanski, Biller, Schoenfeld, Herzog, & Saxe, 1995) or adolescent (Golden et al., 2002; Strokosch, Friedman, Wu, Kamin, 2006) females with AN, and oral contraceptives should not be prescribed for this purpose. Furthermore, oral contraceptives cause exogenously induced monthly menstrual bleeding even at a low weight, which may incorrectly be interpreted as indicative of adequate weight restoration. Studies investigating the use of IGF-l (Grinspoon et al., 1996; Grinspoon, Thomas, Miller, Herzog, & Klibanski, 2002), DHEA (Gordon et al., 1999; Gordon, Grace, et al., 2002), and the bisphosphonates (Golden et al., 2005; Miller et al., 2004, 2011) have proved disappointing.

Current treatment recommendations focus on weight restoration with resumption of spontaneous menses, calcium supplementation (p. 312) (1,000–1200 mg elemental calcium /day), vitamin D supplementation (600 IU/day), and carefully monitored weight-bearing exercise (Golden, 2010).

Treatment to Goal Weight for Adolescents with Anorexia Nervosa

Treatment goal weight should be individualized, taking into account pubertal stage, prior growth percentiles, height, and age. For adolescents, the treatment goal weight is a “moving target,” and normal growth and development necessitates a recalculation of this number every 3 to 6 months. Height and weight tables used for adults are inappropriate for adolescents. The Centers for Disease Control and Prevention growth charts (available at cdc.gov/growthcharts) provide a useful resource of normative height and weight data for children and adolescents in the United States; however, the tables provide only normative weight and BMI data, not specific guidance for what is an “ideal body weight.” Absolute BMI values should not be used in children and adolescents. For example, a BMI of 17.5 would be on the third percentile for a 19-year-old but on the 50th percentile for an 11-year-old.

Treatment goal weight should be the weight at which normal physical and sexual development occurs, and for girls, the weight at which menstruation and ovulation are restored. In postmenarcheal adolescent girls, 86% of patients resumed menses within 6 months of achieving a weight at or above 90% of median weight for age and height (Golden et al, 1997). However, there was wide variability, with some subjects resuming menses at a lower weight and others doing so at a higher weight. When using the CDC growth charts to calculate expected body weight (expected body weight in kilograms = median BMI times height in meters squared), 90% of median weight for age and height corresponds to a weight approximately 95% of expected body weight (Golden, Yang, Jacobson, Robinson, & Shaw, 2012). For those who were previously overweight, treatment goal weight may need to be higher. In a premenarcheal girl or an adolescent boy whose growth and development are not yet complete, treatment goal weight should be 100% of expected body weight in order to maximize growth potential. It is preferable to provide a weight range for treatment goal weight, with a clear message that this range will change with growth and development. This is done in order to avoid focusing on a single weight and to acknowledge that there are daily fluctuations in weight as well as expectations that both height and weight will change as puberty progresses.

Once an individualized treatment goal weight range is reached, serial estradiol levels or pelvic ultrasonography can be used to assess restoration of normal hypothalamic–pituitary–ovarian function and readiness for spontaneous resumption of menses. A serum estradiol level above 30 pg/mL is predictive of resumption of menses within 3 to 6 months (relative risk 4.6, confidence interval 1.9–11.2) (Golden et al., 1997). One clinical approach is to aim for weight maintenance in the treatment goal weight range for 3 months. If after 3 months the patient remains amenorrheic, a serum estradiol level can be measured. If the level is above 30 pg/mL, the patient can wait a further 3 months at that weight in anticipation of resumption of menses. An estradiol level below 30 pg/mL indicates that the treatment goal weight needs to be higher and the patient needs to gain further weight. Another approach is to use serial pelvic ultrasound scans to assess ovarian and uterine maturity to provide an individualized weight when reproductive maturity has been achieved or restored (Allan et al., 2010; Key, Mason, Allan, & Lask, 2001; Lai, De Bruyn, Lask, Bryant-Waugh, & Hankins, 1994; Sobanski, Hiltmann, Blanz, Klein, & Schmidt, 1997; Treasure, Wheeler, King, Gordon, & Russell, 1988).

Summary

Most of the medical consequences of eating disorders are secondary to malnutrition and/or purging and are reversible with nutritional rehabilitation and interruption of binge/purge activity (Table 13.2 provides a summary). Heart (p. 313) rate returns to normal after approximately 12 days, vital sign instability resolves after approximately 2 to 3 weeks, and resting energy expenditure increases slowly and normalizes after approximately 6 weeks (Schebendach et al., 1997; Shamim et al., 2003). The amount of time needed for weight gain varies, and resumption of menses usually occurs within 3 to 6 months after achieving treatment goal weight. Difficulties with body image distortion and preoccupation with weight and shape, however, may take longer to resolve. While most of the medical complications are reversible with weight restoration, growth retardation, reduced BMD, and, possibly, structural brain changes may not be entirely reversible. (p. 314)