EATING DISORDERS IN ADOLESCENCE

ETHNIC AND CULTURAL DIFFERENCES

Eating disorders are usually reported to occur predominantly in young women,
particularly young white women from middle to upper class backgrounds. However, information
regarding ethnic/racial differences among adolescents is somewhat limited. Several studies have
found no racial or ethnic dif-ferences in the prevalence of eating disorder symptoms . . . or risk
factors for eating disorders. However, one consis-tent finding is of lesser body dissatisfaction
among young African American females than among their white coun-terparts (Stice & Bulik,
2008). It is suggested that eating disorders are a culturally related phenomena, particularly
bulimia nervosa (Eddy, Keel, & Leon, 2010; Keel & Klump. 2003). This would suggest that the
more "Westernized* young women from other cultures become, the more likely they are to
develop eating disorders. Within Western culture certain groups may be at particular risk. These
include individuals involved in activities such as gymnastics, wrestling, ballet, and cheerleading
in which weight-control behaviors and abnor-mal eating are used to enhance performance or
appearance (Eddy et aL, 2010; Jacobi et al., 2004; Smolak, Murnen, & Ruble, 2000; Thomas,
Keel. & I leatherton, 2006).
CO-OCCURRING DISORDERS
Eating disorders commonly co-occur with a number of other disorders (O'Brien &
Vincent, 2003; Stice & Bulik, 2008). Lewinsohn, Striegel-Moore, and Seeley (2000) report that
in a community sample of adolescent girls, 90% of those with full syndrome eating disorders
experienced one or more co-occurring disorders. Depression, anxiety disorders, and substance
use disorders, in particular, are commonly reported as co-occurring with eating- and weightrelated difficulties and with anorexia and bulimia nervosa (Fischer & Le Grange, 2007; Lock et
at, 2005; Rawana et al., 2010).
Developmental Course and Prognosis
ANOREXIA NERVOSA
The age of onset of AN is typically during adolescence, with peaks at ages 14 and 18
(Eddy et at, 2010; Halmi et at. 1979). Cases of earlier onset are rare but do exist (Cowers &
Bryant-Waugh, 2004; Lask & Bryant-Waugh, 1992). Some individuals may experience a single
episode; others fluctuate between peri-ods of restoration of normal weight and relapse (perhaps
to dangerously low levels of weight that require hospital-ization). Other individuals may gain

weight and no longer meet the diagnostic criteria for AN, but they continue to engage in eating
disordered behaviors and may meet the criteria for BN or Other (Specified or Unspecified)
Eating Disorders (OED) (APA, 2013; Walsh et al., 2005a). Anorexia nervosa is a serious
disorder, and a substan-tial proportion of young women with the disorder have poor outcomes
although prognosis appears better for adolescents than adult women (Doyle & Le Grange, 2009;
Fairburn & Cowers, 2008; Katzman, 2005; Steinhausen, 1997). Extreme weight loss can lead to
significant medical complications (e.g., anemia, hormonal changes, cardiovascular problems,
dental problems, loss of bone density), and the disorder may be life-threatening (Doyle &
LeGrange, 2009). It has been reported that women with AN are 11-12% more likely to die than
other women of a similar age, many of the deaths resulting from suicide (Birmingham et al..
2005; Stice & Bulik, 2008).
BULIMIA NERVOSA The onset of BN extends from adolescence into early adulthood
with a peak period of onset between 14 and 19 years of age in females (Stice & Bulik, 2008).
Binge eating often begins during or after a period of restrictive dieting driven by extreme
dissatisfac-tion with body shape and weight. The DSM describes the course of the disorder as
either chronic or intermittent, with periods of remission alternating with recurrences of binge
eating. However, over the long term, symptoms of BN diminish in many individuals (APA,
2013). Although some individuals may no longer meet the diagnostic crite-ria for BN, problems
may persist. They may, for example, continue to binge but no longer engage in inappropri-ate
compensatory behaviors. Some of these individuals may meet the criteria for binge eating
disorder or OED, and many meet the criteria for major depressive disor-der (Fairburn et al.,
2000; Lewinsohn et al., 2000; Stice & Bulik, 2008). 'The recurrent vomiting associated with BN
can result in dental problems such as the loss of tooth enamel and gum disease. Other medical
problems such as irrita-tion of the esophagus, alterations of the colon, and fluid and electrolyte
disturbances may also occur, particularly among those who employ purging compensatory
behav-iors (Mailer, 2011).
Etiology
A variety of risk factors and causal mechanisms have been proposed to explain the
development of eating disorders. Indeed, it is likely that AN and BN are multiply deter-mined
and result from a variety of different patterns of influences (Eddy et aL, 2010; Jacobi et al., 2004;
Striegel-Moore & Bulik, 2007). Being female is probably the most reliable risk factor. Other

