Eating disorders in school-aged children

Eating disorders in school-aged children

Beth Watkins, BSca,b,*,Bryan Lask, FRC Psych, FRCPCH, Mphila,c

aDepartment of General Psychiatry, St. George’s Hospital Medical School,

Cranmer Terrace, London SW17 ORE, UKbDepartment of Psychology, University of Reading, Early Gate, Whiteknights,

Reading RG6 6AL, UKcHuntercombe Manor Hospital, Huntercombe Lane South, Taplow,

Maidenhead, Berkshire SL6 OPQ, UK

Eating disorders that occur in childhood are not a new phenomenon. As early

as 1894, The Lancet published a short report concerning a 7-year-old girl who

suffered anorexia nervosa (AN) [15]. Eating disorders have since been reported in

prepubertal children of both sexes [19,25,32]. It seems, however that not all these

children fulfilled existing accepted diagnostic criteria for eating disorders as

stated in ICD-10 [75] or DSM-IV [1].

Confusion has arisen over whether the symptomatology of childhood-onset

eating disorders differs from that in older adolescents and adults. This confusion

has been fuelled by the fact that children who present with restricted eating and

emaciation often receive a diagnosis of AN despite being described as a

heterogeneous group [19,25,28,32]. Given that these disorders occur in children,

many of whom are prepubertal, the question arises of whether the core dis-

turbances in cognitions concerning body weight and shape, which are the hallmark

of the eating disorders of later onset [1], are manifested by these patients. The

question of whether such overvalued ideas are present in children with ‘‘eating

disorders’’ of childhood onset is not answered by the case series that have been

reported to date [19,25,31,32].

The picture is complicated further by the continuum of eating and feeding

difficulties that can occur from birth onward. Weaning problems, selective eating

patterns, and food faddiness in infants and preschool-aged children are relatively

common and generally need not to be a cause for concern, because in most cases, a

child’s growth and development are unaffected [6]. Children usually outgrow

these difficulties, but if they do not, they should be considered more seriously.

1056-4993/02/$ – see front matter D 2002, Elsevier Science (USA). All rights reserved.

PII: S1056 -4993 (01 )00003 -7

* Corresponding author. Department of General Psychiatry, St. George’s Hospital Medical

School, Cranmer Terrace, London SW17 ORE, UK.

E-mail address: [email protected] (B. Watkins).

Child Adolesc Psychiatric Clin N Am

11 (2002) 185–199

Whereas it is developmentally appropriate for an infant to experience these dif-

ficulties as a means of experimentation with new tastes and textures and testing the

impact of their behavior on their care givers, in older children feeding and eating

problems are developmentally inappropriate. By this time, the child’s cognitive

development is much more sophisticated, and eating problems are much more

likely to be related to underlying psychologic issues.

The accounts of the clinical features of eating disorders of childhood onset

suggest that the patients described may well constitute a heterogeneous group. For

example, Fosson et al [19] reported that only 56% of their series of patients with

early-onset AN gave a fear of fatness (a core feature of classic eating disorders) as

their main reason for refusing food. The two attempts to compare the clinical

features of a group of patients with early-onset AN to those with later onset [25,32]

also pointed to heterogeneity among the younger group. Despite the methodologic

limitations of these studies, the findings suggest distinct subgroups within these

younger patients. This finding led Lask and Bryant-Waugh [40] to argue that

various atypical eating disorders of childhood must be distinguished from true AN

of childhood onset; however, these disorders have yet to be studied in depth. These

atypical childhood-onset eating disorders and childhood-onset AN and bulimia

nervosa (BN) are briefly described in the following discussion.

Childhood-onset anorexia nervosa

The age at which a child goes through puberty varies from child to child and is

a complex process that spans 2 to 3 years [66]. It is wise to consider the onset of

AN as ‘‘early’’ or ‘‘late’’ in terms of pubertal development rather than age [57].

Childhood-onset (or early-onset) AN is characterized by determined attempts to

lose weight or avoid weight gain by restricted food intake, self-induced vomiting,

laxative abuse, excessive exercising, or more usually, a combination of one or

more of these practices. Children with AN also often fail to maintain hydration

[31] and may need urgent rehydration. Weight loss in prepubertal children is

worrying because they have relatively low body fat levels. Children also must

maintain a healthy body mass index to support growth and development.

