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Defining Eating Disorders 

Defining Eating Disorders
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Defining Eating Disorders
DOI:
10.1093/9780195173642.003.0014
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date: 16 August 2018

The wide range of human food preferences and of human practices surrounding food preparation and consumption makes the definition of an eating disorder challenging. This challenge is amplified by the fact that dramatic changes occur in energy requirements during adolescence for supporting normal growth and development. For example, between ages 9 and 19, the estimated caloric requirements for girls increases by almost 50% and those for boys, by 80% (Committee on Dietary Reference Intakes, 2002). In addition, dieting related to self-perceived weight status is now extremely common among adolescents (Strauss, 1999). These and other factors provide a fertile environment for the development of disordered eating, yet researchers have paid surprisingly little attention to the task of defining an eating disorder.

The most widely used definitions of eating disorders are those provided by the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM-IV, 2000). Only two distinct syndromes, anorexia nervosa and bulimia nervosa, are described in DSM-IV. A residual category, eating disorder not otherwise specified (EDNOS), is provided for all other disorders of eating. A prominent example within the EDNOS category is binge eating disorder, and tentative criteria for binge eating disorder are presented in an appendix in DSM-IV. As is described in more detail below, it appears that most adolescents and adults who present for treatment of an eating disorder do not meet full criteria for either of the two formally defined syndromes and are therefore classified as having an EDNOS. Precisely how to characterize and subdivide this large heterogeneous group is a significant problem for the field. It should also be noted that the state of being overweight or obese is not considered an eating disorder. The presence of excess body fat is viewed in the DSM-IV system as a general medical problem, not a mental disorder. The relationship between obesity and eating disorders, especially binge eating disorder, is a topic of considerable interest.

Although most eating disorders begin in adolescence, surprisingly little research has focused on this age range. The ability to make firm treatment recommendations for adolescent patients is thus severely limited. In the chapters that follow, our current knowledge of the definition, treatment, and prevention of eating disorders will be reviewed. Chapter 13 includes the etiology of eating disorders; the diagnostic criteria for anorexia nervosa and bulimia nervosa and assessment of how well these 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 anorexia nervosa and bulimia nervosa. Chapter 14 describes psychological and pharmacological treatments for adolescents with eating disorders, and studies of relapse prevention in which psychological or pharmacological interventions are used. Chapter 15 addresses the risk factors for the development of anorexia nervosa and bulimia nervosa, the relationship between treatment of obesity and the development of eating disorders, and prevention. Chapter 16 suggests promising directions for future study in this field.

ETIOLOGY OF EATING DISORDERS

A variety of biological, environmental, and psychosocial factors are associated with the development of an eating disorder, thus such factors may play a causative role in their evolution. However, as is discussed in greater detail in Chapter 15, there is no conclusive evidence that any characteristic or event is specifically associated with the development of anorexia nervosa or bulimia nervosa.

Both of these disorders affect primarily women and usually begin around the time of or soon after puberty, thus developmental factors may play a crucial role in the onset of eating disorders. It is not clear, however, whether biological changes that accompany adolescence, psychological changes, or an interaction between the two types of phenomena account for the occurrence of eating disorders. Social factors may also influence the development of eating disorders among adolescents, as adolescents may model overconcern with body shape and weight, dieting, or binge eating behavior observed among peers. This behavior suggests that contagion may play a role in the development of eating disturbances, although this phenomenon has received little study.

Because these disorders are described primarily in developed countries, Western influence may play an important role, but precisely how cultural factors interact with other phenomena in the development of these disorders is not well understood. Evidence for the impact of Western culture, specifically the influence of mass media, was found in a naturalistic study of adolescents in Fiji, where increased rates of body image and eating disturbances were observed following the introduction of Western media (Becker, Burwell, Gilman, Herzog, & Hamburg, 2002). An experimental study found that exposure to images of the cultural thin-ideal, such as those in fashion magazines, were associated with an increase in negative affect among vulnerable adolescents who reported increased perceived pressure to be thin and body dissatisfaction (Stice, Spangler, & Agras, 2001).

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 development of the eating disorder. There is growing evidence that genetic influences contribute to an individual's vulnerability to develop an eating disorder, but genes specifically linked to the development of anorexia nervosa or bulimia nervosa have not been identified, and it is uncertain how genetic influences may operate to influence the risk of a disorder. In short, despite extensive information about the clinical characteristics of eating disorders and much discussion of potential causes, solid knowledge of the etiology of eating disorders is elusive.

In addition, it is likely that different factors contribute to the onset and maintenance of eating disorders. If risk and maintenance factors are distinct, then prevention efforts and treatment interventions likely need to be aimed at somewhat different targets and, potentially, at different populations. However, there is currently insufficient evidence to differentiate with confidence those factors that increase the risk of developing an eating disorder from those that perpetuate the 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 EATING DISORDERS

Diagnostic Criteria for Anorexia Nervosa

The most widely used diagnostic criteria for anorexia nervosa are those of the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders (DSM-IV, 1994a). The DSM-IV diagnostic system is based on a practical foundation and aims to (1) facilitate meaningful communication among clinicians, (2) aid replication of research findings, (3) gauge treatment efficacy by means of carefully defined criteria, and (4) foster further elucidation of the disorder under investigation. The specific DSM-IV criteria for anorexia nervosa are listed in Table 13.1. None of the criteria in the DSM-IV diagnosis of anorexia nervosa is perfect, and further refinement of the criteria is needed. The World Health Organization's 10th Revision of the International Classification of Diseases and Related Health Problems (ICD-10, 1990) also provides diagnostic criteria similar to those of the DSM-IV for eating disorders. However, there are sufficient differences between the two criteria sets that the populations defined are not identical. In this section we will focus on the DSM-IV criteria, as they are widely employed in the research literature. The first criterion deals with weight loss and would seem to be noncontroversial; however, there is no consensus on how weight loss should be calculated, especially during adolescence. Some investigators emphasize the amount lost from an original baseline, and others emphasize weight loss below a normal weight for age and height. The term refusal in the first criterion is also problematic, because it implies a voluntary decision not to eat. In anorexia nervosa, dieting behavior often has an obsessive quality and is difficult for patients to control, thus inability might be more accurate than refusal.

Table 13.1 DSM-IV Diagnostic Criteria for Anorexia Nervosa

  • A. Refusal to maintain body weight at or above a minimally normal weight for age and height (e.g., weight loss leading to maintenance of body weight less than 85% of that expected; or failure to make expected weight gain during period of growth, leading to body weight less than 85% of the expected)

  • B. Intense fear of gaining weight or becoming fat, even though underweight

  • C. Disturbance in the way in which one's body weight or shape is experienced, undue influence of body weight or shape on self-evaluation, or denial of the seriousness of the current low body weight

  • D. In postmenarcheal females, amenorrhea, i.e., absence of at least three consecutive menstrual cycles (A woman is considered to have amenorrhea if her periods occur only following hormone, e.g., estrogen, administration.)

Specify Type

Restricting type During the current episode of anorexia nervosa, the person has not regularly engaged in binge-eating or purging behavior (i.e., self-induced vomiting or the misuse of laxatives, diuretics, or enemas).

Binge eating/purging type During the current episode of anorexia nervosa, the person has regularly engaged in binge-eating or purging behavior (i.e., self-induced vomiting or the misuse of laxatives, diuretics, or enemas).

Source: Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision, Copyright 2000. American Psychiatric Association.

Many individuals with anorexia nervosa acknowledge the core phenomenon described in Criterion B, an intense fear of gaining weight or becoming fat. However, younger individuals and individuals who are not motivated for treatment sometimes deny that they fear gaining weight, despite engaging in behaviors that strongly suggest an intense fear of fatness. It is possible that this criterion might be better worded to capture the characteristic behaviors rather than focusing on a psychological parameter. Criterion C is complex, as it describes three rather distinct phenomena in an attempt to define the core psychological features of anorexia nervosa. The disturbance in the experience of body weight or shape is observable from statements of feeling fat or of perceiving specific parts of the body as being too large, even when the person is emaciated. Individuals with anorexia nervosa are remarkably successful at remaining underweight, thereby deriving a feeling of accomplishment by evaluating themselves in terms of their thinness. An admission of the seriousness of low body weight would imply an acknowledgment of the necessity of changing behavior and gaining weight, which are overwhelming and terrifying notions.

The final criterion for the diagnosis of anorexia nervosa, amenorrhea, remains controversial. The physiological implications of the amenorrhea are not entirely clear; some investigators have suggested that its presence might be indicative of a primary disturbance of hypothalamic function (Pirke, Fichter, Lund, & Doerr, 1979; Russell, 1969), whereas others maintain that amenorrhea is merely a reflection of dieting and weight loss (Katz, Boyar, Roffwang, Hellman, & Weiner, 1978). Several reports have suggested that the characteristics of individuals who meet all diagnostic criteria for anorexia nervosa except amenorrhea do not differ from those of individuals who meet all the criteria (Cachelin & Maher, 1998; Garfinkel et al., 1996). These observations, in addition to the occasional difficulty of obtaining an accurate history of menstrual patterns from patients, suggest that amenorrhea may be a less useful criterion for anorexia nervosa.

