Classification of Eating Disturbance in Children and Adolescents: Proposed Changes for the DSM-V

Article (PDF Available)inEuropean Eating Disorders Review 18(2):79-89 · March 2010with221 Reads
DOI: 10.1002/erv.994 · Source: PubMed
Childhood and adolescence are critical periods of neural development and physical growth. The malnutrition and related medical complications resulting from eating disorders such as anorexia nervosa (AN), bulimia nervosa (BN) and eating disorder not otherwise specified may have more severe and potentially more protracted consequences during youth than during other age periods. The consensus opinion of an international workgroup of experts on the diagnosis and treatment of child and adolescent eating disorders is that (a) lower and more developmentally sensitive thresholds of symptom severity (e.g. lower frequency of purging behaviours, significant deviations from growth curves as indicators of clinical severity) be used as diagnostic boundaries for children and adolescents, (b) behavioural indicators of psychological features of eating disorders be considered even in the absence of direct self-report of such symptoms and (c) multiple informants (e.g. parents) be used to ascertain symptom profiles. Collectively, these recommendations will permit earlier identification and intervention to prevent the exacerbation of eating disorder symptoms.
Classification of Eating Disturbance in Children and
Adolescents: Proposed Changes for the DSM-V
T. Bravender
, R. Bryant-Waugh
, D. Herzog
, D. Katzman
, R. D. Kriepe
, B. Lask
D. Le Grange
, J. Lock
, M. D. Marcus
, S. Madden
, D. Nicholls
, J. O’Toole
L. Pinhas
, E. Rome
, M. Sokol-Burger
, U. Wallin
, & N. Zucker
Workgroup for Classification of Eating Disorders in Children and Adolescents (WCEDCA)
Nationwide Children’s Hospital, Columbus, OH, USA
Great Ormond Street Hospital, NHS Trust, London, UK
Massachusetts General Hospital, MA, USA
The Hospital for Sick Children and University of Toronto, Canada
Western New York Comprehensive Care Center for Eating Disorders, NY, USA
St George’s Hospital, University of London, Huntercombe Hospitals, London, UK
Regional Eating Disorders Service, Oslo, Norway
Stanford University, Pal Alto, CA, USA
The University of Chicago, Chicago, IL, USA
Fairleigh Dickinson University, Teaneck NJ and Mount Sinai School of Medicine, New York, NY, USA
The Children’s Hospital at Westmead, Australia
Western Psychiatric Institute, Pittsburgh, PA, USA
Kartini Clinic for Childhood Eating Disorders, Portland, OR, USA
Cleveland Clinic Children’s Hospital, Cincinnati, OH, USA
Creighton University, Omaha, NE, USA
Lund University Hospital, Lund, Sweden
Duke University Medical Center and Duke University, Durham, NC, USA
Childhood and adolescence are critical periods of neural development and physical growth. The malnutrition and related
medical complications resulting from eating disorders such as anorexia nervosa (AN), bulimia nervosa (BN) and eating
disorder not otherwise specified may have more severe and potentially more protracted conseque nces during youth than
during other age periods. The consensus opinion of an international workgroup of experts on the diagnosis and treatment of
child and adolescent eating disorders is that (a) lower an d more developmentally sensitive thresholds of symptom severity (e.g.
lower frequency of purging behaviours, significant deviations from growth curves as indicators of clinical severity) be used as
diagnostic boundaries for children and adolescents, (b) behavioural indicators of psychological features of eating disorders be
considered even in the absence of direct self-report of such symptoms and (c) multiple informants (e.g. parents) be used to
ascertain symptom profiles. Collectively, these recommendations will permit earlier identification and intervention to prevent
the exacerbation of eating disorder symptoms. Copyright # 2010 John Wiley & Sons, Ltd and Eating Disorders Association.
eating disorders; classification; children; adolescents; malnutrition
N. Zucker, Department of Psychiatry and Behavioral Sciences, Duke University Medical Center, P. O. 3842, Durham, NC 27705, USA. Tel:
1-919-308-9140; Fax: 1-919-681-7347.
Published online in Wiley InterScience ( DOI: 10.1002/erv.994
Eur. Eat. Disorders Rev. 18 (2010) 79–89 ß 2010 John Wiley & Sons, Ltd and Eating Disorders Association. 79
Anorexia nervosa (AN), bulimia nervosa (BN) and
related eating disorders are psychiatric syndromes that
convey significant risk for medical problems, particu-
larly among youth. AN has a point prevalence of 0.48–
0.7% in adolescent females (Ackard, Fulkerson, &
Neumark-Sztainer, 2007; Hoek, 2006; Hoek & van
Hoeken, 2003). BN occurs in approximately 1–2% of
the adolescent population while clinically significant
bulimic behaviours occur in an additional 2–3% (Hoek
& van Hoeken, 2003). Lewinsohn, Striegel-Moore, and
Steeley (2001) indicate that while the hazard rates for a
diagnosis of AN peak between the ages of 16–17 years,
slopes begin increasing around the age of 10 years
old. For BN, a disorder that was previously reported
to have a later age of onset than AN, the pattern is
similar. The view put forward in this paper is that
the current diagnostic classification system requires
greater sensitivity to the expression of disordered
eating in children and adolescents (Cooper, Watkins,
Bryant-Waugh, & Lask, 2002; Nicholls, Chater, & Lask,
Disturbances in nutrition may be particularly harmful
during vulnerable periods of brain development and
physical growth. Adolescence is well-recognized as a
period of profound alteration in multiple influential
domains: the physical changes of puberty, the social
changes associated with increased peer influence, the
increased opportunities to engage in both maladaptive
and adaptive decisionsall against a backdrop of
intensified emotional reactivity (Casey, Getz, & Galvan,
2008; Casey, Giedd, & Thomas, 2000; Giedd et al., 1996;
Giedd et al., 1999). Many of these changes are
instantiated at the neural level. Accumulating evidence
supports the observation that extensive neural remo-
delling and synaptic pruning occurs in the developing
adolescent brain (Gogtay et al., 2004). Particularly,
brain structures associated with motivated states and
emotional experience have been reported to develop
more rapidly than distributed neural circuitry associ-
ated with cognitive control, a developmental divergence
that has been proposed to account, in part, for the
increase in maladaptive decisions that occur during this
developmental window as emotions hold more sway
than rational cognition. Adaptive negotiation of this
period leads to flexible, adaptive responding, i.e. the
ability to use emotion to guide decisions, not dictate
them (Ochsner & Gross, 2005).
To be sure, these are challenges of typical adolescents.