Incidence and prevalence

No epidemiologic studies have focused solely on childhood-onset AN. A large

study of the incidence of AN was conducted by Rastam et al [54], however, who

screened the entire population of schoolchildren in Goteborg, Sweden. They found

that in the population of 4291 children, 17 had AN, 3 had a partial AN syndrome,

and 3 had BN. The accumulated prevalence for AN (those who had or had had the

disorder) was 0.84%. Crisp et al [17] conducted a survey of London private girls’

schools (believed to be a high-risk group) and found an incidence of AN of only

0.2% in girls aged 15 years or younger. In adolescence, the prevalence rate of AN

is estimated at 0.1% to 0.2% [2,74], but this is almost certainly lower in children

[10]. Although there is no firm evidence of an increase in the incidence of AN of

B. Watkins, B. Lask / Child Adolesc Psychiatric Clin N Am 11 (2002) 185–199186

childhood onset in the last 40 years, there has certainly been an increase in

referrals, as evidenced by rates of referral to Great Ormond Street Hospital. In the

1960s there were one or two referrals per annum, and by 1994, the clinic had

25 referrals in the first 6 months of the year [10].

Sex ratio

Studies of AN in adults and adolescents consistently have shown that 90% to

95% of patients are female [20]. Studies of childhood-onset AN reveal more boys

relative to the number of girls than would be expected. Some studies report as

many as 19% to 30% of boys, although some of these studies reported their sample

to be heterogeneous, which suggests that not all the children in the studies had

‘‘true’’ childhood-onset AN [8,19,26,28,32]. Swift [64] reported similar sex ratios

in childhood-onset AN to the adult and adolescent studies, finding an overall sex

ratio of girls to boys of 9.5 to 1.

Social class bias

Fosson et al [19] have reported that 22 of the 48 children included in their

study came from the higher social classes, whereas Gowers et al [25] reported

that 80% of the 30 children in their study with premenarchal onset had higher

social class backgrounds. Some authors, however, have suggested that for AN

in general, this social class bias is becoming less pronounced over the past

decade [20]. Equally, there are suggestions that more advantaged families have

easier access to health services, although as Lask and Bryant-Waugh [38]

pointed out, this assertion has yet to be tested experimentally in the context of

eating disorders.

Prognosis and outcome

Outcome studies of children and adolescents with AN consistently have

reported a good outcome in one half to two thirds of cases [9,26]. Widely

varying results are reported regarding the prognostic factors, however [47]. For

example, factors that have been associated with a good outcome include (1) good

relationships between the child and the parents [46], (2) short duration of

inpatient treatment [76], and (3) a short interval between onset and hospitalization

[12]. Some studies have shown an onset below the age of 11 years to be

associated with a poor outcome [71], whereas other studies found that the older

the age of onset the poorer the outcome [55].

Factors associated with a poor outcome include (1) depressive features [9], (2)

severe obsessive, riualistic, and social interaction problems [23], and (3) poor fam-

ily functioning [2]. Family functioning and disturbance in relationship between

the parents and their child seems to be recurring themes in the outcome of AN

regardless of age [12,30,50,55,60], but relationships measured vary widely

among studies.

B. Watkins, B. Lask / Child Adolesc Psychiatric Clin N Am 11 (2002) 185–199 187

Generally, for every study that identifies a group of prognostic factors, another

study fails to replicate the significance of those variables. These inconsistencies

and contradictions can be accounted for by methodologic differences and flaws,

including small sample sizes, poor recruitment (often only half the original sample

were followed up), inadequate preliminary intake information, and lack of use

of standardized structured assessment methods. Other methodologic shortcomings

in the existing literature include failure to specify diagnostic criteria and inad-

equate reporting of screening procedures and attrition rates [22].