The DSM-IV suggests that individuals with anorexia nervosa 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). These subtypes were included in the DSM-IV criteria for anorexia nervosa because of data indicating that in comparison with AN-R patients, AN-B/P patients have a higher frequency of impulsive behaviors such as suicide attempts, self-mutilation, stealing, and alcohol and substance abuse (Casper, Eckert, Halmi, Goldberg, & Davis, 1980; Garfinkel, Moldofsky, & Garner, 1980). In addition, the binge eating and purging behaviors of individuals with AN-B/P predispose these individuals to medical problems less frequently associated with AN-R (Halmi, 2002).

Comparison of Anorexia Nervosa in Adolescents and Adults

The DSM-IV system of classification does not suggest that a different set of criteria be employed for adolescents with anorexia nervosa. It is of interest to note that the third edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-III; American Psychiatric Association, 1980) placed the anorexia nervosa criteria in the section on child and adolescent disorders, which reflects the fact that most cases of anorexia nervosa have their onset during adolescent years. Several studies provide information on whether there are substantial differences in the clinical characteristics of adolescent and older individuals with anorexia nervosa.

Halmi, Caspar, Eckert, Goldberg, and Davis (1979) examined correlations between a variety of clinical characteristics and age of onset of anorexia nervosa. Younger patients were hospitalized somewhat sooner than older patients after the onset of their illness, and older age of onset was associated with a greater weight loss from normal. Most of the typical anorectic behaviors and attitudes occurred with a greater frequency in patients with a younger age of onset. In general, however, there were very few significant age-related correlations. Heebink, Sunday, and Halmi (1995) compared clinical characteristics of four age groups of female inpatients on an eating disorders unit: early adolescence (ages 12 through 13), middle adolescence (ages 14, 15, and 16), late adolescence (ages 17, 18, and 19), and adult (age 20 and older). Few psychological differences were observed between the adults and the adolescents. Onset of anorexia nervosa before age 14 and primary amenorrhea were associated with the greatest maturity fears. Among AN-R patients, adolescents aged 17 through 19 had the highest drive for thinness, and the lowest levels of depression and anxiety were seen in patients younger than age 14. These data suggest that eating disorder symptomatology is fairly consistent in presentation over the life cycle.

Fisher, Schneider, Burns, Symons, and Mandel (2001) compared patients between the ages of 9 and 19 years with patients aged 20 to 46. On most variables, there were no significant differences between the adolescents and adults. The adults were more likely to have a history of binge eating, laxative abuse, diuretic and ipecac use, and prior use of psychiatric medications. The adolescents were more likely than adults to have a diagnosis of EDNOS, and the adolescents had a lower global severity score, greater denial, and less desire for help. Although the study showed some age-related differences between adolescents and adults, changes to the DSM-IV diagnostic criteria for the adolescent population were not recommended.

Additionally, in a study comparing the general psychopathology of early-onset anorexia nervosa to that defined as classic adolescent-onset anorexia nervosa (Cooper, Watkins, Bryant-Waugh, & Lask, 2002), the specific eating disorder psychopathology and general psychopathology in the early onset anorexia nervosa group were very similar to those of the late-onset anorexia nervosa sample. Thus, there is little evidence to suggest that the core clinical characteristics of adolescents with anorexia nervosa differ substantially from those of adults, and it does not appear necessary to modify the diagnostic criteria for anorexia nervosa for use with adolescents.

Diagnostic Criteria for Bulimia Nervosa

The DSM-IV diagnostic criteria for bulimia nervosa are listed in Table 13.2. As with anorexia nervosa, the diagnostic criteria for bulimia nervosa are at times difficult to interpret. Criterion A, which provides a definition of a binge eating episode, addresses amount (“larger than most people would eat”), duration (“in a discrete period of time”), and psychological state (“a sense of a lack of control”). The relative importance of these elements and the definitions offered are open to interpretation. For example, many patients with bulimia nervosa state that they are binge eating when they eat amounts of food that are not larger than what most people eat and believe that the sense of loss of control is more important than the amount ingested.

Table 13.2 DSM-IV Diagnostic Criteria for Bulimia Nervosa

  • A. Recurrent episodes of binge eating. An episode of binge eating is characterized by both of the following:

    • i. Eating, in a discrete period of time (e.g., within any 2-hour period), an amount of food that is definitely larger than most people would eat during a similar period of time and under similar circumstances

    • ii. A sense of lack of control over eating during the episode (e.g., a feeling that one cannot stop eating or control what or how much one is eating)

  • B. Recurrent inappropriate compensatory behavior in order to prevent weight gain, such as self-induced vomiting; misuse of laxatives, diuretics, enemas, or other medications; fasting; or excessive exercise

  • C. Binge eating and inappropriate compensatory behaviors both occur on average at least twice a week for 3 months.

  • D. Self-evaluation is unduly influenced by body shape and weight.

  • E. The disturbance does not occur exclusively during episodes of anorexia nervosa.

Source: Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision, Copyright 2000. American Psychiatric Association.

Criterion B, which describes recurrent and inappropriate behaviors, includes some behaviors that are easily characterized (self-induced vomiting) and others that are open to interpretation (for example, what is “misuse” of laxatives and diuretics?). Particularly problematic is the question of what constitutes excessive exercise.

Criterion C requires that the binge eating and inappropriate compensatory behaviors occur on average at least twice a week for 3 months, but studies suggest that individuals with somewhat lower reported frequencies of binge eating closely resemble individuals who meet Criterion C. Criterion D, that self-evaluation is unduly influenced by body shape and weight, is part of the anorexia nervosa criteria as well, and attempts to capture an important psychopathological variable. But the line between “undue influence” and normative overconcern with body shape and weight among female adolescents is uncertain.

Evaluation of DSM-IV Classification for Adolescents with Eating Disorders

One indicator of the utility of the diagnostic criteria for eating disorders is the degree to which they capture the signs and symptoms reported by patients who present for assessment because of distress about their symptoms or because of medical, psychological, or social impairment resulting from these problems. Most patients treated in clinical settings do not meet full criteria for either anorexia nervosa or bulimia nervosa but instead must be grouped into the EDNOS category, which includes some specific examples of eating patterns that do not meet the full criteria for anorexia nervosa or bulimia nervosa but which remains for the most part poorly characterized.

For example, in data collected as part of an eating disorder database system involving five clinical centers (Neuropsychiatric Research Institute/University of North Dakota; University of South Florida; University of Toledo; Ohio State University; University of Chicago) and including a total of 704 patients, the percentage of subjects meeting full criteria for bulimia nervosa ranged from 12% to 20% and for subjects meeting full criteria for anorexia nervosa from 3% to 17%. The percentage of those diagnosed with EDNOS ranged from 49% to 71%. Of the adolescent patients in this database (N = 163), 86 (53%) received a diagnosis of EDNOS. This finding is reflected in other literature as well. Fisher and colleagues (2001) compared adolescents and young adults at presentation to an eating disorder program, and found that the likelihood of EDNOS was high in both populations but was highest among the adolescents. Others have discussed the high rate of EDNOS in adolescents and the inadequacy of the DSM criteria as well (Brewerton, 2002; Dancyger & Garfinkel, 1995; Eliot & Baker, 2001; Engelsen, 1999; Fisher et al., 1995; Muscari, 2002; Nicholls, Chater, & Lask, 2000).

Factors that appear to be risk factors for the later development of eating disorders, which are discussed in detail in Chapter 15, are common among adolescent girls, and some are so common as to be considered normative. A question relevant to both devising prevention efforts and considering the most appropriate diagnostic criteria is where to draw the line, to decide that a clinically significant eating problem has developed. Are cognitive concerns sufficient, are early behavioral symptoms necessary, or does a well-established pattern of such behaviors need to emerge? Prior research has shown that the altering of severity criteria would result in substantial changes in base rates of bulimia nervosa (Thaw, Williamson, & Martin, 2001).

Alternatives to DSM-IV Classification

As described above, the DSM-IV system fails to provide useful categories for a substantial number of individuals with significant eating disorder symptoms. A possible alternative to the DSM-IV categories for an adolescent population is provided by the Diagnostic and Statistical Manual for Primary Care (DSM-PC), Child and Adolescent Version (Wolraich, Felice, & Drotar, 1996), developed by the American Academy of Pediatrics. This manual provides a broader classification scheme and includes a hierarchy of clinical presentations that do not reach full DSM-IV diagnostic criteria but that nonetheless deserve clinical attention. “Variations” represent minor dysfunctional symptoms related to eating or body image and “problems” reflect more serious disturbances. The utility of this system has received little empirical examination. The clinical characteristics of individuals in these categories are unknown, as is the prevalence of these characteristics. In addition, it is not known how often or whether DSM-PC variations or problems advance to become DSM-IV full syndromes. Nonetheless, this system provides a potentially useful method for defining a wide range of important eating problems among adolescents.

In an attempt to describe the wide range of eating problems seen among children, the Great Ormond Street criteria were developed (Lask & Bryant-Waugh, 2000). These criteria include determined weight loss, abnormal cognitions about body weight and shape, and morbid preoccupation with body weight and shape for the diagnosis of anorexia nervosa. The bulimia nervosa criteria include recurrent binges and purges, a sense of lack of control, and morbid preoccupation with shape and weight. A unique feature of these criteria is the inclusion of specific criteria for additional disorders, such as food avoidance emotional disorder, selective eating, functional dysphagia, and pervasive refusal syndrome. The utility of the Great Ormond Street criteria is just beginning to be explored empirically.