Any insult or trauma during this period of vulnerability
greatly complicates these developmental challenges,
while trauma or neglect prior to this period may cause
divergence from a healthy developmental trajectory that
becomes potentiated via the maturational processes of
adolescence (Cook, Ciorciari, Varker, & Devilly, 2009;
De Bellis & Kuchibhatla, 2006). Frank malnutrition or
the threat of self-imposed malnutrition (whether or not
it is actually realized) are traumatic experiences that
threaten the well-being and physical status at any stage
of development. It stands to reason that nutritional
disturbance or deficit, defining features of eating
disorders, during particularly vulnerable developmental
periods can result in excessive and potentially
permanent physical and psychological consequences
(De Souza, 2006). As adequate nutrition is the necessary
substrate for all biological growth, the fact that the
malnutrition of eating disorders principally begins in
adolescence and can also onset prior to adolescence
necessitates flexibility in diagnostic boundaries based
on developmental stage. Modifications to adult-defined
boundaries of illness are needed to address the
associated morbidity in the short term and to prevent
more serious morbidity in the longer term (Eisle, Dare,
Russell, Szmukler, le Grange, & Dodge, 1997; Madden,
Morris, Zurynski, Kohn, & Eliot, 2009; Peebles, Wilson,
& Lock, 2006). The failure to capture unique age-
sensitive nuances of eating disturbance impedes case
identification and the opportunity for early interven-
tion. Further, insensitivity to the developmental
expression of nutrition inadequacy obscures differential
diagnosis and inhibits identification and differentiation
of related clinically significant childhood nutritional
presentations and disorders (Cooper et al., 2002;
Nicholls, Christie, Randall, & Lask, 2001; Watkins &
Lask, 2002). This paper is intended to address these
important issues by proposing changes to diagnostic
criteria delineated in the current edition of Diagnostic
and Statistical Manual of Mental Disorders (DSM-IV;
American Psychiatric Association, 1994) to reflect
pivotal developmental manifestations of symptom
expression in children and adolescents. While this
opinion was framed while considering the criteria
outlined in the DSM-IV specifically, the issues
80 Eur. Eat. Disorders Rev. 18 (2010) 79–89 ß 2010 John Wiley & Sons, Ltd and Eating Disorders Association.
Eating Disturbance in Children and Adolescents T. Bravender et al.
addressed are also germane to current revisions being
considered for revisions to the International Statistical
Classification of Diseases and Related Health Problems
(ICD-10; World Health Organization, 2004).
A realistic goal for the current revision to the DSM-IV is
the creation of empirically validated amendments to
existing criteria that characterize developmentally
sensitive alterations in symptom expression seen in
children and adolescents. There are important gaps in
the current research literature pertaining to child and
adolescent eating disorder diagnosis as summarized by
the following research questions. First, do eating
disorders described in the DSM-IV appear in childhood
in a similar manner to adults? If so, an adult with AN
and a child with AN would present with the same
features. Second, do currently defined DSM-IV
diagnoses appear in childhood and young adolescence,
yet manifest in ways developmentally consistent with
cognitive and emotional maturity? If so, a child can be
diagnosed with AN, but given, as an example,
maturational limitations in abstract reasoning, she
might be unable to identify or articulate the fears of
fatness associated with adult illness manifestations and
thus displays a child-specific manifestation of AN.
Nevertheless, her behaviour might be entirely consist-
ent with avoidance of any weight gain. Third, do
children and adolescents manifest different eating
disorders than described in older samples? For example,
dietary restriction and weight loss without the stated
fear of fatness may be a different psychological entity
entirely to AN, and might not be associated with
concerted efforts to avoid gaining weight. The working
group determined the body of evidence was too limited
to adequately adjudicate novel and separate diagnoses
in children and adolescents (question 3), but con-
sidered this an area for future research. However, there
is evidence that, in some cases, eating disorders as
expressed in childhood and adolescence differ from
their adult-expressed counterparts (question 1). Thus,
our goal with this paper is to consider the current body
of research in disordered eating in children and
adolescents, to view the current diagnostic criteria in
light of cognitive and developmental milestones of
childhood and adolescence, and to integrate this body
of evidence to arrive at proposed developmentally
sensitive adaptations of existing criteria (question 2).
Recommended changes to
existing cognitive criteria
in AN and BN
Recommendation 1: Behavioural indicators should be
permitted to substitute for internally referenced
cognitive criteria.
Recommendation 2: Wording should be added that
alerts healthcare professionals to developmental
limitations that may preclude the ability to endorse
a cognitive criterion.
Diagnostic criteria for eating disorders that require
complex abstract reasoning may not be valid for
children or adolescents. Formal thought is defined as
the ability to integrate two or more lower-order,
concrete processes to arrive at an intangible higher
order process (e.g. refusing food and exercising
excessively to manage fears of being overweight)
(Marini & Case, 1994). In typically developing
adolescents, formal thought emerges around 11–13
years old, while complex abstract reasoning continues
to evolve into late adolescence (Rosso, Young, Femia, &
Yurgelun-Todd, 2004). Capacity for complex abstract
reasoning is necessary to meet current criteria. For
example, to determine the value of body weight and
appearance in the determination of self-worth, an
individual needs to rank several abstract constructs
(such as trustworthiness, loyalty, attractiveness and
interpersonal competence) pertinent to self-evaluation.
This capacity to describe internal experiences or
compare and articulate multiple abstract concepts are
not present in some children and adolescents.
The ability to perceive risk also continues to evolve
throughout adolescence (Boyer, 2006). Risk perception
requires a child or adolescent to appreciate relative
probabilities and to weigh these relative perceptions
both immediately and in the future (Boyer, 2006). For
example, Criterion C for AN relates to denial of the
seriousness of low body weight (Table 1). To perceive
the seriousness of low body weight, a child must be able
to consider the risk of their current weight relative to
the risk of an alternative weight (such as being normal
weight or overweight) and to project the long-term
serious implications of this weight. While research has
been inconsistent, a conservative interpretation is that
some preadolescents have difficulty perceiving the
Eur. Eat. Disorders Rev. 18 (2010) 79–89 ß 2010 John Wiley & Sons, Ltd and Eating Disorders Association. 81
T. Bravender et al. Eating Disturbance in Children and Adolescents
relative risk of alternative outcomes (Levin & Hart,
2003), while both young and older adolescents may
exhibit difficulties in appreciating distal negative
Behavioural indicators may serve as valid substitutes
when internal experiences cannot be articulated in a
manner consistent with adult presentations. Impor-
tantly, we cannot distinguish whether lack of endorse-
ment of a cognition-based criterion is due to
developmental insensitivity or to differences in symp-
tom expression. However, given aforementioned
limitations in cognitive development, behavioural
indicators should be permitted to serve as substitutions
for reliable descriptions of internal experiences. For
example, severe and determined food restriction or
selectivity that is designed to yield a low body weight
(e.g. refusal to eat any fat or carbohydrates) could be
considered as a proxy for expressed fear of weight gain.