The clinical presentation of true AN in childhood is similar to that in

adulthood. There has been some debate, however, as to whether these children

display the abnormal cognitions associated with weight and shape that are

characteristic of AN. This question has been tested using a standardized

diagnostic assessment tool, which is an adaptation of the eating disorder

examination [7,18]. Cooper et al [77] compared children with a prepubertal/

premenarchal onset to children who had a postpubertal/postmenarchal onset and

found that the two groups were indistinguishable in terms of weight and shape

concerns. It has been noted clinically, however [6], that boys do present slightly

differently from girls. Boys with AN tend to be more concerned about being

‘‘flabby’’ than fat and want to become more muscular rather than lose weight.

They often equate being overweight with being unhealthy rather than unattractive.

They are similar to girls, however, because they avoid eating foods that they

regard as fattening or unhealthy and usually exercise excessively, with the end

result being a significant weight loss.

Bulimia nervosa

Bulimia nervosa is rare in school-aged children. When it does occur, as with

adults, it is characterized by episodes of overeating in which the sufferer

experiences a loss of control. These episodes are usually followed by compen-

satory behaviors designed to avoid weight gain, for example, self-induced

vomiting, laxative or diuretic abuse, excessive exercising, and periods of fasting

or severe food restriction. The weight and shape concerns characteristic of AN are

also core features of BN. Sufferers of BN often engage in self-harm and have poor

self-image.

Although rare, Cooper et al [77] reported five cases of prepubertal BN,

whereas Bryant-Waugh [6] reported a 7-year-old child who received a clinical

diagnosis of BN. Previously, Bryant-Waugh and Lask [10] reported a referral

rate of up to five cases per year of BN with an onset below the age of 14 years,

which represented approximately 10% of their annual referrals. Many women

with BN, who typically only present for treatment after many years of having

the disorder, often report that their bulimia started in early adolescence, which

suggests that the disorder can remain ‘‘hidden’’ for many years. Although BN

has been reported in men [45], there have been virtually no reports of this

disorder in boys.


Atypical childhood-onset eating disorders

None of the atypical childhood-onset eating disorders has been well studied,

and their clinical features and nosologic status are uncertain. What is known about

these conditions is that there is dysfunctional behavior around food, but the

fundamental psychologic disturbance is unclear. This disorder is in contrast with

AN, in which the individual’s distorted cognitions regarding his or her body are

assumed to be driving the food-avoiding behaviors. It is only in the past 25 years

that children with eating disorders have come to be regarded as a subgroup of

interest. The literature on all aspects of eating disorders specifically relating to this

younger population remains sparse, and although there is descriptive literature

regarding the differentiation of the childhood-onset eating disorders, no stand-

ardized methods of assessment have been used to test this notion.

Food avoidance emotional disorder

Food avoidance emotional disorder (FAED) is a term used to describe children

who have a primary emotional disorder in which food avoidance is a prominent

feature [28]. These children present with mood disturbance coupled with

significant weight loss and food avoidance but do not have the same preoccu-

pation with weight and shape, nor do they have a distorted view of their own

weight or shape that is characteristic of anorexia nervosa. They can be extremely

physically unwell as a result of their low weight and can suffer from growth

impairment. Their mood disturbance may take the form of mild depression,

anxiety, obsessionality, or phobias, especially for specific foods. Higgs et al [28]

suggested that FAED may be an intermediate condition between AN and

childhood emotional disorder (with no eating disorder), a partial syndrome of

AN with an overall more favorable prognosis. The characteristics of FAED were

originally set out as follows:

� A disorder of the emotions in which food avoidance is a prominent

symptom in the presenting complaint� A history of food avoidance or difficulties (eg, food fads or restriction)� A failure to meet the criteria for AN� The absence of organic brain disease, psychosis, illicit drug abuse, or

prescribed drug-related side effects

Although organic brain disease is an exclusion criteria, it has been noted that

many children with FAED do have other physical illnesses or disorders. They

seem to develop food avoidance as part of their emotional response to physical ill

health, and in such cases the food avoidance is not a direct symptom of the child’s

illness [6].

There are no reports of the incidence, prevalence, or sex ratio of FAED. A

study of consecutive series of 88 children who presented with childhood onset

eating disorder at two specialist clinics [77] over the course of 2 years found that


FAED was the most common clinical diagnosis after AN, with approximately

29% (ie, 26 children) receiving a diagnosis of FAED. The ratio of girls to boys in

this FAED group was 4:1.