Summary

The DSM-IV criteria for anorexia nervosa and bulimia nervosa are widely used and are useful in recognizing and describing both adolescents and adults with severe disturbances of eating behavior. However, it is not completely clear how several of the criteria for both anorexia nervosa and bulimia nervosa should be interpreted. The criterion requiring amenorrhea for the diagnosis of anorexia nervosa is particularly problematic and may need to be eliminated. The available literature strongly suggests that the criteria sets provided by DSM-IV fail to describe many adolescents and adults with clinically significant eating problems. Indeed, EDNOS is the most common diagnosis assigned in eating disorder programs. Thus, the DSM-IV criteria may need to be broadened, and other categories for less severely affected individuals may need to be added.

DEMOGRAPHICS AND PREVALENCE OF EATING DISORDERS

Despite exponential growth in eating disorders research the past few decades (Theander, 2002), epidemiological research has lagged behind research in other areas, such as studies of the clinical presentation of eating disorders and research on treatment interventions. Although the symptoms of eating disorders are known to originate primarily during adolescence, epidemiological studies have focused principally on adult populations. Consequently, data on the prevalence and distribution of anorexia nervosa and bulimia nervosa among adolescents are quite limited.

Even among adults, knowledge about the number of individuals having an eating dis order or about particular vulnerability to developing anorexia nervosa, bulimia nervosa, or their variants (for review, see Striegel-Moore & Cachelin, 2001) is limited. For example, only one study in the United States, conducted about 25 years ago, has provided prevalence data for eating disorders based on a nationally representative sample (Robins & Regier, 1991). Rates of bulimia nervosa were not documented, as this disorder had not yet been introduced into the psychiatric nomenclature.

Experts have concluded that eating disorders occur in approximately 1% (anorexia nervosa) to 3% (bulimia nervosa) of women, and prevalence rates among men are approximately one tenth of those observed in women (for review, see Hoek, 2002). Large samples are needed to describe even the most easily identified epidemiological parameters such as gender or ethnicity, and as the review by Hoek, van Hoeken, and Katzman (2003) illustrates, even in samples exceeding 1,000 girls, some studies have not identified a single girl with past or current anorexia nervosa (e.g., Johnson-Sabine, Wood, Patton, Mann, & Wakeling, 1988). Because of the rather preliminary stage of epidemiological research among adolescent samples, studies based on relatively small or select samples or only on self-report are not reviewed in this chapter.

Fifteen recent studies (summarized in Tables 13.3 and 13.4) have provided interview-based information about the prevalence of anorexia nervosa and bulimia nervosa as defined by DSM-III (1980) and DSM-IV criteria. In some instances, the prevalence of partial syndrome eating disorders in community-based samples was also determined. Some studies recruited not only adolescents but also younger children or adults; these studies are also reviewed (e.g., Newman et al., 1996).

Table 13.3 Two-stage Studies of Prevalence of Anorexia Nervosa and Bulimia Nervosa in Community Samples of Adolescents

Subjects

Methods

Prevalence Rates (%)d

AN

BN

Study

Country

(city or state)

Samplea

Age (years)

Sample Size (response rate in %)

Screeningb Interview (response rate in %)

Diagnostic Criteriac

Point

Lifetime

Point

Lifetime

Whitaker et al., 1990

United States (county in New Jersey)

1

13–18

F 2544

M 2564

(91)

EAT-40 Interview

(75)

DSM-III

F

M

0.3

0

F

M

2.5

0.2

Rathner & Messner, 1993

Italy (Brixen)

2

11–20

F 517

M 0

(81)

EAT, ANIS Interview

(88)

DSM-III-R

F

0.58

F

0

Wlodarczyk-Bisaga & Dolan, 1996

Poland

(Warsaw)

2

14–16

F 747

M 0

(93)

EAT-26 Interview

(92)

DSM-III-R

F

0

F

0

Graber et al., 2003

United States

New York City

3

Mean:16

F 155

M 0

EAT

SCID

DSM-III-R

F

3.9

F

3.2

Szabo & Tury, 1991

Hungary (Debrecen)

2

14–18

F 416

M 119

(49)

EAT-40, BCDS, ANIS Interview

DSM-III-R

F—

M—

F

M

0

0

Steinhausen et al., 1997

Switzerland (Zurich Canton)

2

14–17

F 276

M 307

EDE-S

DISC-P

DSM-III-R

F

M

0.7

0

F

M

0.05

0

Verhulst et al., 1997

Netherlands

4

13–18

F/M 853

(82)

CBCL DISC-C/-P

(91)

DSM-III-R

F/M

0.3

F/M

0.3

Santonastaso et al., 1996

Italy (Padova)

2

16

F 359

M 0

(91)

EAT-40, BMI Interview

(93)

DSM-IV

F

0

0

F

0.5

1.0

Rosenvinge et al., 1999

Norway

(Buskerud)

2

15

F 464

M 214

(78)

EDI

DSED

DSM-IV

F

M

0.4

0

F

M

1.1

0

a 1 = entire enrollment of grades 9 through 12 in a single New Jersey county, including public, private and parochial schools; 2 = public school students; 3 = private school students; 4 = national probability sample.

b ANIS, Anorexia Nervosa Inventory Scale; BCDS, Bulimic Cognitive Distortions Scale; BMI, Body Mass Index; CBCL, Children's Behavior Check List; DISC, Diagnostic Interview Schedule for Children (DISC-P, parent version, DISC-C, child version); DSED, Diagnostic Survey for Eating Disorders; EAT, Eating Attitudes Test; EDE-S, Eating Disorder Examination, screening version; EDI, Eating Disorder Inventory; SCID, Structured Clinical Interview for DSM-IIIR.

c DSM, Diagnostic and Statistical Manual for Mental Disorders (DSM III, 3rd edition; DSM III-R, 3rd, revised edition; DSM IV, 4th edition).

d AN, anorexia nervosa; BN, bulimia nervosa; F, female; M, male; Point, point prevalence, based on 6 months (Verhulst et al., 1997), 12 months (Steinhausen et al., 1997), or “current” (i.e., at the time of the interview; Rathner & Messner, 1993; Rosenvinge et al., 1999; Santonastaso et al., 1996; Szabo & Tury, 1991; Wlodarczyk-Bisaga & Dolan 1996).

Table 13.4 Interview-based Studies of Prevalence of Anorexia Nervosa and Bulimia Nervosa in Community Samples of Adolescents

Subjects

Methods

Prevalence Rates (%)c

AN

BN

Study

Country

(city or state)

Sampleb

Age (years)

Sample Size (response rate in %)

Interviewc

Diagnostic Criteriad

Point

Lifetime

Point

Lifetime

Lewinsohn et al., 1993

United States

(Oregon)

1

15–18

F 797(61)

M 711

K-SADS

DSM-III-R

F 0

M 0

0.74

0

F 0.49

M 0

1.6

0.14

Newman et al., 1996

New Zealand

(Dunedin)

2

21

F 469(84)

M 492

DIS

DSM-III-R

F 0.9

M 0.0

F 1.5

M 0.4

Wittchen et al., 1998

Germany

(Munich)

3

14–24

F 1488(71)

M 1533

M-CIDI

DSM-IV

F 0.3

M 0

1.0

0.1

F 0.7

M 0

1.7

0

Johnson, Cohen, Kasen, et al., 2002a

United States

(New York)

4

9–23

F 366

M 351

DISC-I

DSM-IV

F 0

M 0.28

F 4.0

M 0.28

McKnight Investigators, 2003

United States (Arizona, California)

1

11–14

F 1103

M 0

MEDE

DSM-IV

F 0

F0.37

Emerson, 2003

Great Britain

5

5–15

F/M 10,438

DAWBA

DSM-IV

F/M 0.1–0.4

(current eating

disorder)

a Rates reported reflect the number of respondents who either at early adolescence (9 to 19 years) or mid-adolescence (11 to 23 years) assessment met criteria.

b 1 = school students; 2 = entire birth cohort 4/72–3/73; 3 = city residents; 4 = representative sample of two counties; 5 = national sample.

c DAWBA, Development and Well-Being Assessment; DIS, Diagnostic Interview Schedule; DISC-I, Diagnostic Interview Schedule for Children; K-SADS, Kiddie Schedule for Affective Disorders and Schizophrenia; M-CICI, Munich-Composite International Diagnostic Interview; MEDE, McKnight Eating Disorder Examination.

d DSM, Diagnostic and Statistical Manual for Mental Disorders (DSM III-R, 3rd, revised edition; DSM IV, 4th edition).

e AN, anorexia nervosa; BN, bulimia nervosa; F, female; M, male; point, point prevalence, based on 3 months (McKnight Investigators, 2003), 12 months (Johnson, Cohen, Kasen, et al., 2002a; Lewinsohn et al., 1993; Newman et al., 1996; Wittchen et al., 1998), or “current” (i.e., at the time of the interview; Emerson, 2003).

Prevalence Studies of Anorexia Nervosa and Bulimia Nervosa: Methodological Considerations

Ideally, epidemiological studies recruit adequately large, representative population samples and provide detailed information about the sampling frame, recruitment procedures, and participation rates. Because eating disorders are fairly uncommon in adults (Hoek, 2002), sample sizes of several thousand (for studies focused on girls) to tens of thousands of participants (for studies focusing also on eating disorders in boys) are needed for stable estimates of eating disorders. Most studies reviewed in this chapter had fewer than 1,000 participants and only one study had over 10,000. Regrettably, the latter did not report detailed information about eating disorder cases, leaving unknown the specific disorders found (anorexia nervosa or bulimia nervosa) or the gender of those affected by an eating disorder (Emerson, 2003).