There are several precedents for this type of accom-
modation within the existing body of DSM-IV criteria
(e.g. anxiety disorders). Moreover, parents or other
caregivers can be enlisted as additional informants in
assessing the presence and severity of behavioural
indicators of the psychological features of AN and BN, a
strategy utilized in measures of other forms of
psychopathology in children and adolescents (e.g.
depression) (Table 1).
Changes to weight loss criterion
in AN
Recommendation 3: Wording should be added to
existing weight loss criteria that emphasizes the
importance of an individual’s previous growth and
maturational trajectory in the determination of
healthy weight status rather than population-refer-
enced cut point in the determination of clinical
While extreme weight loss or failure to make
expected weight gain is a clinically significant symptom
of AN (de Monleon et al., 1998), the sensitivity of
current weight criteria in the detection of clinical
severity has been questioned by numerous empirical
investigations, professional organizations and national
treatment guidelines (Hebebrand, Casper, Treasure, &
Schweiger, 2004; Nicholls & Stanhope, 2000). Malnu-
trition has been convincingly demonstrated to nega-
tively impact every system of the body both in
individuals with AN and those who are malnourished
due to environmental or medical causes (de Monleon
et al., 1998; Misra et al., 2004; Misra et al., 2005; Misra
et al., 2006; Nicholls & Stanhope, 2000). Of importance,
however, is that the timing of severe weight loss may
have more damaging effects at certain pivotal periods of
development and may argue for more conservative
definitions of weight loss during these sensitive periods
(Nicholls, Wells, Singhal, & Stanhope, 2002). To
illustrate, Peebles, Wilson, and Lock (2006) compared
children with AN, defined as 13 years of age or younger,
with older adolescent patients. Children were reported
to exhibit a lower percentage ideal body weight, a
shorter duration of illness, and a shorter temporal
trajectory of weight loss (Peebles et al., 2006), high-
lighting the rapidity with which weight loss may confer
potential harm. To be sure, a prepubescent child is
likely to have lower fat stores than an adult (Nicholls
et al., 2002).Thus, milder percentage weight loss may
Table 1 Symptoms in current eating disorder diagnoses that reference cognitive events or experiences
AN Criterion B: Intense fear of gaining weight, or becoming fat, even though underweight
Children may not verbally endorse fear of fatness despite determined food refusal (of a quantitative and/or qualitative nature) that results in
severe weight loss. This may either be a manifestation of anorexia nervosa in younger ages or reflect an alternative diagnosis. Specific fear of
weight gain or compensatory behaviours may become apparent once weight restoration efforts commence. Behavioural indicators and/or
parental report should serve as valid sources of information for this criterion.
AN Criterion C: Disturbance in the way in which one’s body weight or shape is experienced, undue influence of body weight
and shape on self-evaluation, or denial of the seriousness of the current low body weight
Children and young adolescents may lack the capacity to appreciate abstract concepts such as self-worth or to describe the experience of
their bodies in other than concrete or somatic terms. Children and both younger and older adolescents have a reduced capacity for general
risk appraisal, and thus may fail to appreciate the specific risk of extreme weight loss behaviours.
BN Criterion D: Self-evaluation is unduly influenced by body shape and weight
Children and young adolescents may lack the capacity to appreciate abstract concepts such as self-worth or to describe the experience of
their bodies in other than concrete or somatic terms.
82 Eur. Eat. Disorders Rev. 18 (2010) 79–89 ß 2010 John Wiley & Sons, Ltd and Eating Disorders Association.
Eating Disturbance in Children and Adolescents T. Bravender et al.
have more immediate negative impact such as severe
dehydration (Nicholls et al., 2002; Peebles et al., 2006).
Of importance, while an adult needs to resolve
symptoms to improve health, children and adolescents
continue to grow and develop somatic processes with
high-energy demands. Increased nutrition is necessary
during this critical window to enable these processes to
occur. To illustrate, malnourishment during adoles-
cence is associated with low turnover of bone with
increased bone resorption without concomitant bone
formation, a pattern different from that seen in
menopausal women (Lennkh et al., 1999). While
weight restoration is an important determinant of
bone mineral density, there appears to be a critical
window during which such repair can occur (Brooks,
Ogden, & Cavalier, 1998; Valla, Groenning, Syversen, &
Hoeiseth, 2000). To avoid the negative impact of
malnourishment and to reflect the valid nutritional
status of a child or adolescent adequately, developmen-
tally sensitive definitions are required to ensure
children are able to access appropriate treatment.
Accordingly, an alternative strategy to reliably define
ideal weight for children and adolescents is to consider
developmental trends in growth and physical maturity
for that individual. To be sure, current weight criteria
were never meant to be interpreted literally, but rather
to be used as a guide to determine when an individual’s
weight history warranted concern. In practice, however,
these guidelines are far too often literally interpreted
with potentially deleterious consequences as individuals
may be denied access to care by third party payers due
to failure to meet an arbitrary defined threshold. Thus,
upcoming revisions have two challenges. First, weight
criteria should be framed in a manner that is
developmentally sensitive. Second, criteria must be
framed so that they are clinically useful with no
potential for misuse. Combined, such precautions
would ensure that those who need care are not denied
such treatment based on their weight loss history.
Current diagnostic complexity is due, in part, to the
challenge of defining an optimal weight range for a
growing child or adolescent. The degree of variation in
physical development at any one age during puberty is
wide; for example, some children may be prepubertal,
while others may have reached full adult maturity by the
age of 12. With regard to eating disorders, this range can
be widened further, since underweight can result in
pubertal delay or interruption. An average 16 year old
female, with the onset of menarche at 12.5 years of age,
could therefore have reached full adult height and
weight, and thus be appropriately compared to centile
charts or reported as standard deviations from
population medians. However, if the eating disorder
onsets early, she may still have the height of an 11 or 12
year old, making weight centiles more difficult to
interpret. This is mainly an issue for premenarcheal
onset AN, since linear growth decelerates after
menarche with an average height gain averaging
approximately 7 cm (2.8 inches) (Rosen, 2004). Further
complicating this issue is that while there are strong
correlations between degree of emaciation and the
frequency and severity of the medical sequelae of
starvation, there is no ‘threshold’ effect below which
signs and symptoms of malnutrition occur (Swenne &
Engstrom, 2005).
