Handbook of Eating Disorders - part 3 pps

Serotonin activity: rDisturbances of brain serotonin activity have been described in patients with anorexia nervosa and bulimia nervosa.. rThere are distinct differences in serotonin act

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Structural neuroimaging techniques:

rThere is sufficient evidence of a relationship between eating disorders and altered brain

structures

rMorphological brain alterations are most likely a consequence of endocrine and metabolic

reactions to starvation, regardless of whether starvation leads to an underweight state(‘pseudoatrophy’)

rHowever, there are individual cases in whom the brain alterations continue to exist.

rImprovement in MRI technique will shed more light on the regional distribution of

struc-tural brain abnormalities

Functional neuroimaging techniques:

rThe functional abnormalities may be partly secondary to weight loss but may also reflect

underlying primary brain dysfunction

rCognitive activation and symptom provocation paradigms might elucidate typical brain

activation patterns in eating disorder patients

rRe-assessment should be performed upon recovery to determine if the structural and

functional abnormalities are strictly secondary to the abnormal eating behavior or related

to underlying traits

rThe enormously rapid development of new technology in structural and functional

neu-roimaging techniques will allow more precise observation of the brain

Serotonin activity:

rDisturbances of brain serotonin activity have been described in patients with anorexia

nervosa and bulimia nervosa

rWhether abnormalities are a consequence or a potential antecedent of pathological eating

behavior remains a major question

Handbook of Eating Disorders Edited by J Treasure, U Schmidt and E van Furth.

rThere are distinct differences in serotonin activity between recovered and ill patients with

anorexia or bulimia nervosa (challenge tests, CSF 5-HIAA)

rIt cannot be ruled out that subjects at risk of an eating disorder might have trait

abnor-malities in the regulation of brain serotonin function that might make them vulnerable toabnormal eating behavior (as a way to ‘treat’ abnormal serotonin activity) or to dieting-induced decreases in plasma tryptophan

rIn addition, a disturbance of serotonin activity may also explain associated

psychopatho-logical features (e.g obsessionality, depression) that are common to both anorexia andbulimia nervosa

Table 5.1 Results of CT and MRI studies in patients with eating disorders

r Enlargement of external CSF spaces (enlargement of cortical sulci, narrowing of the gyri)

r Enlargement of internal CSF spaces (ventricular enlargement)

r Decreased total gray matter volume

r Decreased total white matter volume

r Mild atrophy of the thalamus and midbrain area

r Reduced pituitary size

Since a considerable number of normal-weight bulimic patients display the same kind ofsulcal widening as anorexic patients, malnutrition cannot be the only explanation for thesestructural brain abnormalities However, bulimic patients show low T3and elevatedβ-HBA

values as a consequence of intermittent starvation Hypercortisolemia may contribute rectly to the brain abnormalities Hypercortisolism is a common finding in eating disordersand similar structural brain changes can be found in patients with Cushing syndrome andthose taking corticosteroids (Table 5.2)

di-As mentioned previously, the abnormalities are usually reversible with weight restoration;however, there are individual cases in whom the brain alterations continue to exist unalteredover a period of one year after the body weight has returned to normal Change that persistsmight be due to residual damage of the brain (‘scar’) or persistent abnormal metabolism.The results of neuropathologic examinations of patients who died of anorexia nervosarevealed ventricular enlargement, but also neuronal loss and gliosis in the cerebral cortex.However, persistence of changes might also be a consequence of comorbid disorders such

as alcoholism Even though there is no good evidence for a primary structural deficit,this possibility for explaining a persistent brain alteration can not be completely excluded.Technological advances in MRI should shed more light on the regional distribution of tissueshrinkage

From a clinical standpoint, CT and MRI are useful for identifying structural lesionsinvolving the hypothalamus which have been reported in emaciated patients (‘diencephalic

Table 5.2 Significant clinical correlates with CT and MRI findings

Positive correlations betweenr serum/urinary cortisol and total/cortical CSF volumes

r lowest BMI and total gray matter volumes

r serum creatinine and total/cortical gray matter volumes

r total protein and central gray matter volume

Negative correlations between

r urinary free cortisol and central gray matter volumes

r body weight and external CSF volumes

r lowest BMI and total/external CSF volumes

r T3(as a sign of starvation) and CSF volumes

No correlations

r estradiol, LH, FSH, prolactin

r duration of illness

r age

wasting’), but such cases are extremely rare Both CT and MRI should be used clinically

in patients who have atypical symptoms of eating disorders such as food aversions withoutbody image disturbances (Swayze, 1997)