There are few reports of outcome in these children. Higgs et al [28] suggest

that children with FAED have an overall better outcome than children with AN,

but no formal studies have been conducted.

Selective eating

Children who are selective eaters eat very few different foods and sometimes

are particular about the brand of food or where the food was bought. Their diet is

usually high in carbohydrates and often includes crisps, bread, biscuits, or chips.

These children usually include milk or fruit juice in their diet. Attempts to widen

their range of foods are usually met with extreme distress and resistance. The

children do not have a distorted body image or the preoccupation with weight or

shape that is characteristic of AN and BN. Growth and development in selective

eaters do not seem to be affected by their eating habits. Nicholls et al [48] have

suggested that selective eating may be a variant of normal eating behavior, a

stereotyped behavior in developmental disorder or an emotional (phobic) disorder.

Parental requests for help and advice are often precipitated by the impact that

selective eating patterns have on social functioning, and by increasing parental

concern as the child gets older. Although parents are able to manage the child’s

extreme fussiness by providing access to favored foods at home, they are unable

to do so once the child gets older and starts to take part in social events such as

sleepovers and school trips. In childhood, selective eaters are usually referred

because of parental concerns about the adequacy of nutrition, despite the fact that

children tend to thrive. Once into adolescence, however, the concerns relate to

social and peer-group difficulties. Most selective eating problems tend to resolve

eventually as peer group influences become stronger, and the need to conform in

adolescence often results in the relaxation of the limits placed on dietary intake.

There are no reports of the incidence, prevalence, or sex ratio of FAED in the

general population. In a consecutive series of 88 children who presented with

childhood-onset eating disorder, however Cooper et al [77] found that 19% (ie,

17 children) of the sample had selective eating and that boys were overrepresented

(76% of the group), which is in broad agreement with Nicholls et al [48], who

found a ratio of boys to girls of 4:1 in their study of selective eaters.

In terms of outcome, Nicholls et al [48] found that after a mean follow-up of

2.6 years, the eating habits of 50% of their sample of 20 children with selective

eating had not changed, whereas the eating habits of 38% had improved, and 12%

had worsened.

Functional dysphagia

The characteristic feature of functional dysphagia is a fear of swallowing,

vomiting, or choking, which makes the child anxious about and resistant to eating


normally, which results in a marked avoidance of food. This avoidance tends to

be of foods of a certain type or texture. Children with this disorder do not have

the characteristic weight and shape concerns seen in children with AN or BN.

Usually there is an easily identifiable precipitant, such as having witnessed

someone choking while eating, having choked on a piece of food, having had

traumatic gastrointestinal investigations, or experiencing abuse that becomes

associated with particular textures, tastes, or types of food.

Little information has been reported about this disorder, and its incidence is

unknown. In a consecutive series of 88 children with childhood-onset eating

disorder [77], only 1 child received a diagnosis of functional dysphagia.

Pervasive refusal syndrome

Pervasive refusal is a term that was first used in 1991 to describe a small group

of children who presented with a potentially life-threatening condition manifested

by a profound and pervasive refusal to eat, drink, walk, talk, or care for themselves

in any way over a period of several months [39]. These children usually present as

underweight and often dehydrated, but it is unclear whether they have distorted

cognitions regarding weight and shape because they are unwilling to communi-

cate. An additional and striking feature is their determined resistance to any form

of help. Lask et al [39] suggested that the condition may be understood as an

extreme form of posttraumatic stress disorder. Further cases of children with this

condition have been reported [43,51,69], with the hypothesis that it is a model of

learned helplessness. One other case has been reported since in the literature [67],

which casts doubt on this theory because the child was only 4 years old and would

‘‘not have the developmental capacity to sustain the cognitive generalization for

helplessness.’’ There is much yet to be understood about this rare but life-

threatening disorder.

Origin of childhood-onset eating disorders

This section reports on the origin of the childhood-onset eating disorders.