Reporting nutritional status in terms of BMI
standard deviation units or centiles (or %BMI)
provides an additional strategy to address problems
with interpretation of weight by adjusting weight for
height, age and sex. Many countries now have their own
national reference centile charts for BMI for age.
International BMI cut-offs for child overweight and
obesity have been developed, and recently Cole, Flegal,
Nicholls, and Jackson (2007) used similar methodology
in order to improve international comparison of BMI
in underweight growing children. While these guide-
lines provide a laudable advance in increasing the
consistency in the definition of thinness across the
developmental spectrum, such reference BMI centiles
only account for age and sex and do not take
developmental maturity into account. Finally, as
evidence of the potential for harm when criteria are
interpreted literally, Madden et al. (2009) characterized
the expression of early onset eating disorders in a
nationally representative sample of 5–13 year old
Australian youth. Of importance, while only 51% met
current weight criteria as defined by current diagnostic
criteria, 61% had life-threatening complications of
malnutrition (Madden et al., 2009). Accommodation
for individual developmental trends is needed (Table 2).
Changes to amenorrhea
requirement in AN
Recommendation 5: Multiple physical systems should
be evaluated for the clinical management of eating
disturbance, but no single system should be required
for diagnosis.
Eur. Eat. Disorders Rev. 18 (2010) 79–89 ß 2010 John Wiley & Sons, Ltd and Eating Disorders Association. 83
T. Bravender et al. Eating Disturbance in Children and Adolescents
The requirement of amenorrhea in the diagnosis of
AN is invalid for prepubescent children (Nicholls et al.,
2000) inappropriate for males (Abraham, Pettigrew,
Boyd, Russell, & Taylor, 2005), and is not reliably
reported by patients (Abraham et al., 2005; Swenne,
Belfrage, Thurfjell, & Engstrom, 2005). The inadequacy
of this criterion is widely accepted (National Institute
for Clinical Excellence, 2004; Society for Adolescent
Medicine, 2003) as research investigations with both
adolescents and adults do not consistently require this
feature in defining their clinical populations, (Lock,
Couturier, & Agras, 2006; Walsh et al., 2006). Further,
treatment recommendations from professional organ-
izations advise clinicians that while medical signs,
symptoms and complications help characterize the
clinical picture, they are not sufficient for diagnosis
(National Institute for Clinical Excellence, 2004). Thus,
what is the role or necessity of menstrual dysfunction in
the diagnosis of child and adolescent eating disorders
(ED)? The principle here is that for eating disturbance
to be clinically significant there must be some evidence
of physical risk or impairment. A review of the evidence
suggests a middle ground: A recommendation that
thorough diagnostic evaluation of children and adole-
scents take an expansive view of biological systems and
consider a diverse array of biological abnormalities as
contributing to the clinical picture of child and
adolescent diagnosis, but not mandating specific
abnormalities within a single system in the body for
The clinical profile of AN complicates determination
of sexual maturation rating. In females, the emaciated
physical state and low estrogen associated with AN may
reduce breast size and distort a healthcare professional’s
assessment of sexual maturity rating. In males, similar
regression may be witnessed in the effects of lowered
testosterone on rating of Tanner stage (Tanner &
Preece, 1998).
Dysfunction in diverse physical systems may provide
alternative or additional indicators of malnutrition
resulting from disturbed eating in children and
adolescents (Shamim, Golden, Arden, Filiberto, &
Shenker, 2003). Several laboratories have supported the
presence of significant medical abnormalities in diverse
biological systems in both inpatient (Shamim et al.,
2003) and outpatient (Misra et al., 2004) adolescents
with ED. Such variation demonstrates that there is not
likely to be one specific metabolic profile in children,
adolescents or adults with AN. Rather, there may be an
array of physiological signs in individuals with AN that
aid in diagnosis (Table 3).
Changes to binge eating criteria
in BN and binge eating disorder
Recommendation 6: The experience of loss of control
irrespective of the amount of calories consumed during
an eating episode should be considered the hallmark of
binge eating behaviour in children.
Table 3 Hypothalamic-pituitary axis dysfunction
Anorexia Criterion D: In post-menarcheal females, amenorrhea i.e. the absence of at least three consecutive cycles (A woman is
considered to have amenorrhea if her periods occur only following hormone replacement, e.g. estrogen administration)
The effects of malnutrition evidence great variability. Clinicians should evaluate changes in multiple systems (e.g. cardiac, endocrine,
gastrointestinal) for clinical management but refrain from using a single physical sequelae as a diagnostic requirement (in children and
Table 2 Weight criteria for the diagnosis of anorexia nervosa
AN Criterion 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 that expected)
In children and adolescents, consideration should be given to weight and height trends such as deviation from previous growth trajectories,
percentage of weight loss and/or BMI centiles for age, rather than reliance on particular weight values in the determination of clinical
threshold and severity.
In children and adolescents, the deleterious effects of weight loss may appear at a lower percentage weight lost relative to adults.
84 Eur. Eat. Disorders Rev. 18 (2010) 79–89 ß 2010 John Wiley & Sons, Ltd and Eating Disorders Association.
Eating Disturbance in Children and Adolescents T. Bravender et al.
Recommendation 7: Binge episodes should be a
persistent symptom for diagnosis, but a lower
frequency and duration are clinically significant in
children. Episodes should occur at least once a month
during the previous 3-month period for diagnosis.
Although adolescents with aberrant eating beha-
viours exhibit many features in common with adults,
indicators of disordered eating in children are age-
specific and require assessment strategies sensitive to
developmental context. In the DSM-IV (American
Psychiatric Association, 1994), binge eating is defined
by consumption of an excessively large amount of food
paired with the subjective experience of a loss of control
over eating (American Psychiatric Association, 2000).