Most studies were conducted in European countries (ranging from Norway to Italy) and included populations representing Western industrialized nations. Five studies were conducted in the United States (Graber, Tyrka, & Brooks-Gunn, 2003; Johnson, Cohen, Kasen, & Brook, 2002; Lewinsohn, Hops, Roberts, Seeley, & Andrews, 1993; McKnight Investigators, 2003; Whitaker et al., 1990) and one was done in New Zealand (Newman et al., 1996). A considerable variety of sampling frames was used (ranging from the recruitment of girls at a single school, to the use of sophisticated stratification schemes, to the recruitment of an entire birth cohort in a particular county). Only two studies recruited national probability samples of children in a particular age range (Emerson, 2003: Great Britain; Verhulst, van der Ende, Ferdinand, & Kasius, 1997: the Netherlands). Unfortunately, although they included both girls and boys, neither study reported gender-specific eating disorder rates. None of the studies examined ethnic differences in the prevalence of eating disorders.

In nine studies (summarized in Table 13.3) a two-stage case-finding approach was used: a questionnaire was given to the entire sample and was followed by a diagnostic interview of those individuals whose responses to the initial screening suggested the presence of an eating disorder. In some studies, a random subset of those participants who screened negatively for an eating disorder were also interviewed. The two-stage screening approach permits a relatively cost-effective assessment of large samples through use of an inexpensive survey method first, reserving the expensive interview method for those participants whose self-report responses suggest the presence of an eating disorder. The quality of the two-stage method depends in part on the participation rates at each assessment. For example, some data suggest that screening efforts may miss eating disorder cases and thus underestimate the prevalence of eating disorders (Fairburn & Beglin, 1990). The sensitivity of the screening instrument is also important: in an uncommon disorder, the omission of even a few cases because of an insensitive screen produces underestimates of the true prevalence of the disorder.

In six studies (summarized in Table 13.4), there was no initial screening; rather, the entire sample participated in a diagnostic interview. In general, eating disorder status was assessed in the context of a comprehensive evaluation of psychiatric disorders, rather than in an interview focused specifically on eating disorders. This approach can be advantageous—because participants are not recruited specifically for a study of eating disorders, participation rates are likely unaffected by the participants' attitudes about eating disorders (e.g., wanting to avoid detection of one's eating disorder). There are also limitations to using a one-step assessment design. These studies generally have lower participation rates than those of two-stage studies, possibly because of a greater subject burden from the requirement that all participants complete the diagnostic interview. Also, in an effort to reduce assessment time and subject burden, interviewers usually employ a branched approach to diagnostic assessment: “gated” questions about the key symptom(s) are required for a diagnosis; if these are answered negatively, any further assessment of symptoms is terminated (Feehan, McGee, Raja, & Williams, 1994). Hence, unless the participant acknowledges the initial question (e.g., voluntary efforts to achieve low weight in the case of anorexia nervosa, and recurrent binge eating in the case of bulimia nervosa), no further information is gathered about eating disorder symptoms. It is unclear whether the clinical presentation of eating disorders in children is less prototypic than that in adults. If it is, then a higher number of cases among children would be missed using a one-step approach.

The prevalence rate is the actual number of cases in a population at a certain point in time. Some studies only report either point prevalence rates or “lifetime” rates, and a few studies report both point-prevalence and lifetime rates. Point prevalence is reported over various time frames, ranging from the present (or the time of interview) to within the last 12 months. Lifetime prevalence can be a problematic term, given that participants may have not yet reached the age of maximum risk for developing an eating disorder. In the studies reviewed in this chapter, lifetime prevalence connotes the number of individuals who ever met criteria for anorexia nervosa or bulimia nervosa. Retrospective reports of age of onset from adult samples suggest that full-syndrome status is not reached until mid-to late adolescence (16–18 years) or even young adulthood (18–21 years). In adult community samples, the mean age of onset of anorexia nervosa ranges from 16 to 19 years (Fairburn, Cooper, Doll, & Welch, 1999; Garfinkel et al., 1996; Walters & Kendler, 1995) and that of bulimia nervosa ranges from 18 to 20 years (Garfinkel et al., 1995; Kendler et al., 1991). Few eating disorders begin before age 10 or after age 25, and the rate of new cases climbs steadily in between those ages (Bushnell, Wells, Hornblow, Oakley-Browne, & Joyce, 1990; Lewinsohn, Striegel-Moore, & Seeley, 2000). Hence, “lifetime” prevalence, especially in young samples, should be adjusted to reflect these age-related patterns.

Prevalence Studies of Anorexia Nervosa and Bulimia Nervosa: Major Findings

Full-Syndrome Anorexia Nervosa

Full-syndrome current anorexia nervosa is not uncommon among adolescent girls, with rates ranging from 0% to 0.9%, depending on the study. Epidemiologically, it is undetectable among boys. It is difficult to discern a clear trend in prevalence rates for girls because of the considerable variations in methodology used across studies. Those studies in which no girls were identified with a diagnosis of current anorexia nervosa included relatively young samples (ages 11 to 16 years; McKnight Investigators, 2003; Santonastaso, Zanetti, Sala, & Favaretto, 1996; Wlodarczyk-Bisaga & Dolan, 1996). Rathner and Messner (1993) initially observed a 0.39% rate for anorexia nervosa, but found additional cases for a total rate of 0.58%, and reported that none of the current cases identified in their Italian sample were under age 15 years. In a randomly selected population sample of 15-year-old girls in Southern Norway, by contrast, about 4 in 100 current anorexia nervosa cases were found (Rosenvinge, Borgen, & Boerresen, 1999). An earlier study from the Mayo Clinic had a prevalence rate of 0.48% among 15-to 19-year-old girls, a rate higher than that for any other age group (Lucas, Beard, O'Fallon, & Kurland, 1991).

In a large study of 14-to 24-year-old Germans, Wittchen, Nelson, and Lanchner (1998) oversampled 14-and 15-year-olds, which may explain why only 0.3% of current anorexia nervosa cases were identified among the female participants, despite the wider age range of the study sample. A relatively large number of girls with current anorexia nervosa (0.7%) was observed in a Zurich Canton sample of 14-to 17-year-olds. In this study, confirmatory interviews were conducted with a parent, rather than with the child, as in most other studies (Steinhausen, Winkler, & Meier, 1997). Denial is a hallmark of anorexia nervosa, and future studies are needed to determine whether parental reports result in better detection of anorexia nervosa than that from child self-report only. Finally, the highest point prevalence rate (past 12 months), 0.9%, was reported in a New Zealand study (Newman et al., 1996) and was based on diagnostic interviews when the girls were 21 years old. This well-controlled, longitudinal study of an entire birth cohort of children born between April 1972 and March 1973 had previously reported prevalence rates for major mental disorders, but not eating disorders, based on assessments at ages 11 years (Anderson, Williams, McGee, & Silva, 1987), 13 years (Frost, Moffitt, & McGee, 1989), 15 years (McGee et al., 1990), and 18 years (Feehan, McGee, & Williams, 1993; Feehan et al., 1994). It is unclear whether rates from earlier assessments would have been similar to those found in the other large-scale studies conducted in the United States (Johnson, Cohen, Kasen, & Brock, 2002; Lewinsohn et al., 1993) or the large Munich study (Wittchen et al., 1998) in which a majority of girls were younger than 21 years.

For girls, lifetime rates (ever having met criteria for anorexia nervosa) range considerably, with rates as low as 3 in 100 (Whitaker et al., 1990) in a study using DSM III criteria (which are more restrictive for anorexia nervosa than later editions of the DSM) and as high as 3.9 (Graber et al., 2003).

Partial-Syndrome Anorexia Nervosa

Only a few studies have provided data about partial anorexia nervosa, and when such data are reported, typically rates for partial anorexia nervosa have exceeded those for full-syndrome anorexia nervosa (McKnight Investigators, 2003; Rathner & Messner, 1993; Wittchen et al., 1998). Wittchen and colleagues (1998) found an additional 1.3% of females and 0.4% of males who fell “just short one DSM IV criterion” (p. 116) for having ever experienced anorexia nervosa, for a combined lifetime rate of partial anorexia nervosa or anorexia nervosa of 2.3% in females and 0.5% in males. In the young sample from the McKnight study, five girls (0.37%) met criteria for current partial anorexia nervosa, defined as meeting all but the amenorrhea criteria (McKnight Investigators, 2003, p. 249). Despite the use of quite liberal criteria for partial anorexia nervosa (“at least one DSM IV criterion not met,” p. 385), Rosenvinge and colleagues (1999) found no cases of partial anorexia nervosa in their sample of 15-year-olds. Not surprisingly, rates of partial anorexia nervosa also seem to be correlated with age of the sample, with higher rates found in samples of older girls. For example, Rathner and Messner (1993) found no partial anorexia nervosa among the younger girls (ages 11 to 14 years), but found a rate of 1.3% among the older girls (15 to 20 years).