factors, however, are needed to help explain the gender difference and the development of eating
disorders.
BIOLOGICAL INFLUENCES Eating and the biologi-cal mechanisms behind it are
complex; thus, numerous biological mechanisms have been studied. There is some suggestion
that prenatal sex hormone exposure (lower testosterone and higher estrogen) may be associated
with eating-disordered behavior. Also, the onset of anorexia nervosa is most often around
puberty. While there is no definitive explanation of why puberty may increase risk, it is
hypothesized that hormonal changes during puberty may moderate genetic influences on eatingdisordered behavior (Eddy et al., 2010; Klump et at, 2007). Research on biological influences
has also focused on neurobiological and genetic influences. Eating behav-ior can both be
influenced by and effect changes in neurobiological and neuroendocrine systems, so determining causal relationships is not easy. It has been difficult to determine whether a particular
biological difference found in young women with eating disorders placed them at initial risk for
the disorder or has resulted from changes in the biological system due to disordered eating.
Research suggests differences in neurotransmitter (e.g., serotonin, norepinephrine) activity are
associated with eating disorders (Eddy et al, 2010; Halmi, 2009; Jacobi et at. 2004; Kaye et aL,
2008; Klump & Gobrogge, 2005). For example, serotonin plays a major role in the inhibition of
feeding, and decreased serotonin activity has been observed in individuals with anorexia and
bulimia nervosaboth during the illness and after recovery. A genetic contribution to eating
disorders has also been suggested (Eddy et al.. 2010; Halmi, 2009; Jacobi et aL, 2004; Klump &
Gobrogge, 2005; Striegcl-Moore & Bulik, 2007).
WEIGHT HISTORY Family weight history and the indi-vidual's previous weight history
are frequently considered as possible risk factors. For example, there is debate about the idea that
the self-starvation that is characteristic of AN begins as an attempt to control genuine
overweight. It has been suggested that comments that the young girl is 'getting plump' may
stimulate normal dieting, which evolves into anorexic refusal to eat. Similar considerations have
been discussed regarding BN, and there does seem to be evidence that supports personal and
family history of overweight as a risk factor (Wilson et at. 2003). Some young women with such
a history may become bulimic. Their problematic behaviors may begin as more typical attempts
to reduce weight that could not meet the thin cultural ideal. However, the frequency of dieting
among adolescent girls raises the question of why some girls who begin this common social