Associated features of binge eating include the context
in which eating occurs (e.g. in private), affective states
that follow disturbed eating (e.g. shame and guilt), and
the physiological state of the individual (e.g. feeling
uncomfortably full following the episode). The assess-
ment of these behaviours and experiences in children
requires age-specific strategies. Such strategies include
the use of concrete examples and developmentally
sensitive metaphors (e.g. a loss of control is similar to ‘a
ball rolling down a hill’) (Tanofsky-Kraff, Yanovski,
Wilfley, Marmarosh, Morgan, & Yanovski, 2004). When
such strategies are employed, a subgroup of children
endorses symptom profiles consistent with adult defi-
nitions of binge eating. However, an additional group
endorses the subjective experience of loss of control
without accompanying excessive food intake. As high-
lighted by Marcus and Kalarchian (2003), the clinical
significance of loss of control relative to the quantity of
calories consumed may provide a more developmentally
valid index of aberrant eating. Indeed, in cross-sectional
studies, any loss of control eating (i.e. one or more
episodes) reported over the previous 4-week period is
associated with greater adiposity (Neumark-Sztainer &
Hannan, 2000; Tanofsky-Kraff et al., 2004); elevations in
psychiatric symptoms such as depression, anxiety and
body image disturbance (Glasofer et al., 2007; Tanofsky-
Kraff, Faden, Yanovski, Wilfley, & Yanovski, 2005);
excessive weight gain (Tanofsky-Kraff, Yanovski, Schvey,
Olsen, Gustafson, & Yanovski, 2009b); and increased
vulnerability to the abundant environmental triggers for
dysregulated eating such as excessive food availability
(Tanofsky-Kraff et al., 2009a). Thus, consistent with the
recommendations of Marcus and Kalarchian (2003) and
supported by recent findings about the clinical
implications of loss of control (Tanofsky-Kraff et al.,
2009b), it may be that the experience of loss of control is
an important consideration in the determination of
clinical impairment irrespective of the amount of food
Despite similar symptom presentations in children
and adolescents relative to adults, lower symptom
thresholds are recommended. Research characterizing
atypical eating patterns in adolescent BN and compar-
ing threshold to subthreshold forms of this disorder
indicate significant overlap in levels of impairment,
patterns of psychiatric comorbidity, (Binford & le
Grange, 2005; Eddy, Celio-Doyle, Hoste, Herzog, & Le
Grange, in press), and medical sequelae, (Le Grange,
Loeb, Van Orman, & Jellar, 2004) supporting the
inadequacy of current diagnostic thresholds. Indeed,
this finding is not unique to adolescents (Le Grange
et al., 2006). Current data suggest that the frequency
and duration criteria for binge eating and purging in
DSM-IV are not adequate (Crow, Agras, Halmi,
Mitchell, & Kraemer, 2002; Sullivan & Kendler,
1998). Further, specific boundaries distinguishing
subthreshold BN are extremely varied. Notwithstand-
ing, in children, there is added motivation to consider
lower thresholds for diagnosis given the greater impact
of similar medical sequelae at fragile developmental
stages. Evidence to date supports the clinical signifi-
cance of at least one episode of loss of control eating
occurring for 3 months, a recommendation describing
both a lower symptom frequency and shorter duration
of symptom expression. This practice is consistent with
other childhood diagnoses (e.g. for dysthymic disorder
the duration is 1 year instead of 2 years for adults). In
sum, aberrant eating in children and adolescents
overlaps significantly with adult manifestations, but
behaviours do differ. The conservative strategy is to
alert the healthcare community to divergent presenta-
tions and to consider a lower threshold of severity to
protect children and adolescents from harmful sequelae
of their disorders (Tanofsky-Kraff, Marcus, Yanovski, &
Yanovski, 2008) (Table 4).
Changes to criteria for
inappropriate compensatory
mechanisms in BN
Recommendation 8: Lower thresholds of both symptom
frequency and duration should be used to designate
Eur. Eat. Disorders Rev. 18 (2010) 79–89 ß 2010 John Wiley & Sons, Ltd and Eating Disorders Association. 85
T. Bravender et al. Eating Disturbance in Children and Adolescents
clinical levels of inappropriate compensatory mech-
anisms in children and adolescents.
Given the potential severity of extreme weight loss
strategies on growth and development, lower thresholds
of symptom severity are needed for children and
adolescents (Table 5). There is significant inter-
individual variation in the response to extreme weight
loss behaviours, variation that complicates the deter-
mination of a threshold of severity. For example, while
some children may manifest electrolyte abnormalities
with subthreshold levels of symptom frequency, for
others, laboratory results may fail to reveal significant
medical sequelae until a chronic disease course has
significantly progressed. Given the unpredictability of
relating symptom frequency and duration to medical
impairment, coupled with the severe cost of ‘missing’ a
serious disorder due to insensitive thresholds, the
conservative strategy is the consideration of lower
symptom thresholds for both symptom frequency and
symptom duration. This strategy would alert clinicians
to the serious nature of extreme weight loss behaviours
increasing the sensitivity of detection of severe clinical
Subthreshold levels of extreme weight loss behaviours
are clinically significant, predicting both increased
symptom severity as well as concurrent impairment in
functioning. For example, in a representative com-
munity sample of 2516 adolescents, Neumark-Sztainer,
Wall, Guo, Story, Haines, and Eisenberg (2006) report
that subthreshold levels of extreme weight loss
behaviour predict a one-point increase in BMI relative
to adolescents not engaging in these behaviours.
Further, the presence of these behaviours at baseline
resulted in a 3-fold increase in the likelihood of
overweight at follow-up. Individuals who engage in
extreme weight loss behaviours were less likely to
engage in health-promoting weight maintenance
strategies such as fruit and vegetable consumption
(Story, Neumark-Sztainer, Sherwood, Stang, & Murray,
1998). Several studies comparing the diagnosis of BN to
subthreshold forms of this disorder found no difference
in comorbid symptom severity or treatment response
(Binford & le Grange, 2005; Le Grange, Crosby,
Rathouz, & Leventhal, 2007; Schmidt et al., 2007).
These results portend harm: Adolescents engaging in
even subthreshold levels of extreme weight loss
strategies are positioned on a harmful trajectory
predictive of unhealthy weight management and
increased eating disturbance and appear to be as ill
as threshold forms of BN.
The purpose of the DSM ‘is to provide clear
descriptions of diagnostic categories in order to enable
clinicians and investigators to diagnose, communicate
about, study and treat people with various mental
Table 4 Binge eating
Bulimia Criterion A: Recurrent episodes of binge eating. An episode of binge eating is characterized by both of the
following:(1) 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. (2) 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)
In children and younger adolescents, the subjective experience of a loss of control may be a particularly robust indicator of aberrant eating
behaviour. However, care must be taken to ensure that children understand what is meant by loss of control through the use of
developmentally appropriate assessment strategies such as concrete examples or age-appropriate metaphors (e.g. the experience is ‘like a
ball rolling down a hill’ (Tanofsky-Kraff et al., 2004)). Behavioural indicators of loss of control eating such as secretive eating, food seeking in
response to negative affect and food hoarding should be considered in children younger than 12 years of age.
Given the prognostic significance of binge eating in children and young adolescents in relation to symptom severity and chronicity, a lower
threshold for diagnosis should be considered
Table 5 Compensatory behaviours
Bulimia Criterion B: Recurrent inappropriate compensatory behaviour in order to prevent weight gain, such as self-induced
vomiting; misuse of laxatives, diuretics, enemas or other medications; fasting or excessive exercise
In children and younger adolescents, a lower threshold of symptom frequency and duration should be considered due to potential for acute
medical sequelae in younger ages.