Full-Syndrome Bulimia Nervosa

Reported prevalence rates for current bulimia nervosa in girls vary considerably, and with the possible exception of age of the sample, these variations do not seem to reflect methodological differences across the studies. Only two studies found any current male cases and the reported rates were very low (Johnson, Cohen, Kasen, et al., 2002; Wittchen et al., 1998). Rates for females (0.5% or less) were reported to be low in several European countries (e.g., Italy: Rathner & Messner, 1993; Switzerland: Steinhausen et al., 1997; Hungary: Szabo & Tury, 1991; the Netherlands: Verhulst et al., 1997; Poland: Wlodarczyk-Bisaga & Dolan, 1996) but not uniformly so (e.g., Norway: Rosenvinge et al., 1999; Germany: Wittchen et al., 1998).

Studies reporting relatively higher point prevalence rates have tended to include older participants. Specifically, 12-month prevalence rates were 0.7% in the female Munich sample (ages 14 to 24; Wittchen et al., 1998), 1.5% in the female Dunedin sample (age 21; Newman et al., 1996), and an astonishingly high 4% in the U.S. sample of students from New York state (Johnson, Cohen, Kasen, et al., 2002). In this study, any student who had met criteria during either early adolescence or mid-adolescence (spanning the ages 9 to 23 years) was counted. Johnson, Cohen, Kasen, and Brook have published several reports on eating disorders in their sample, and in one of these they indicated that in early adolescence (mean age 13.8, range 9–19 years), the 12-month prevalence for bulimia nervosa among girls was 1.4% (Johnson, Cohen, Kotler, Kasen, & Brook, 2002). It further bears noting that in general, rates were higher in the studies that employed a one-time assessment strategy rather than the more common two-stage approach. Consistently, the studies found that bulimia nervosa is very rare among adolescent boys (Lewinsohn et al., 1993; Wittchen et al., 1998; Woodside et al., 2001). In most studies, there were no cases of current or lifetime male bulimia nervosa, and when such cases were detected, they were far less common than female cases.

Partial-Syndrome Bulimia Nervosa

As has been observed for anorexia nervosa, partial-syndrome bulimia nervosa is more common than full-syndrome bulimia nervosa (Johnson, Cohen, Kasen, et al., 2002; McKnight Investigators, 2003; Newman et al., 1996; Rathner & Messner, 1993; Rosenvinge et al., 1999; Wittchen et al., 1998). Rathner and Messner (1993) found no full-syndrome bulimia nervosa cases and reported that the two girls with partial bulimia nervosa (0.39%) were among the older girls (>15 years). In the study conducted by the McKnight Investigators (2003), 1.2% of girls met criteria for partial bulimia nervosa, for a combined rate of partial bulimia nervosa and bulimia nervosa of 1.6%. A fairly inclusive definition of partial bulimia nervosa was used: all cases in which either binge eating and purging were less frequent than that required by DSM-IV or subjective binges occurred in the presence of at least weekly purging were reported (McKnight Investigators, p. 249).

Using another broad definition, the presence of “all but one of the required symptoms,” Wittchen and colleagues (1998) identified 1.5% female partial bulimia nervosa cases and 0.6% male partial bulimia nervosa cases. The combined rate of partial bulimia nervosa and bulimia nervosa was 3.2% in females and 0.6% in males. Finally, in what may be the most inclusive definition, “at least one DSM IV criterion not met,” Rosenvinge at al. (1999) detected 1% of girls but no boys with partial bulimia nervosa. Although it is clear that a broader definition of bulimia nervosa results in increased rates, the lack of a systematic definition of partial bulimia nervosa makes it impossible to draw any conclusions about the prevalence of more broadly defined bulimia nervosa in adolescents.

Prevalence of Binge Eating Disorder

Only three studies have reported specifically on the prevalence of binge eating disorder (defined mutually exclusively from partial bulimia nervosa or eating disorder not otherwise specified). The McKnight Investigators (2003) reported that 0.59% of the 11-to 14-year-old girls in their study met 3-month point prevalence criteria for binge eating disorder. Using 12-month prevalence criteria, Johnson, Cohen, Kasen, et al. (2002) identified no male binge eating disorder cases and reported 0.55% of female binge eating disorder cases. The highest rates were found by Rosenvinge and colleagues (1999), who reported that 1.5% of the 15-year-old school girls and none of the boys studied met point prevalence (time frame not specified) for binge eating disorder. As described earlier, this particular study found relatively high rates for all eating disor ders, considering the young age of the sample, yet there is no apparent explanation for these high rates (e.g., some obvious methodological peculiarity).

In clinical samples, onset of binge eating disorder (as determined by retrospective report) has been described to occur later than that of bulimia nervosa (Wilfley, Schwartz, Spurrell, & Fairburn, 2000). There are some indications from nonrepresentative community samples that in adults, binge eating disorder is more prevalent than bulimia nervosa (Spitzer et al., 1993; Spitzer, Williams, Kroenke, Hornyak, & McMurray, 2000). On the basis of the very limited evidence, this does not seem to be the case, but the evidence of binge eating disorder in adolescents is too preliminary to permit firm conclusions. Given the emerging data about recurrent binge eating as a risk factor for obesity (Fairburn, Cooper, Doll, Norman, & O'Connor, 2000), future studies need to include the requisite diagnostic questions to identify binge eating disorder in adolescents.

Conclusions from the Data on Prevalence

The prevalence of anorexia nervosa and bulimia nervosa in adolescent samples clearly is lower than rates reported for adult samples. The lack of studies with adequate sample sizes and the considerable variation in methodology make it difficult to answer confidently the question of

    Red Flags Signaling the Potential Development of an Eating Disorder
  • An abnormally low weight or significant fluctuations in weight not due to medical illness
  • Purging behaviors intended to induce weight loss
  • Persistent intense concerns with weight or shape
  • Persistent attempts to diet or lose weight despite being at a normal or low weight
  • Social withdrawal and isolation for activities involving food and/or eating
  • Unexplained amenorrhea
how many adolescents experience an eating disorder. A major gap in studies from the United States is the lack of data adequately representing the ethnic diversity of its population.

Experts have expressed concern that the data on prevalence of eating disorders in adolescents are misleading because the strict diagnostic criteria do not permit diagnosis of anorexia nervosa or bulimia nervosa among adolescents who show evidence of the core features of these disorders yet have not yet developed the requisite severity or duration of symptoms (Golden et al., 2003). Examination of the prevalence of behavioral eating disorder symptoms, is therefore indicated. These symptoms may represent the first signs of development of a full-syndrome disorder, and data on their prevalence thus give an indication of the size of the “at-risk” group.

Symptoms of Eating Disorders in Adolescent Girls and Boys

In 1990, the Centers for Disease Control and Prevention developed the Youth Risk Behavior Surveillance System to monitor health risk behaviors that contribute markedly to the leading causes of death, disability, and social problems among youth and adults in the United States. The system includes national, state, and local school-based Youth Risk Behavior Surveys (YRBS; 2003) conducted every 2 years, of representative samples of 9th through 12th grade students. Students complete the anonymous surveys during a class period at school. In the 2001 YRBS (Grunbaum et al., 2002), the overall participation rate was 63% but varied considerably across states. The YRBS includes questions about current attempts to lose weight and questions about weight loss or weight maintenance efforts, such as vomiting, diet pills, and “other methods.”

Consistently, the YRBS has found that about two of every three female students report trying to lose weight, compared to one in four male students. Trying to gain weight is quite common among boys (about 40%), whereas only a minority of girls (about 8%) engage in efforts to become heavier (Grunbaum et al., 2002; Lowry et al., 2002; Middleman, Vasquez, & Durant, 1998). The YRBS also includes questions about behav iors that are considered in the DSM to be “inappropriate compensatory behaviors.” Data collected in 1999 and 2001 suggest that inappropriate efforts to lose weight or keep from gaining weight are disturbingly common, especially among girls. Specifically, in 1999, fasting, use of diet pills, and vomiting or laxative abuse were reported by 18.8%, 10.9%, and 7.5% of girls, respectively, compared to 6.4%, 4.4%, and 2.2% of boys (Lowry et al., 2002). Data for 2001 showed similar rates for these behaviors (Grunbaum et al., 2002).

The YRBS includes an ethnically diverse sample, permitting the examination of ethnic group differences in the prevalence of weight-related behaviors. In 2001, white and Hispanic girls were found to be significantly more likely than black girls to report inappropriate compensatory behaviors. Almost one in four (23.1%) female Hispanic students and one in five white students (19.7%), compared to 15% of black students, reported that she had gone without eating for 24 or more hours to control her weight. Vomiting or laxative use to control weight was reported by 10.8%, 8.2%, and 4.2% of Hispanic, white, and black girls, respectively (Grunbaum et al., 2002). These findings suggest that additional study of disordered eating among minority groups is needed. Whether girls in this sample would meet diagnostic criteria for an eating disorder is unclear, because the YRBS does not include questions covering the complete set of diagnostic criteria for anorexia nervosa and bulimia nervosa. Nevertheless, a considerable subset of female students practice potentially health-damaging behaviors, such as vomiting, which is cause for concern.

Although the YRBS does not assess binge eating, a recent study of boys and girls in public middle and high schools has provided information about binge eating in adolescents (Ackard, Neumark-Sztainer, Story, & Perry, 2003). Binge eating was considered present if the child answered “yes” to a question about overeating with loss of control, at least a few times a week, and feeling upset “some” or “a lot” by overeating. More girls (3.1%) than boys (0.9%) met criteria for binge eating, and the results suggested that binge eating was significantly correlated with body mass index (BMI) in girls and boys. Binge eating was only slightly more common in white girls (2.6%) than in black (1.6%) or Hispanic (1.7%) girls, and was reported by a surprisingly large number of Asian American girls (5.9%). Therefore, binge eating may occur among ethnically diverse groups.