ritual persist well beyond the point of socially desired slimness. Research regarding the
mechanisms that might link early dieting and weight concerns to eating disorders for some girls
is ongoing (Eddy et al., 2010).
TEMPERAMENT/PERSONALITY TRAITS The tempera-ment quality of negative
affectivity has been associated with eating disordered behaviors and attitudes. But negative
affectivity is also associated with other dis-orders such as anxiety and depression that frequently
co-occur with eating disorders. Thus, this tempera-ment quality may be a non-specific risk factor
for eat-ing disorders (Eddy et al., 2010). The relationship between certain personality traits and
eating disorders also has received considerable attention. For example, perfectionism (striving
for unreasonably high standards and defining one's worth based on accomplishments) has been
reported to be associated with eating disorders (Bardone-Cone et al., 2007). However, research
does not support viewing perfectionism and other personality traits such as obsessionality,
impulsivity, restraint, and conformity as preexisting risk factors for specific eating disorders. At
best, the relationship between personality traits and eating disorders remains unclear.
Alternatively. personality traits may be factors that affect the course of an eating disorder, or they
may be consequences of an eating disorder (Walsh et al., 2005b; Wonderlich et al., 2005).
SEXUAL ABUSE Reports based on clinical cases have suggested early sexual abuse as a
cause of eating disor-ders. Reviews suggest a small but significant association between
childhood sexual abuse and eating-disordered behavior (Smolak & Murnen, 2002). The nature of
this relationship remains unclear. However, sexual abuse would appear to be a risk factor for
psychopathology in general, rather than a specific risk for the development of eating disorders
(Eddy et al.. 2010; Jacobi et al.. 2004; Walsh et at, 2005b). This, of course, does not mean that
clinicians working with young people should not con-sider the occurrence of sexual abuse, which
may be part of a pathway to eating disturbance for some individuals of a pathway to eating
disturbance for some individuals (Feldman & Meyer, 2007; Wonderlich et al., 2001).
CULTURAL INFLUENCES AND BODY DISSATISFACTION Any discussion of the
development of eating disorders is likely to address cultural influences and gender roles for
women and the problem of body dissatisfaction (Eddy et al., 2010; Smolak & Murnen, 2004;
Striegel-Moore & Bulik. 2007). Our society's emphasis on and valuing of slim and young bodies,
particularly for women, likely contributes to body dissatisfaction and the development of eating
disorders (Mirkin, 1990; Striegel-Moore & Bulik, 2007). For example, Dittmar, Halliwell & lye

(2006) asked the question, "Does Barbie make girls want to be thin?" Many young girls own at
least one Barbie doll. Barbie is excep-tionally thin and her body proportions are unattainable and
unhealthy. In the study, girls ages 5 to 8 were exposed to picture-book images of either Barbie
dolls. Emme dolls (body proportions of a dress size 16), or neutral stimuli without any
descriptions of bodies. Girls exposed to Barbie reported lower body esteem and greater desire for
a thinner body than girls in the other conditions. This was particularly true for younger girls.
Girls exposed to Emme did not differ from those who viewed neutral images. Such findings raise
concerns that at a very young age girls may internalize a thin ideal.
Intervention
As we have seen, eating disorders likely develop from and are maintained by a variety of
influences, and there is considerable heterogeneity among individuals with eating disorders.
Thus. interventions that address multiple influences are needed and we briefly highlight some
approaches. In general, there is more research supporting interventions for BN than for AN.
However, interventions specifically targeting adolescents with BN are limited and. thus,
recommendations regarding BN are based largely on controlled studies with adults (APA, 2006;
Keel & Haedt. 2008; Wilson, Grilo, & Vitousek, 2007). With regard to adolescents with AN,
there is evidence supporting family-based approaches.
FAMILY APPROACHES Family therapy for eating disorders derives from the
observation by clinicians of varying persuasions that families are intimately involved in the
maintenance of this behavior. Family therapy is wide-spread in clinical practice, but research
support is more limited. There is support for the effectiveness of family interventions for
adolescents with AN (Keel & Haedt, 2008; Robin & lc Grange. 2010; Wilflcy et al., 2012) and
the evidence is strongest for the Maudsley family-based treatment for AN (FBT-AN; Eisler et al.,
2010; Lock & lc Grange, 2005). This approach avoids viewing families as pathological and
blaming them for the development of AN. The position taken is that the causes of the disor-der
are unknown and the family is considered the most important resource for the adolescent's
recovery. Thus, the goal is to remobilize family resources to work with the professionals rather
than seeking to 'treat the family." Treatment, which initially involves intense support of the
family that is gradually faded over time, is broadly divided into three phases. The first phase is
highly focused on the eating disorder. Weeding, and weight gain and also seeks to reinvigorate
the parents in their role as agents of change. Families are encouraged, with therapist consul-