86 Eur. Eat. Disorders Rev. 18 (2010) 79–89 ß 2010 John Wiley & Sons, Ltd and Eating Disorders Association.
Eating Disturbance in Children and Adolescents T. Bravender et al.
disorders’ (p. xxxvii) (American Psychiatric Associ-
ation, 1994). The goal of this consensus opinion is to
improve the description of AN, BN and Eating Disorder
Not Otherwise Specified as they pertain to children and
adolescents, to improve case identification, treatment
and research efforts in that segment of the population at
highest risk for onset of these serious eating disorders.
In diagnosing child and adolescent eating disorders, the
data on proposed criteria modifications are convincing
and their import compelling, while the breadth of
research is relatively small. This is due, in part, to the
strategies that have been employed in the ascertainment
of childhood eating disturbance, i.e. extrapolating from
adult-defined symptoms. While clinically significant
but atypical presentations of eating disturbance also
appear prominently in the adult population, develop-
mental considerations increase the likelihood of such
symptom constellations obscuring true AN or BN
‘caseness’ among children and adolescents. The risks
secondary to misdiagnosis during key periods of growth
and development are grave. Advances in the diagnosis
and research of eating disturbance in children and
adolescents can only occur by adopting developmen-
tally sensitive frameworks and methodologies. We
recommend examining the topography and expression
of symptoms of relevance for eating disorders through
the lens of a developmental trajectory, and defining
child and adolescent eating pathology at the intersect of
deviation from both healthy development and adult-
defined diagnostic criteria.
This paper is in memory of Dr Mae Sokol-Burger whose
tireless efforts with young children and adolescents will
help us aid countless future children.
Abraham, S. F., Pettigrew, B., Boyd, C., Russell, J., & Taylor,
A. (2005). Usefulness of amenorrhea in the diagnoses of
eating disorder patients. Journal of Psychosomatic Obstetrics
and Gynecology, 26, 211–215.
Ackard, D. M., Fulkerson, J. A., & Neumark-Sztainer, D.
(2007). Prevalence and utility of DSM-IV eating disorder
diagnostic criteria among youth. International Journal of
Eating Disorders, 40, 409–417.
American Psychiatric Association. (1994). Diagnostic and
statistical manual of mental disorders (4th ed.). Washing-
ton, DC.
American Psychiatric Association. (2000). Diagnostic and
statistical manual of mental disorders-text revision
(4th ed.). Washington, DC: American Psychiatric
Binford, R. B., & le Grange, D. (2005). Adolescents with
bulimia nervosa and eating disorder not otherwise speci-
fied-purging only. International Journal of Eating Dis-
orders, 38, 157–161.
Boyer, T. W. (2006). The development of risk-taking: A
multi-perspective review. Developmental Review, 26, 291–
Brooks, E. R., Ogden, B. W., & Cavalier, D. S. (1998).
Compromised bone density 11.4 years after diagnosis
of anorexia nervosa. Journal of Women’s Health, 7,
Casey, B. J., Getz, S., & Galvan, A. (2008). The adolescent
brain. Developmental Review, 28, 62–77.
Casey, B. J., Giedd, J. N., & Thomas, K. M. (2000). Structural
and functional brain development and its relation to
cognitive development. Biological Psychology, 54, 241–
Cole, T. J., Flegal, K. M., Nicholls, D., & Jackson, A. A.
(2007). Body mass index cut-offs to define thinness in
children and adolescents International survey. British
Medical Journal, 335, 166–167.
Cook, F., Ciorciari, J., Varker, T., & Devilly, G. J. (2009).
Changes in long term neural connectivity following
psychological trauma. Clinical Neurophysiology, 120,
Cooper, P. J., Watkins, B., Bryant-Waugh, R., & Lask, B.
(2002). The nosological status of early onset anorexia
nervosa. Psychological Medicine, 32, 873–880.
Crow, S. J., Agras, W. S., Halmi, K., Mitchell, J. E., &
Kraemer, H. C. (2002). Full syndromal versus subthres-
hold anorexia nervosa, bulimia nervosa, and binge eating
disorder: A multicenter study. International Journal of
Eating Disorders, 32, 309–318.
De Bellis, M. D., & Kuchibhatla, M. (2006). Cerebellar
volumes in pediatric maltreatment-related posttraumatic
stress disorder.
de Monleon, J. V., Simonin, G., Giraud, P., Achache, F.,
Sokolowsky, M., Battista, M., et al. (1998). Statural
growth deficiency due to anorexia nervosa. A case in a
patient with an unaffected identical twin. Annales de
Pediatrie, 45, 702–706.
De Souza, R. G. (2006). Body size and growth: The signifi-
cance of chronic malnutrition among the Casiguran Agta.
Annals of Human Biology, 33, 604–619.
Eddy, K., Celio-Doyle, A., Hoste, R., Herzog, D., &
Le Grange, D. (2008). Eating disorder not otherwise
specified (EDNOS): An examination of EDNOS presen-
tations in adolescents. Journal of the American Academy of
Child and Adolescent Psychiatry, 47, 156–164.
Eur. Eat. Disorders Rev. 18 (2010) 79–89 ß 2010 John Wiley & Sons, Ltd and Eating Disorders Association. 87
T. Bravender et al. Eating Disturbance in Children and Adolescents
Eisler, I., Dare, C., Russell, G. F., Szmukler, G., le Grange, D.,
& Dodge, E. (1997). Family and individual therapy in
anorexia nervosa. A 5-year follow-up. Archives of General
Psychiatry, 54, 1025–1030.
Giedd, J. N., Blumenthal, J., Jeffries, N. O., Castellanos, F. X.,
Liu, H., Zijdenbos, A., et al. (1999). Brain development
during childhood and adolescence: A longitudinal MRI
study. Nature Neuroscience, 2(10), 861–863.
Giedd, J. N., Vaituzis, A. C., Hamburger, S. D., Lange, N.,
Rajapakse, J. C., Kaysen, D., et al. (1996). Quantitative
MRI of the temporal lobe, amygdala, and hippocampus in
normal human development: Ages 4–18 years. Journal of
Comparative Neurology, 366, 223–230.
Glasofer, D. R., Tanofsky-Kraff, M., Eddy, K. T., Yanovski,
S. Z., Theim, K. R., Mirch, M. C., et al. (2007). Binge
eating in overweight treatment-seeking adolescents. Jour-
nal of Pediatric Psychology, 32, 95–105.