Summary

Epidemiological research on eating disorders in adolescence is limited in several important ways. Nationally representative samples, including ethnic minority children, are needed to determine the prevalence of eating disorders among American youth. Studies of ethnic minorities in European countries (e.g., Bhugra & Kamaldeep, 2003) and among adolescents in non-Western countries (e.g., Huon, Mingyi, Oliver, & Xiao, 2002; Nobakht & Dezhkam, 2000) have reported significant rates of eating disorders among minorities. These results indicate that eating disorder research should be more inclusive in its sampling frames.

While the diagnostic criteria for anorexia nervosa and bulimia nervosa are well articulated, definitions of eating pathology that fail to meet diagnostic criteria are quite varied. Since eating pathology that fails to reach diagnostic significance may represent the early stages of a full-syndrome eating disorder for some adolescents, a more uniform definition of partial syndrome is needed. Studies should also include criteria for binge eating disorder to permit estimates of the prevalence of this syndrome.

The lack of a uniform instrument for measuring eating disorder symptoms also limits current epidemiological research. One-step assessment studies that use standardized psychiatric interviews, in which individuals “skip out” of the eating disorder module if a gated question is answered negatively, may have produced an underestimation of eating pathology, especially in young samples, in whom the clinical presentation of anorexia nervosa or bulimia nervosa could be atypical (Kreipe et al., 1995). Finally, parent reports might improve the detection of anorexia nervosa, a disorder in which denial is a hallmark.

Eating disorders may be transient (albeit in many cases recurrent) and point prevalence rates may therefore not reflect fully the extent of eating pathology in adolescents (Patton, Coffey, & Sawyer, 2003). Even if an adolescent's eating disorder is time limited and nonrecurring, it may represent a marker for psychopathology that conveys important clinical information. For example, Johnson, Harris, Spitzer, & Williams (2000) demonstrated that an adolescent's history of an eating disorder is associated with elevated risk for other Axis I disorders in adulthood. Adolescent eating disorders, even when fully remitted, are associated with a broad range of indicators of impaired psychosocial functioning (Striegel-Moore, Seeley, & Lewinsohn, 2003).

Information about the incidence of eating disorders requires longitudinal data. Although a few studies have included longitudinal follow-ups, these studies have not focused specifically on eating disorders and did not provide incidence data. There is one exception, however. Lewinsohn and colleagues (2000) classified an eating disorder sample into onset prior to or after age 19 and reported that first incidence for anorexia nervosa was significantly more likely to occur prior to age 19. An incidence rate for anorexia nervosa of 0.1% was found for the age group of 19–23 years. For bulimia nervosa, the incidence rates for before age 19 and after were comparable: 1.5% and 1.3%, respectively. Clearly, more detailed data are needed on the incidence of eating disorders.

In conclusion, epidemiological research of eating disorders is quite limited. In light of the considerable public health significance of anorexia nervosa and bulimia nervosa and their spectrum variants, such research is urgently needed.

COMORBIDITY, OUTCOME, AND DIAGNOSTIC MIGRATION

In addition to examining the diagnostic categories and prevalence of eating disorders, it is important to know what other emotional and psychological problems individuals with eating disorders are prone to develop and to describe what is likely to occur over time to individuals with eating disorders. Knowledge of comorbidity, outcome, and migration between diagnostic categories is important in helping to refine the definition of adolescent eating disorders and in assessing the effectiveness of treatment. A number of studies have addressed comorbidity, course, and outcome of adult patients with eating disorders, but studies of adolescents have only included patients with anorexia nervosa.

Comorbidity of Anorexia Nervosa

The lifetime rates of psychiatric comorbidity among patients with anorexia nervosa are approximately 80% (Halmi et al., 1991). Affective disorders, anxiety disorders, substance use disorders, and personality disorders are commonly associated with anorexia nervosa. The affective disorder that most commonly co-occurs with anorexia nervosa is major depressive disorder, with a lifetime comorbidity of 50%–68% (Herzog, Nussbaum, & Marmor, 1996). Lifetime rates of anxiety disorders are between 55% and 65% (Godart, Flament, Perdereau, & Jeammet, 2002; Halmi et al., 1991); the most common comorbid anxiety diagnoses are social phobia (55%) and obsessive-compulsive disorder (OCD) (25%–69%; Godart et al., 2002; Halmi et al., 1991). Lifetime prevalence of substance use disorders ranges between 12% and 21% (Herzog, Keller, Sacks, Yeh, & Lavori, 1992; Stock, Goldberg, Corbett, & Katzman, 2002), compared to 11% of women in the general population (Bulik, Sullivan, McKee, Weltzin, & Kaye, 1994). Patients with AN-B/P are more likely than those with AN-R to manifest substance use disorders (Herzog, Keller, Sacks, et al., 1992; Stock et al., 2002).

When patients with anorexia nervosa present for treatment, over 70% report an additional current psychiatric disorder. Approximately 66% have a co-occurring affective disorder, 49% are diagnosed with a personality disorder, 5% have a substance use disorder, and 56% report an anxiety disorder (Braun, Sunday, & Halmi, 1994; Herpertz-Dahlmann et al., 2001; Herzog, Keller, Sacks, et al., 1992; Wonderlich & Mitchell, 1997). Cluster C personality disorders, which include avoidant, dependent, obsessive-compulsive, and passive-aggressive personality disorder, are also common among patients with anorexia nervosa (Herzog, Keller, Lavori, Kenny, & Sachs, 1992).

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

Comorbidity of Bulimia Nervosa

Nearly 83% of patients with bulimia nervosa report a lifetime history of an additional psychiatric disorder (Fichter & Quadfleig, 1997); affective disorders, anxiety disorders, substance use disorders, and personality disorders are commonly associated with bulimia nervosa. While there is a significant amount of variability in the rates of comorbidity, more than 50% of patients with bulimia nervosa have a lifetime history of a mood disorder. Major depressive disorder has been shown to be the most common mood disorder diagnosis among patients with bulimia nervosa. In community samples, approximately one third are depressed, 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 ranges from 13% to 65% (Herzog, Keller, Sacks, et al., 1992). Social phobia (17%) and OCD (8%–33%) are the most frequently diagnosed anxiety disorders in bulimia nervosa, and panic disorder is also commonly observed (Brewerton et al., 1995; von Ranson, Kaye, Weltzin, Rao, & Matsunaga, 1999). The lifetime prevalence of substance use disorders is approximately 25% (Bulik et al., 1994), and patients with bulimia nervosa most frequently abuse alcohol, cocaine, and marijuana. Patients with bulimia nervosa and substance use disorders commonly exhibit impulsivity in multiple domains, including suicide attempts, self-injurious acts, and stealing.

When patients with bulimia nervosa present for treatment, approximately 75% meet criteria for an additional psychiatric disorder (Fichter & Quadfleig, 1997). Approximately 50% have a co-occurring affective disorder, 34% have a substance use disorder, and 56% have an anxiety disorder (Halmi et al., 2002; Herzog, Keller, Sacks, et al., 1992; Mitchell, Specker, & de Zwaan, 1991; Wonderlich & Mitchell, 1997). Cluster B personality disorders, such as antisocial, borderline, histrionic, and narcissistic personality disorder, are also common in bulimia nervosa (Herzog, Keller, Lavori, et al., 1992).

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

Outcome of Anorexia Nervosa

The available data suggest that approximately 50%–70% of adolescents with anorexia nervosa recover, 20% are improved but continue to have residual symptoms, and 10%–20% have chronic anorexia nervosa (Herpertz-Dahlmann et al., 2001; Morgan, Purgold, & Welbourne, 1983; Steinhausen, 2002; Steinhausen et al., 1997). Adolescents with anorexia nervosa 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. Those anorexia nervosa 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, 1997; Strober et al., 1997; Wentz, Gillberg, Gillberg, & Rastam, 2001). Relapse is common after weight gain in hospitalized patients, with up to one third of adolescent anorexia nervosa patients relapsing soon after discharge (Herzog et al., 1999; Strober et al., 1997).

Anorexia nervosa has one of the highest mortality rates among psychiatric disorders. Approximately 5.6% of patients diagnosed with anorexia nervosa die per decade of illness (Sullivan, 1995), and anorexia nervosa patients are 12 times more likely to die than women of a similar age in the general population (Keel et al., 2003). Although the combined mortality rate for anorexia nervosa among adolescents and adults is over 5% (Steinhausen, 2002), the mortality rate during adolescence is low. The most common causes of death among patients with anorexia nervosa are suicide and the effects of starvation. The suicide rate among women with anorexia nervosa is 57 times higher than that for women of a similar age in the general population (Keel et al., 2003). Some studies have found lower weight at presentation, longer duration of illness, and severe alcohol use to be associated with higher risk of mortality (Keel, Mitchell, Miller, Davis, & Crow, 1999; Patton, 1988).

Few variables are consistently associated with outcome in anorexia nervosa, but the most positive outcomes are seen in patients between the ages of 12 and 18 with a short duration of illness. Poor outcome is associated with extremely low weight at presentation and, in some studies, by vomiting. The relationship of binge eating to outcome of anorexia nervosa is not clear, as patients with AN-R and those with AN-B/P have a similar time to recovery (Herzog et al., 1999).