Because most of the literature in this area is about AN, the focus of this section is

on AN, although it still considers relevant information regarding the other

childhood-onset eating disorders. No one factor has been identified as the cause

of eating disorders. It is wise to consider a multifactorial model with possible

contributory factors, including genetic, biologic, psychologic, personality, famil-

ial, and sociocultural.

Genetic factors

Although there are no studies regarding genetic factors and childhood-onset

AN, there are several adult studies that Lask [38] has argued are almost certainly

applicable to the younger population. Several studies have pointed to a significant

familial aggregation in AN and BN [58,62,63,68]. It has been found that first-


degree relatives of sufferers of AN and BN are generally eight times more likely to

have one of the disorders themselves in comparison to even the highest reported

rates in the general population [17]. These studies, however, cannot exclude any

environmental factors that may be in play. Twin studies provide a more compelling

case for genetic factors being involved. The concordance for AN in monozygotic

twins is approximately ten times greater than for dizygotic twins [29,58,70],

whereas the concordance for narrowly defined BN in monozygotic twins is almost

three times greater than for dizygotic twins [34].

Lask [38] has suggested that there are two likely pathways—biologic

vulnerability and psychologic vulnerability—through which genetic loading

exerts its effects to produce an eating disorder.

Biologic vulnerability

Although biologic abnormalities are commonly found, it is unclear whether

these are a cause or a consequence of AN. For example, an endocrine

disorder that affects the hypothalamic-pituitary-gonadal axis in AN has been

suggested [57]. Similarly, dysfunction being triggered by stress in individuals

who may have abnormal sensitivity in the hypothalamic tissues also has been

cited [73]. The generally accepted view, however, is that most endocrine

changes are a consequence rather than a cause of weight loss, increased exer-

cise, and purging [78].

The role of polypeptides, which play a part in gastric emptying, also has been

studied. Adult studies have confirmed that delayed gastric emptying occurs in AN

[59], although this finding has not been confirmed in children [56]. To some extent

these peptides also work centrally by acting as neurotransmitters with receptor

sites in the brain [42] and are associated with the peripheral satiety system. High

levels of a particular peptide, cholecystokinin, are associated with a sense of

satiety. Silver and Morley [59] found high levels of this peptide in sufferers of AN,

whereas individuals with BN had low levels of cholecystokinin. It is unclear,

however, whether these levels are a consequence of the eating disorder or

a precipitant.

Recently the role of serotonin activity has been considered. High levels of

serotonin are associated with rigidity and constraint, whereas low levels are

associated with impulsivity. Strober [61] suggests that low levels of serotonin

may predispose an individual to BN, which is characterized by impulsivity,

whereas high levels may predispose to AN, which is characterized by

rigidity and constraint. The role of serotonin activity, however, is not yet

fully understood.

Studies of brain structure and function in adults with AN have shown

abnormalities of structure and function [27,33,36]. It seems likely, however, that

they are a result of weight loss and dehydration, because they generally reverse

after weight gain. A study of children and adolescents with AN showed a

unilateral reduced cerebral blood flow in the anterior portion of the temporal lobe

[24]. This abnormality in cerebral blood flow is hard to explain in terms of


starvation or dehydration, and it has been suggested that this finding may

constitute evidence of a primary abnormality in the limbic system [14].

Psychologic vulnerability

Children with AN often present as being perfectionistic, having always been

well behaved, conscientious, high achieving, popular, and successful. These

children seem to have an inability to express negative emotions such as anger,

anxiety, or sadness [38]. This perfectionistic type of personality may contribute to

the ability to exert the restraint required to maintain a low weight.

A commonly associated feature is that of low self-esteem [13,41]. Children

with AN tend to have a poor self-image and see themselves as failures, bad, and

unworthy. Such a perception may, in part, be reinforced by the perfectionistic

traits, which impose such high standards that failure is inevitable.