Gogtay, N., Giedd, J. N., Lusk, L., Hayashi, K. M., Green-
stein, D., Vaituzis, A. C., et al. (2004). Dynamic mapping
of human cortical development during child through
early adulthood. Proceedings of the National Academy of
Sciences of the United States of America, 101, 8174–
Hebebrand, J., Casper, R., Treasure, J., & Schweiger, U.
(2004). The need to revise the diagnostic criteria for
anorexia nervosa. Journal of Neural Transmission, 111,
Hoek, H. W. (2006). Incidence, prevalence and mortality of
anorexia nervosa and other eating disorders. Current
Opinion in Psychiatry, 19, 389–394.
Hoek, H. W., & van Hoeken, D. (2003). Review of the
prevalence and incidence of eating disorders. Inter-
national Journal of Eating Disorders, 34, 383–396.
Le Grange, D., Binford, R. B., Peterson, C. B., Crow, S. J.,
Crosby, R. D., Klein, M. H., et al. (2006). DSM-1V
threshold versus subthreshold bulimia nervosa. Inter-
national Journal of Eating Disorders, 39, 462–467.
Le Grange, D., Crosby, R., Rathouz, P., & Leventhal, D.
(2007). A randomized controlled comparison of family-
based treatment and supportive psychotherapy for ado-
lescent bulimia nervosa. Archives of General Psychiatry, 64,
Le Grange, D., Loeb, K., Van Orman, S., & Jellar, C. (2004).
Adolescent bulimia nervosa: A disorder in evolution?
Archives of Pediatrics and Adolescent Medicine, 158, 478–482.
Lennkh, C., de Zwaan, M., Bailer, U., Strnad, A., Nagy, C.,
El-Giamal, N., et al. (1999). Osteopenia in anorexia
nervosa: Specific mechanisms of bone loss. Journal of
Psychiatric Research, 33, 349–356.
Levin, I. P., & Hart, S. S. (2003). Risk preferences in young
children: Early evidence of individual differences in reac-
tion to potential gains and losses. Journal of Behavioral
Decision Making, 16, 397–413.
Lewinsohn, P. M., Striegel-Moore, R. H., & Seeley, J. R.
(2001). Epidemiology and natural course of eating dis-
orders in young women from adolescence to young
adulthood. Journal of the American Academy of Child
and Adolescent Psychiatry, 39, 1284–1292.
Lock, J., Couturier, J., & Agras, W. S. (2006). Comparison of
long-term outcomes in adolescents with anorexia nervosa
treated with family therapy. Journal of the American
Academy of Child and Adolescent Psychiatry, 45, 666–672.
Madden, S., Morris, A., Zurynski, Y. A., Kohn, M., & Eliot,
E. J. (2009). Burden of eating disorders in 5-13-year-old
children in Australia. Medical Journal of Australia, 190,
Marcus, M. D., & Kalarchian, M. A. (2003). Binge eating in
children and adolescents. International Journal of Eating
Disorders, 34, S47–S57.
Marini, Z., & Case, R. (1994). The Development of Abstract
Reasoning About the Physical and Social World. Child
Development, 65, 147–159.
Misra, M., Aggarwal, A., Miller, K. K., Almazan, C., Worley,
M., Soyka, L. A., et al. (2004). Effects of anorexia nervosa
on clinical, hematologic, biochemical, and bone density
parameters in community-dwelling adolescent girls.
Pediatrics, 114, 1574–1583.
Misra, M., Miller, K. K., Stewart, V., Hunter, E., Kuo, K.,
Herzog, D. B., et al. (2005). Ghrelin and bone metabolism
in adolescent girls with anorexia nervosa and healthy
adolescents. Journal of Clinical Endocrinology and Metab-
olism, 90, 5082–5087.
Misra, M., Miller, K. K., Tsai, P., Gallagher, K., Lin, A., Lee,
N., et al. (2006). Elevated peptide YY levels in adolescent
girls with anorexia nervosa. Journal of Clinical Endocrin-
ology and Metabolism, 91, 1027–1033.
National Institute for Clinical Excellence. (2004). Core
interventions in the treatment and management of anor-
exia nervosa, bulimia nervosa, and related eating dis-
orders. Retrieved from
Neumark-Sztainer, D., & Hannan, P. J. (2000). Weight-
related behaviors among adolescent girls and boys: Results
from a national survey. Archives of Pediatrics & Adolescent
Medicine, 154, 569–577.
Neumark-Sztainer, D., Wall, M., Guo, J., Story, M., Haines,
J., & Eisenberg, M. (2006). Obesity, disordered eating, and
eating disorders in a longitudinal study of adolescents:
How do dieters fare 5 years later? Journal of the American
Dietetic Association, 106, 559–568.
Nicholls, D., Chater, R., & Lask, B. (2000). Children into
DSM don’t go: A comparison of classification systems for
eating disorders in childhood and early adolescence.
International Journal of Eating Disorders, 28, 317–324.
Nicholls, D., Christie, D., Randall, L., & Lask, B. (2001).
Selective eating: Symptom, disorder or normal variant.
Clinical Child Psychology and Psychiatry, 6, 257–270.
88 Eur. Eat. Disorders Rev. 18 (2010) 79–89 ß 2010 John Wiley & Sons, Ltd and Eating Disorders Association.
Eating Disturbance in Children and Adolescents T. Bravender et al.
Nicholls, D., & Stanhope, R. (2000). Medical complications
of anorexia nervosa in children and young adolescents.
European Eating Disorders Review, 8, 170–180.
Nicholls, D., Wells, J. C., Singhal, A., & Stanhope, R. (2002).
Body composition in early onset eating disorders. Euro-
pean Journal of Clinical Nutrition, 56, 857–865.
Ochsner, K. N., & Gross, J. J. (2005). The cognitive control of
emotion. Trends in Cognitive Sciences, 9, 242–249.
Peebles, R., Wilson, J. L., & Lock, J. D. (2006). How do
children with eating disorders differ from adolescents
with eating disorders at initial evaluation? Journal of
Adolescent Health, 39, 800–805.
Rosen, D. S. (2004). Physiologic growth and development
during adolescence. Pediatrics in Review, 25, 194–200.
Rosso, I. M., Young, A. D., Femia, L. A., & Yurgelun-Todd,
D. A. (2004). Cognitive and emotional components of
frontal lobe functioning in childhood and adolescence. In
R. E. Dahl, & S. E. Spear (Eds.), Adolescent brain develop-
ment: Vulnerabilities and opportunities (pp. 355–362).
New York, NY: New York Academy of Sciences.
Schmidt, U., Lee, S., Beecham, J., Perkins, S., Treasure, J., Yi,
I., et al. (2007). A randomized controlled trial of family
therapy and cognitive behavior therapy guided self-care
for adolescents with bulimia nervosa and related dis-
orders. American Journal of Psychiatry, 164, 591–598.