Outcome of Bulimia Nervosa

Most adolescents and adults with bulimia nervosa improve over time, with recovery rates ranging from 35% to 75% at 5 or more years of follow-up (Fairburn et al., 2000; Fichter & Quadfleig, 1997; Herzog et al., 1999). Bulimia nervosa is a chronic relapsing condition, and approximately one third of individuals with bulimia nervosa relapse (Keel & Mitchell, 1997), often within 1 to 2 years of recovery (Herzog et al., 1996). Although approximately 50% of patients with bulimia nervosa recover, the remaining individuals continue to be symptomatic, often with substantial impact on physical and psychosocial functioning. Mortality is a rare outcome in bulimia nervosa, with rates as low as 0.5% (Keel et al., 1999). Few prognostic factors have been consistently reported across studies of bulimia nervosa, 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 poor outcome (Bulik, Sullivan, Joyce, Carter, & McIntosh, 1998; Fairburn, Stice, et al., 2003; Keel et al., 1999).

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 bulimia nervosa to anorexia nervosa (Kassett, Gwirtsman, Kaye, Brandt, & Jimerson, 1988), the most frequent change among diagnostic categories is from the subtype AN-R to AN-B/P, reflecting the development of bulimic symptomatology. Some individuals gain weight in association with the binge eating, leading to a change in diagnostic status from the subtype AN-R or AN-B/P to bulimia nervosa. In one study, more than 50% of AN-R patients, both adolescents and adults, developed bulimic symptomatology (Eddy et al., 2002), and only a small fraction of patients with AN-R remained in that diagnostic subtype. The remaining patients with AN-R who did not develop binge eating or purging were partially or fully recovered. It is unknown what factors lead to the development of bulimic symptoms among patients with AN-R, and what the precise time course of this development is.

Summary

The occurrence of other psychiatric disorders is extremely common in association with both anorexia nervosa and bulimia nervosa, and this complicates treatment. Unfortunately, many treatment studies of eating disorders exclude patients with serious comorbid disorders, such as substance use disorders. Adolescents with anorexia nervosa have a better prognosis when they receive treatment early in the course of their illness. However, anorexia nervosa is a severe psychiatric disorder, and those who remain ill have high rates of psychiatric comorbidity and are at risk for premature death. Diagnostic migration appears to be common between AN-R to AN-B/P and AN-B/P to bulimia nervosa. Little is known about the course and outcome of bulimia nervosa among adolescents, but among adults, bulimia nervosa is a chronic relapsing condition with a 50% recovery rate and a low mortality rate.

MEDICAL COMPLICATIONS OF EATING DISORDERS

Eating disorders are associated with significant medical morbidity and mortality. Most complications of eating disorders result from physiologic 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. In an adolescent whose growth and development are not yet complete, however, 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 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%–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 anorexia nervosa and bulimia nervosa are listed in Table 13.5. Individuals with symptoms of both disorders (e.g., patients with AN-B/P) are at risk for complications of both. Adolescents who have symptoms of eating disorders but do not meet full criteria for anorexia nervosa or bulimia nervosa may also be at risk of complications. Most of the complications occur with equal frequency in adults and adolescents. In contrast to adults, however, 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 13.5 Signs and Symptoms in Adolescence

Factor

Anorexia Nervosaa

Bulimia Nervosa

Weight

Markedly decreased

Usually normal

Menstruation

Absent

Usually normal

Skin/extremities

Growth of fine downy hair (lanugo)

Cold blue hands and feet (acrocyanosis)

Swelling of feet (edema)

Calluses on back of hand

Cardiovascular

Low heart rate (bradycardia)

Hypotension

Gastrointestinal

Elevated liver enzymes

Delayed gastric emptying

Constipation

Salivary gland enlargement

Dental erosion

Esophagitis

Hematopoietic

Normochromic, normocyctic anemia

Leukopenia

Low erythrocyte sedimentation rate

Fluid/electrolytes

Increased blood urea nitrogen

Increased creatinine

Hyponatremia

Hypokalemia

Hypochloremia

Alkalosis

Endocrine

Hypoglycemia

Low estrogen or testosterone

Low luteinizing hormone

Low follicle stimulating hormone

Low to normal thyroxine

Normal thyroid stimulating hormone

Increased cortisol

Delayed puberty

Growth retardation

Skeletal

Osteopenia

a Individuals with anorexia nervosa who engage in binge eating with or without purging may also develop signs and symptoms of bulimia nervosa.

Partially adapted from Walsh, B. T. (2001). Eating disorders. In E. Braunwald, S. L. Hauser, A. S. Fauci, D. L. Longo, J. L. Jameson, & D. L. Kasper (Eds.), Harrison's Principles of Internal Medicine (15th ed., p. 488).

Medical Complications of Anorexia Nervosa

The most notable medical complications of anorexia nervosa result from malnutrition. Subcutaneous tissue is lost, muscle wastes, 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 in color. 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 changes in pulse and blood pressure. There may be generalized muscle weakness.

In anorexia nervosa, life-threatening complications include electrolyte disturbances and cardiac arrhythmias. Patients may present with dehydration and abnormal serum levels of sodium, potassium, chloride, 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 to either satisfy hunger urges or 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 of cardiac arrhythmias and sudden unexpected death seen in the “refeeding syndrome” (Kohn, Golden, & Shenker, 1998).

Resting pulse rates among patients with anorexia nervosa may be as low as 30–40 beats per minute (Palla & Litt, 1988) and systolic and diastolic blood pressures are low. Within the first 4 days of hospitalization, 60%–85% of patients demonstrate orthostatic pulse changes on stand ing (Shamim, Golden, Arden, Filiberto, & Shenker, 2003). Electrocardiographic (EKG) abnormalities have been noted in up to 75% of hospitalized adolescent patients (Palla & Litt, 1988; Galetta et al., 2002). A prolonged QTc interval, one type of EKG abnormality, is of particular concern because it appears to precede ventricular arrhythmias and sudden death in patients hospitalized with anorexia nervosa (Isner, Roberts, Heymsfield, & Yager, 1985). A pericardial effusion (fluid around the heart) can develop in very malnourished patients (Silverman & Krongrad, 1983). Mitral valve prolapse has been reported in patients with anorexia nervosa (Johnson, Humphries, Shirley, Mazzoleni, & Noonan, 1986; Meyers, Starke, Pearson, & Wilken, 1986), but the apparent prolapse is reversible with weight restoration, whereas true prolapse is a permanent degeneration of the mitral valve (Schocken, Holloway, & Powers, 1989). 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 anorexia nervosa and reflect delayed gastric emptying and decreased intestinal motility. Liver enzymes are elevated in 4%–38% of patients with anorexia nervosa (Mickley, Greenfeld, Quinlan, Roloff, & Zwas, 1996; Palla & Litt, 1988; Sherman, Leslie, Goldberg, Rybczynski, & St. Louis, 1994). 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%–62% of cases and may lead to a yellowish discoloration of the skin (Sherman et al., 1994; Boland et al., 2001). 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 in anorexia nervosa. Rapid weight loss is associated with gallstone formation. With malnutrition, the metabolic rate slows down as an adaptive response to starvation. In anorexia nervosa, measured resting energy expenditure may be 65%–70% of predicted values (Schebendach et al., 1995). Consequently, in the malnourished state, caloric requirements are lower. 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 anorexia nervosa, resulting in low white blood cell, red blood cell, and platelet counts. Leukopenia (low white blood cell count) has been reported in one to two thirds of patients with anorexia nervosa 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 hematologic abnormalities are reversed with nutritional rehabilitation.

The major neurological complications of eating disorders are seizures and cerebral atrophy, found on computed tomography (CT) and magnetic resonance imaging (MRI) scans (Enzmann & Lane, 1977; Golden et al., 1996; Katzman et al., 1996; Nussbaum, Shenker, Marc, & Klein, 1980). Muscle weakness and a peripheral neuropathy can also occur. Neuropsychological testing has demonstrated impairment of attention, concentration, and memory, with deficits in visuospatial ability (Kingston, Szmukler, Andrewes, Tress, & Desmond, 1996). Although 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. It may be that these changes 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 anorexia nervosa 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, but even with intervention, 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 decreased ability to concentrate urine (Mecklenberg, Loriaux, Thompson, Andersen, & Lipsett, 1976). There is activation of the hypothalamic–adrenal axis with high levels of serum cortisol. Clinically, patients with anorexia nervosa 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 anorexia nervosa prior to the completion of puberty (Palla & Litt, 1988; Russell, 1985). Amenorrhea is a cardinal feature of anorexia nervosa, caused by a combination of malnutrition, increased exercise, emotional stress, low body weight, and decreased stores of body fat. Pituitary and ovarian hormones controlling menstruation are all low and the uterus and ovaries shrink in size (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). A recent study found that women who had a history of anorexia nervosa in the past had pregnancy rates similar to those of healthy controls and were no more likely to have received treatment for infertility (Bulik, Sullivan, Fear, Pickering, & Dawn, 1999). The women with a history of anorexia nervosa, however, were more likely to have a miscarriage, presumably because they continued with inappropriate weight-control behaviors during pregnancy.