The clinical impression of children with atypical childhood-onset eating

disorders is that they are psychologically vulnerable. For example, Higgs et al

[28] found that children with FAED were more likely to have suffered life events

that disrupt and permanently alter family life than children who had emotional

disorders without food avoidance. With regard to personality, Nicholls et al [48]

report that selective eaters have a rigidity of behavior and difficulty adjusting to

new experiences that would fit with characteristics seen in autistic spectrum

disorders. Lask [38] has noted that children with atypical childhood-onset eating

disorders seem to have somewhat sensitive personalities, but further information

is needed to confirm a clinical impression.

Psychologic and family factors

There are many psychologic theories of eating disorders but little empirical

support for them. For example, one early theory for eating disorders was that self-

starvation is a defense against the sexual fantasies of oral impregnation [72].

None of the psychodynamic theories were conducive to generating empirical

hypotheses or predicting outcome.

Palazzoli [52] has suggested a developmental theory of how an infant

progresses through stages in relating to his or her mother. She argued that the

future anorectic has a confused ambivalent identification with her mother due to

unresolved problems in the oral incorporation stage of normal development

which impede the crucial stage of separation individuation. Self-starvation thus

becomes an attempt by the anorectic girl to end the feminisation of her body and

to minimise her confused ambivalent identification with her mother.

Bruch [4] also suggested that the refusal to eat and fear of fatness have their

roots in early mother-child interactions. She argued that gratifying early feeding

experiences enable the infant to trust both the mother, in that she will respond to

cues from the infant, and herself, in that the infant’s own internal sensation of

hunger and other appetites are accurate. When the mother persistently fails to

provide responses to the infant’s cues, the infant becomes untrusting of her on


ability to identify her internal state. The infant neither learns to identify hunger

correctly nor to distinguish it from other states of bodily need or emotional

arousal. This lack of emotional containment leads the child to become totally

compliant with the mother’s needs, in an effort to maintain a fragile connection

with her mother. As the child grows, she fails to develop a sense of herself

as independent or entitled to take any initiative, and continues to gain maternal

approval by absolute compliance. The consequences of this is a paralysing sense

of ineffectiveness.

Bruch [4] suggested that AN develops in this situation because, for these

children, ‘‘their own bodies become the arena for their only exercise of control.’’

Sociocultural theorists have pointed to the shift to thinness as a Western cultural

norm during the twentieth century [21]. Although there seems to be general

agreement that Western cultural pressure on women to be thin does contribute to

the development of eating disorders [4,16], Brumberg [5] has noted that eating

disorders have been reported throughout medical history.

Sociocultural ideals, however, may well be a factor in the development of an

eating disorder. In groups in which thinness is deemed to be particularly

important, for example in ballet dancers and models, there are high rates of

AN [20,65]. Children of migrant parents from non-Western cultures, in which AN

has not been reported, are also presenting with eating disorders [3,11]. The

emergence of eating disorders in these populations may relate to adoption of

Western values and subsequent intrapersonal and intrafamilial conflicts [10].

Minuchin et al [44] have postulated the ‘‘psychosomatic family.’’ They state

that ‘‘in these families, the child’s psychosomatic symptoms play an important

role in maintaining the family’s status quo, and blocking change.’’ It is suggested

that four key styles of family interacting are characteristic of such families:

enmeshment, overprotectiveness, rigidity, and conflict avoidances. There is no

empirical support for this view, however, and some empirical evidence contra-

dicts Minuchin’s hypotheses [10,35,53]. Similarly, clinical impressions of these

families do not support Minuchin’s suggestions. In summary, there is as yet no

evidence of a particular family style that predisposes to AN or any other eating

disorders [10].

There is an emerging literature about the families of children with atypical

eating disorders, particularly their mothers. Nicholls et al [48] reported a psy-

chiatric history in 4 of 20 mothers of selective eaters, whereas Watkins et al

(unpublished data) found that 35% of mothers of children with FAED had a

history of an eating disorder. These are only preliminary studies that require

replication, however.

In summary, a complex mix of factors contributes to the development of the

early-onset eating disorders. Some of these factors (eg, genetic, personality,

biologic) predispose to the illness (ie, they are necessary preconditions for its

emergence); others (eg, stressful events) precipitate the illness) ; still others (eg,

the way in which the illness is managed) may perpetuate it [38]. To complicate the

situation further, some factors (eg, family dysfunction) may precipitate and

perpetuate the illness.