tation, to work out for themselves the best way to Weed their anorexic child. Once the adolescent
is gaining weight and eating takes place with minimal struggle, the second phase begins. Eating
disorder symptoms are the main sub-ject of sessions, but the goal is to assist the family in finding ways to return control back to the adolescent. As this occurs other family issues can begin to
be reviewed. Once the adolescent achieves a healthy weight the final phase is undertaken.
General issues of adolescent development and the ways they have been affected by AN are
addressed. The goal is to assure that the adolescent is back on a normal developmental trajectory
and that the family is prepared to manage typical developmental concerns (Eisler et al., 2010).
Two modes of family involvement in FBT-AN have been compared: conjoint family therapy
(CFT), in which the whole family is seen together, and separated family therapy (SFT), in which
the same therapist sees the adolescent individually and the parents in separate sessions. Overall,
CFT and SFT produced significant and comparable weight gain, improved menstrual functioning, and improved psychological functioning by the end of treatment and at a 5-year follow-up
(Eisler et al., 2000; 2007). For a subset of families in which mothers were highly critical,
adolescents who received SFT achieved greater weight gain during follow-up than did those who
received CFT. Family involvement may have to be tailored to the family and/or adjusted over the
course of treatment. A family-based therapy for adolescents with BN, adapted from FBT-AN, has
been developed (le Grange & Locke. 2010). Although initial findings are promising (Le Grange
et al., 2007), there is still only limited research regarding its effectiveness.
COGNITIVE-BEHAVIORAL TREATMENTS Cognitive-behavioral treatment (CBT) of
BN has appreciable research support and is viewed by many as a treatment of choice for this
disorder (Mitchell, Agras, & Wonderlich, 2007; Wilfley et al., 2012; Wilson, 2010). Controlled
research has shown the cognitive behavioral approach to the treatment of BN to be superior to no
treatment and to alternative treatments, including pharmacother-apy and a variety of other
psychotherapies. However, treatment evidence is based largely on adult samples that include
some older adolescents (APA, 2006; Keel & Hacdt, 2008). Treatment involves a multifaceted
program that is largely based on the rationale that a dysfunctional schema for self-evaluation
one that overvalues shape and weight and their controlis what maintains eating disorder
pathology (Cooper & Fairburn, 2010; Fairburn, 1997). According to this view, these cognitions
regarding shape and weight are the primary features of the disorder and other featuressuch as
dieting and self-induced vomitingare secondary expressions of these concerns. The 'dietary

slips and binges that are part of the pattern of behavior among individuals with BN are most
likely to occur in response to negative moods or adverse events. In the initial stage of treatment,
the patient is educated regarding BN, and the cognitive view of the dis-order is made clear.
During this early stage, behavioral techniques are also employed to reduce bingeing and
compensatory behaviors (e.g., vomiting) and to estab-lish control over eating patterns. These
techniques are supplemented with cognitive restructuring techniques, and as treatment
progresses, there is an increasing focus on targeting inappropriate weight-gain concerns and on
training self-control strategies for resisting binge eat-ing. Next, additional cognitively oriented
interventions address inappropriate beliefs concerning food, eating, weight, and body image.
Finally, a maintenance strategy to sustain improvements and to prevent relapses is also included.
As discussed earlier, most adolescents do not meet the diagnostic criteria for AN or BN. Their
prob-lems may be diagnosed in the general OED category. Thus, adolescents seeking treatment
may present with a wide range of eating-disorder problems. Fairburn and colleagues (Cooper &
Fairburn, 2010; Fairburn, Cooper. & Shafran. 2003) have developed a cognitive-behavioral
individualized treatment program based on a etransdi-agnostic" model of eating disorders. This
intervention is an 'enhanced" version of CBT for Bulimia (CBT-E). The program matches
specific therapeutic interventions to the particular eating-disorder features of the individ-ual,
rather than providing treatment based on diagnosis. Fairburn and colleagues (2009) have
evaluated CBT-E with a population of adults either meeting diagnostic cri-teria for BN or for
those with symptoms that do not meet full BN diagnostic criteria (e.g., OED). The treatment was
comparably effective for both groupsabout half of the treated individuals reached a level on
eating disor-der measures that was close to the mean of a community sample. The success of
CBT-E for individuals who do not meet full diagnostic criteria for BN further suggests that a
cognitive-behavioral approach may also be appropriate for adolescents.
INTERPERSONAL PSYCHOTHERAPY Interpersonal psychotherapy (IPT) focuses on
interpersonal problems involved in the development and maintenance of a disorder. Research
suggests that IPT also may be an effective treat-ment for BN in adults (Tanofsky-Kraff &
Wilfley. 2010). This therapeutic approach does not directly target eating symptoms, but seeks to
enhance interpersonal function-ing and communication skills. The rationale for such an approach
is based, in part.on research indicatingpoor inter-personal functioning in individuals with BN and
the role of interpersonal influences (e.g., actions of peers, friends, family; comparison with