Shamim, T., Golden, N. H., Arden, M., Filiberto, L., &
Shenker, I. R. (2003). Resolution of vital sign instability:
An objective measure of medical stability in anorexia
nervosa. Journal of Adolescent Health, 32, 73–77.
Society for Adolescent Medicine. (2003). Eating disorders in
adolescents. Journal of Adolescent Health, 33, 496–503.
Story, M., Neumark-Sztainer, D., Sherwood, N., Stang, J., &
Murray, D. (1998). Dieting status and its relationship to
eating and physical activity behaviors in a representative
sample of US adolescents. Journal of the American Dietetic
Association, 98, 1127–1132.
Sullivan, P. F., & Kendler, K. S. (1998). Typology of common
psychiatric syndromes. An empirical study. British Journal
of Psychiatry, 173, 312–319.
Swenne, I., Belfrage, E., Thurfjell, B., & Engstrom, I. (2005).
Accuracy of reported weight and menstrual status in
teenage girls with eating disorders. International Journal
of Eating Disorders, 38, 375–379.
Swenne, I., & Engstrom, I. (2005). Medical assessment of
adolescent girls with eating disorders: An evaluation of
symptoms and signs of starvation [see comment]. Acta
Paediatrica, 94, 1363–1371.
Tanner, J. M. & Preece M. A. (Eds.). (1998). The physiology
of human growth (Vol. Symposium 29). Cambridge:
Cambridge University Press.
Tanofsky-Kraff, M., Faden, D., Yanovski, S. Z., Wilfley,
D. E., & Yanovski, J. A. (2005). The perceived onset of
dieting and loss of control eating behaviors in overweight
children. International Journal of Eating Disorders, 38,
Tanofsky-Kraff, M., Marcus, M. D., Yanovski, S. Z., &
Yanovski, J. A. (2008). Loss of control eating disorder
in children age 12y and younger: Proposed research
criteria. Eating Behaviors, 9, 360–365.
Tanofsky-Kraff, M., McDuffie, J. R., Yanovski, S. Z.,
Kozlosky, M., Schvey, N. A., Shomaker, L. B., et al.
(2009a). Laboratory assessment of the food intake of
children and adolescents with loss of control eating.
American Journal of Clinical Nutrition, 89, 738–745.
Tanofsky-Kraff, M., Yanovski, S. Z., Schvey, N. A., Olsen,
C. H., Gustafson, J., & Yanovski, J. A. (2009b).
A prospective study of loss of control eating for
body weight gain in children at high risk for adult
obesity. International Journal of Eating Disorders, 42,
Tanofsky-Kraff, M., Yanovski, S. Z., Wilfley, D. E., Marmar-
osh, C., Morgan, C. M., & Yanovski, J. A. (2004). Eating-
disordered behaviors, body fat, and psychopathology in
overweight and normal-weight children. Journal of Con-
sulting and Clinical Psychology, 72, 53–61.
Valla, A., Groenning, I. L., Syversen, U., & Hoeiseth, A.
(2000). Anorexia nervosa: Slow regain of bone mass.
Osteoporosis International, 11, 141–145.
Walsh, B. T., Kaplan, A. S., Attia, E., Olmsted, M., Parides,
M., Carter, J. C., et al. (2006). Fluoxetine after weight
restoration in anorexia nervosaA randomized con-
trolled trial. Journal of the American Medical Association,
295, 2605–2612.
Watkins, B., & Lask, B. (2002). Eating disorders in school-
aged children. Child and Adolescent Psychiatric Clinics of
North America, 11, 185–199.
World Health Organization. (2004). International statistical
classification of diseases and related health problems,
10th Revision (2nd ed.). Geneva: World Health
Eur. Eat. Disorders Rev. 18 (2010) 79–89 ß 2010 John Wiley & Sons, Ltd and Eating Disorders Association. 89
T. Bravender et al. Eating Disturbance in Children and Adolescents
    • "This change mostly stemmed from evidence that a substantial proportion of patients with anorexia nervosa do not endorse fear of gaining weight/fatness. In particular, there is evidence that non-Western and younger presentations are less likely to express fear of gaining weight/fatness [18, 3]. This shift is therefore particularly important for children and young adolescents. "
    Full-text · Article · Sep 2015
    • "However , when using the previous DSM-IV nomenclature (American Psychiatric Association, 2000), 40% to 60% of people seeking treatment for an ED fell into the eating disorder not otherwise specified (EDNOS) category, with clinical features similar to those seen in AN or BN, albeit at varying degrees of acuity or in different symptom combinations (Fairburn & Bohn, 2005; Fairburn et al., 2007; Peebles et al., 2010). Further, it has been argued that the DSM-IV criteria did not adequately capture ED symptoms in children and adolescents (Bravender et al., 2010). For example, in a US nationwide study, Le Grange et al. found that 81% of adolescents with an ED were classified as having EDNOS, making it overwhelmingly the most common ED diagnosis in this age group (Le Grange et al., 2012). "
    [Show abstract] [Hide abstract] ABSTRACT: Objectives: DSM-5 changes for eating disorders (EDs) aimed to reduce preponderance of non-specified cases and increase validity of specific diagnoses. The objectives were to estimate the combined effect of changes on prevalence of EDs in adolescents and examine validity of diagnostic groupings. Method: A total of 3043 adolescents (1254 boys and 1789 girls, Mage = 14.19 years, SD = 1.61) completed self-report questionnaires including the Eating Disorder Diagnostic Scale. Results: Prevalence of full-threshold EDs increased from 1.8% (DSM-IV) to 3.7% (DSM-5), with a higher prevalence of bulimia nervosa (1.6%) and the addition of the diagnosis of purging disorder (1.4%); prevalence of binge eating disorder was unchanged (0.5%), and non-specified cases decreased from 5.1% (DSM-IV) to 3.4% (DSM-5). Validation analyses demonstrated that DSM-5 ED subgroups better captured variance in psychopathology than DSM-IV subgroups. Discussion: Findings extend results from previous prevalence and validation studies into the adolescent age range. Improved diagnostic categories should facilitate identification of EDs and indicate targeted treatments.
    Article · Dec 2014
    • "Such measures, which although currently awaiting tests of reliability and validity , may move towards addressing the deficiencies in our field in assessing the eating disorder pathology of adolescents in FBT. They may also lie in accordance with broader changes to be introduced in DSM-5, which allow for more behavioural indicants of the psychological features of AN (Bravender et al., 2011). Thus, we recommend that future research trials adopt measures which index parental reports of their child's eating disorder pathology. "
    Full-text · Article · Jan 2014
Show more