Management and treatment

With regard to all of the childhood-onset eating disorders, a comprehensive

approach to treatment is essential. Childhood-onset eating disorders have the

potential to damage health severely, the patient often has a lack of insight into the

seriousness of the illness, and there are often battles around control. It is vital to

create a therapeutic alliance with the primary care givers and provide them with

information and education to help them to take complete responsibility for the

child’s health [38].

Assessment of the physical state is a priority, with early rehydration and

reversal of any electrolyte imbalance a must. Re-feeding and weight restoration

must be early goals. The restoration of normal eating patterns is an intermediate

aim, along with addressing the underlying intrapersonal and interpersonal prob-

lems that may have contributed to and helped to maintain the illness [10].

The sine qua non of the treatment program is parental counsel, possibly

combined with family therapy. Individual approaches to treatment should include

attention to motivational enhancement and problem-focused or cognitive-behav-

ioral techniques. Psychodynamic methods may be of value in deeply entrenched

problems that are not alleviated by other approaches.

There is a somewhat limited role for psychotropic medication in this popu-

lation. Antidepressant medications such as the selective serotonin reuptake

inhibitors (SSRIs) can be helpful in any of the eating disorders if there is clinical

evidence of depression and in BN. Anxiolytic agents may have some limited value

when anxiety levels are high; however, they should be used judiciously. Vitamins,

calcium, and other essential nutrients may be used to supplement a poor diet, but

there is no place for laxatives or estrogen.

The establishment of normal eating patterns is not a high priority, but a healthy

dietary intake is essential. How this is achieved is best determined in discussion

with the parents or care givers. Whatever techniques are used, they must be

applied consistently between the caregivers and consistently over time. This is

most likely to occur if the caregivers are in agreement with each other about how

to proceed and are not too uncomfortable with the techniques chosen.

Determination of a healthy weight range is best achieved by the use of pelvic

ultrasound for girls [37,49]. For boys, population norms are the only standard

available. In general, children must achieve a body mass index of 19 or more to

ensure that they are within a healthy range.

Hospitalization is indicated when there is electrolyte imbalance, dehydration

that has not been reversed within 24 hours, peripheral circulatory collapse, a body

mass index below 14, failed outpatient treatment.

A detailed review of treatment has been provided elsewhere [6].

Stages of recovery

Lask [38] has observed that specific behaviors seem to predominate at certain

times throughout the course of many of the childhood-onset eating disorders,


particularly AN but also FAED and pervasive refusal syndrome. It is useful to

consider these in terms of ‘‘stages.’’ The first stage is that in which the child seems

to be preoccupied with food intake and weight to the exclusion of everything else,

except possibly school work, and is unable to recognize that he or she has a

problem. As the presenting problems begin to improve, the child gradually moves

into stage 2. The child goes through a stage of increased assertiveness and

expresses powerful negative emotions toward parents or caregivers with a seeming

disregard of the impact of these feelings. Lask [38] has suggested that it is

imperative that the child enter and resolve stage 2 if he or she is to recover. Stage 2

behavior gradually is replaced by more age-appropriate expressions of emotion

(stage 3). There is overlap in these three stages, which often leads to confusion and

distress for the patient and the family. If this overlap can be tolerated, however,

recovery can occur [38].

Summary

It is widely accepted that eating disorders do occur in children. There is a

growing literature on childhood-onset AN, and it seems that the core behavioral,

psychologic, and physical features are similar to those in adults. The differences

between children and adults also must be taken into account, however. Because

children have lower levels of body fat, they tend to become emaciated and suffer

the effects of starvation far more quickly than adults, which must be taken into

account when considering treatment. Although cases of childhood-onset BN have

been reported, they are so rare that empirical research is difficult. Clinical features

reported regarding the atypical childhood-onset eating disorders generally concur,

although empirical testing of these features has yet to be developed. Theories as

to why children develop these disorders need further development. The general

consensus is that all childhood-onset eating disorders must be considered using a

multidimensional model that takes into account physical, psychologic, social, and

family factors in origin, assessment, and treatment.

References

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Eating disorders in school-aged children