others) on the development of body image and self-esteem (Tanofsky-Kraff & Wilflcy, 2010). An
assessment of the individual's interpersonal history is obtained. One or more of four
interpersonal problem areas are the focus of the intervention: interper-sonal deficits,
interpersonal role disputes, role transitions, and grief.
PHARMACOLOGICAL TREATMENT Although case reports suggest that different
pharmacological treat-ments can be successful with eating-disordered patients, controlled
research, particularly regarding adolescents, is either lacking or presents a somewhat more
cautious pic-ture. There seems to be little support for the effectiveness of any pharmacological
approach in the treatment of AN; however, the use of medications continues to be explored
(APA, 2006; Crow et al., 2009; Kaplan & Howlett, 2010). In controlled studies with adults,
SSR1s, such as fluoxetine, or other antidepressant medications have been reported to be effective
in treating BN (Broft. Berner, & Walsh, 2010). Effectiveness may be limited to only some
patients. and medication would not appear to be the primary treatment of choice. The role of
medica-tion in treating BN in adolescents remains unclear and research is limited (Broft et al.,
2010). Moreover, caution is indicated regarding side effects with individuals who are already
psychologically and physiologically at risk.
PREVENTION There is a considerable prevalence among adolescents of eatingdisordered behavior that does not meet the criteria for anorexia or bulimia nervosa or is
considered "subclinical." In addition, signs of eating-disordered behavior and attitudes in
younger children are frequent. Thus, there is reason to think in terms of pre-vention (Wilfley et
al., 2011). However, empirical stud-ies on the prevention of eating disorders are relatively
limited. Evaluations of universal prevention programs have largely focused on programs that
target older youths (Walsh et al., 2005b). Some programs address issues related to healthy weight
regulation (HWR) and focus on issues such as restrictive dieting, body image, and social and
cultural influences. Other programs focus on broader issues such as self esteem and social
competence (SESC) as a way to prevent the onset of eating-disordered behavior and attitudes.
Evidence is limited. but does offer some suggestion regarding interventions (Walsh et al..
2005b). There are some promising findings for SESC approaches among middle-school students.
For example, Steiner-Adair and colleagues (2002) employed a curriculum that taught recognition
and critical evalu-ation of cultural messages and prejudices regarding appearance, weight, and
eating, and was designed to help seventh-grade girls become more assertive and support-ive of

each other. Eating disorder knowledge and weight-related body esteem were significantly higher
by the end of the curriculum, and remained high at a 6-month follow-up. It seems less clear
whether programs using the HWR approach are of benefit for middle-school children, and
universal prevention programs targeting high school students have found no significant effects
on attitudes or behavior. Given these findings and limited studies it is unclear whether universal
interventions are effective in preventing eating disorders. Targeted prevention studies have
primarily focused on interventions for self-selected samples of older adoles-cents and college
students. Research suggests that these interventions may reduce risk factors for high-risk individuals, at least in the short term, but care should be taken in generalizing these findings to
adolescents or younger children (Walsh et al., 2005b).