The most serious complication of prolonged amenorrhea and a low estrogen state is osteopenia, a substantial reduction in bone mass. In anorexia nervosa, osteopenia may occur after a relatively short duration of illness (Bachrach, Guido, Katzman, Litt, & Marcus, 1990; Grinspoon et al., 2000). Osteopenia is related to a combination of poor nutrition, low body weight, estrogen deficiency, excessive exercise, and high levels of cortisol in the blood stream. The degree of osteopenia in anorexia nervosa is more severe than that seen in women with other conditions associated with amenorrhea and a low estrogen state. This finding suggests that in addition to estrogen deficiency, nutritional factors play an important role (Grinspoon et al., 1999).

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 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 anorexia nervosa during adolescence will not reach her peak bone mass, thus she will be at increased risk of developing fractures. Because of the lower peak bone mass, the increased fracture risk may persist for years after recovery from anorexia nervosa. Recent studies have demonstrated that more than 90% of adolescents and young adults with anorexia nervosa have reduced bone mass at one or more skeletal sites (Golden, 2003; Grinspoon et al., 2000). Osteopenia that occurs in adolescence may not be completely reversible (Rigotti, Neer, Skates, Herzog, & Nussbaum, 1991; Soyka et al., 2002). Weight gain is associated with some improvement in bone mineral density, but levels do not return to normal (Bachrach, Katzman, Litt, Guido, & Marcus, 1991). A recent study conducted on women who had been in recovery from anorexia nervosa for an average of 21 years found that bone mineral density of the hip remained lower than that of controls, and a relatively high percentage of patients reported a history of pathologic bone fractures (Hartman et al., 2000). Although there are no proven therapies and estrogen has been shown to be ineffective, recent studies have shown that insulin-like growth factor-1 (IGF-1), a nutritionally dependent hormone, may prevent bone loss (Grinspoon, Thomas, Miller, Herzog, & Kilbanski, 2002).

Medical Complications of Bulimia Nervosa

For patients with bulimia nervosa, fluctuations in body weight can be observed, and reflect 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), which are 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, although not to the same degree as that seen in patients with anorexia nervosa.

Ipecac, a medication used to induce vomiting after accidental poisoning, is abused by some patients with bulimia nervosa. Ipecac contains the alkaloid emetine, which is toxic to both skeletal and cardiac muscle, and 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 bulimia nervosa (Schiff et al., 1986).

Enlargement of the parotid and salivary glands occurs in 10% to 30% of patients with bulimia nervosa and is thought to be secondary to binge eating and vomiting (Ogren, Huerter, Pearson, Antonson, & Moore, 1987). Erosion of the dental enamel is most evident on the lingual aspects of the anterior teeth and is caused by the gastric acid. Recurrent vomiting leads to gastroesophageal reflux, esophagitis, tears of the esophagus, and, less frequently, esophageal rupture. Small tears may be evidenced by blood-stained vomiting. Esophageal rupture is a catastrophic event and is usually fatal. Esophagitis is associated with epigastric or retrosternal chest pain and warrants treatment.

Treatment of Medical Complications

The goals of medical management of patients with eating disorders are acute medical stabilization, normalization of eating behaviors, and reversal of medical complications. For patients with anorexia nervosa, weight restoration is an important 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 and, in particular, during the first 7–10 days of refeeding. It is during this time when the “refeeding syndrome,” consisting of cardiac, neurologic, and hematologic complications, is most likely to occur. The syndrome can occur after intravenous, nasogastric, or oral refeeding. Hypophosphatemia occurs in over one quarter of adolescents hospitalized with an-orexia nervosa (Ornstein, Golden, Jacobson, & Shenker, 2003). Hypophosphatemia is more likely to occur in those who are very malnourished (less than 70% of ideal body weight) and may predispose patients to ventricular arrhythmias and sudden death.

The refeeding syndrome can be prevented by monitoring of heart rate and serum electrolytes (especially phosphorus) during the first 7–10 days of treatment. Caloric requirements of children and adolescents with anorexia nervosa are usually higher than those for adults and may be 3,000–4,500 kcals/day. The rate of weight gain should be 2–3 lbs/week for inpatient programs, 1–2 lbs/week for partial hospitalization programs (when such programs are step-down programs from inpatient units), and 0.5–1 lb/week for outpatient management (American Psychiatric Association Work Group on Eating Disorders, 2000).

Treatment of Osteopenia in Anorexia Nervosa

Few controlled trials have evaluated the treatment of osteopenia in anorexia nervosa, and fewer still have specifically focused on adolescents; most studies enrolled only a modest number of subjects. Therefore, the preferred treatment of anorexia nervosa–related osteopenia 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 there have been no published controlled trials with anorexia nervosa patients. The Institute of Med icine recommends a dietary intake of 1,300 mg/day of calcium for healthy girls aged 9–18 years (Standing Committee on the Scientific Evaluation of Dietary Reference Intakes for Calcium, 1997) and the American Academy of Pediatrics recommends a calcium intake of 1,200–1,500 mg/day for adolescents (American Academy of Pediatrics Committee on Nutrition, 1999). Without scientific evidence demonstrating the efficacy of calcium supplementation in adolescents with anorexia nervosa, it may be most prudent to suggest calcium supplementation for patients whose dietary intake contains less than the recommended amount.

A number of studies have shown that body weight, and particularly lean body mass, is a significant determinant of bone mineral density in healthy subjects (Glastre et al., 1990; Henderson, Price, Cole, Gutteridge, & Bhagat, 1995; Southard et al., 1991) and in those with anorexia nervosa (Bachrach et al., 1990; Goebel, Schweiger, Kruger, & Fichter, 1999; Golden et al., 2002; Gordon, Goodman, et al., 2002; Grinspoon et al., 1999; Soyka et al., 2002). Although bone mineral density increases with weight gain, even with weight restoration, osteopenia is not entirely reversible (Bachrach et al., 1991; Golden et al., 2002; Hartman et al., 2000; Rigotti et al., 1991).

Both weight-bearing and resistance exercise programs increase bone mineral density of the spine in children and young women (McKay et al., 2000; Snow-Harter, Bouxsein, Lewis, Carter, & Marcus, 1992), but exercise programs for patients with anorexia nervosa have not been studied. Excessive exercise, commonly used by patients with anorexia nervosa 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 osteopenia in adolescents with anorexia nervosa (Robinson, Bachrach, & Katzman, 2000), on the assumption that estrogen deficiency contributes to the bone loss. The only randomized controlled trial published to date (Klibanski, Biller, Schoenfeld, Herzog, & Saxe, 1995) found no significant increase in bone mineral density for adult subjects with anorexia nervosa randomly assigned to receive estrogen treatment, in comparison to those who did not receive hormone treatment. The only suggestion of benefit was for those who were very malnourished (<70% of ideal body weight); hormone treatment may have provided a protective effect. In that subgroup, spinal bone mass increased 4% in those who received estrogen, but decreased 20.1% in those who did not. Golden et al. (2002) found that estrogen-progestin treatment in adolescents did not significantly increase bone mineral density, compared with standard treatment at 1-year follow-up. In subjects followed for 2–3 years, osteopenia was persistent and in some cases progressive, despite weight gain, in both experimental treatment groups (estrogen-progestin treatment and standard care).

Thus, there is currently no evidence of efficacy of hormone replacement therapy for the treatment of osteopenia in anorexia nervosa. Furthermore, prescribing estrogen to a young adolescent may cause premature closure of the epiphyses, which might result in further growth arrest. Ongoing randomized controlled trials are evaluating the use of new modalities such as IGF-l (Grinspoon et al., 1996, 2002), dehydroepiandrosterone (DHEA; Gordon et al., 1999; Gordon, Grace et al., 2002), and the bisphosphonates for the treatment of osteopenia in anorexia nervosa. Current treatment recommendations include weight restoration with resumption of menses, calcium (1,300–1,500 mg/day) and vitamin D (400 IU/day) supplementation, and carefully monitored weight-bearing exercise (Golden, 2003).

Treatments to Increase Weight in Adolescents

The goal weight should be set in treatment on an individual basis, taking into account pubertal stage, prior growth percentiles, and height and age. For adolescents, the goal weight is a “moving target,” and normal growth and development necessitate a recalculation of this number every 6 months. Height and weight tables used for adults are inappropriate for adolescents. The National Center for Health Statistics (NCHS) tables provide a useful resource of normative height and weight data for children and adoles cents in the United States (National Center for Health Statistics, 1973); however, the tables provide only normative weight data, not specific guidance for what is an “ideal body weight.”

The goal, or “ideal,” weight should be the weight at which normal physical and sexual development occurs; for girls this is the weight at which menstruation and ovulation are restored. In postmenarcheal girls, a weight approximately 90% of ideal body weight (the median weight for age and height according to the NCHS tables) is a reasonable goal weight, since 86% of patients who achieve that weight will resume menses within 3 to 6 months (Golden et al., 1997). 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 ideal body weight to maximize growth potential.

Summary

Most of the medical consequences of eating disorders are secondary to malnutrition and are reversible with nutritional rehabilitation and interruption of binge–purge activity. Heart rate returns to normal after approximately 12 days, vital sign instability resolves after approximately 21 days, 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 3–6 months after achieving treatment goal weight. Difficulties with body image distortion and preoccupation with weight and shape, however, may take longer to resolve. Although most of the medical complications are reversible, growth retardation, osteopenia, and, possibly, structural brain changes may not be entirely reversible.