Functional Imaging

These techniques allow the identification of possible brain dysfunction even where thereare no structural changes Currently, SPECT, PET, MRS and fMRI have only researchapplications for patients with eating disorders PET and SPECT require the introduction

of manufactured radioactive compounds The major advantage of SPECT over PET is thelonger half-lives of SPECT’s isotopes, which do not require an on-site cyclotron A majordisadvantage is that SPECT has poorer image resolution than PET

Positron Emission Tomography

Most PET studies of eating disorders have evaluated glucose metabolism (metabolic rate,blood flow) with the use of 18-fluorodeoxyglucose (FDG) At rest with eyes closed, patientswith anorexia nervosa usually present an absolute global and regional hypometabolism ofglucose However, this can also be found in low-weight patients with depression and is mostlikely a consequence of starvation since it disappears after weight gain Most recentlyregional cerebral blood flow (rCBF) was investigated using PET in 9 women in long-termrecovery from BN (Frank et al., 2000) There were no differences between bulimics andcontrols, suggesting that alterations in rCBF during the ill state of bulimia nervosa may be

a state-related phenomenon Both, anorexic and normal-weight bulimic patients have beenshown to have relative parietal hypometabolism which persisted after weight gain in someanorexic patients (Delvenne et al., 1995, 1997a, 1997b, 1999) The authors hypothesise thatthis might be a characteristic of eating disorders, a primary cerebral dysfunction, which may

be related to distortions of body image However, it might also be a particular sensitivity ofthis cortical region to nutritional factors In their most recent study Delvenne et al (1999)found that patients with anorexia nervosa showed an increased relative glucose metabolism

in the inferior frontal cortex and in the basal ganglia compared to controls, confirming thefinding by Herholz et al (1987) This might be due to a more pronounced reduction incortical than in basal ganglia glucose metabolism and may be related to increased vigilance

or anxiety in patients compared to controls

Two studies of glucose metabolism in bulimia applied PET scans together with tive activation tasks which stimulate particular regions of brain activity (Wu et al., 1990;Andreason et al., 1992) Bulimics showed an abnormal hemispheric lateralization (leftgreater than right hemispheric asymmetry as opposed to healthy controls in whom right

cogni-is greater than left) in the parietotemporal region and parts of the frontal lobes, which peared to be independent of the mood state (similar findings were reported for depressionand OCD) It is an open question whether the loss of normal right activation in some areashas a role in the aetiology of this disorder

ap-Another option is symptom provocation studies, which have already been performed inpatients with anxiety disorders In healthy subjects the confrontation with desirable food

stimuli was associated with decreases in left temporo-insular cortical blood flow (Gordon

et al., 2000) Further studies are needed to elucidate brain activity patterns in patients witheating disorders using the same provocation paradigms

Specific ligands for serotonin and dopamine sites can be utilised to clarify the involvement

of these neurotransmitter systems in eating disorders Data of PET with altanserin, a tonergic ligand that binds to 5-HT2areceptors, in 9 women who had recovered from bulimianervosa versus 12 normal controls, have shown reduced 5-HT2abinding in the medial orbitalfrontal cortex, an area involved in regulating emotional and impulse control (Kaye et al.,2001) A study in 16 women recovered from anorexia nervosa versus 23 controls demon-strated significantly reduced altanserin binding in mesial temporal and cingulate corticalregions (Frank et al., 2002) These studies suggest that altered 5-HT neuronal system activitymay persist after recovery from BN or AN

sero-Single Photon Emission Tomography

SPECT is a functional imaging technique that is mainly used for studies of regional cerebralblood flow (rCBF) SPECT studies in adults with eating disorders have been inconclusive.Krieg et al (1989) reported no change in regional blood flow in patients with anorexianervosa before and after eating or when compared with a control group Nozoe et al (1993)reported an increase in rCBF in response to food intake in the left inferior frontal cortex

in patients with anorexia nervosa Gordon et al (1997) showed unilateral temporal lobehypoperfusion in 13 out of 15 children and adolescent patients with anorexia nervosa Theauthors speculate as to whether this is a primary finding since temporal lobe hypoperfu-sion persisted in three patients who had regained normal weight Furthermore, changes inthe brain secondary to starvation would be expected to produce global and symmetricalchanges

SPECT can also be used to study neurotransmitter systems In addition to those pounds used for measuring blood flow, iodine labeled ligands for the muscarinic, dopamin-ergic, and serotonergic receptors can be used [123]Beta-CIT SPECT studies are used toinvestigate the availability of brain serotonin transporters (SERT) and dopamine transporters(DAT) Tauscher et al (2000) performed scans in 10 medication-free, bulimic patients and

com-10 age-matched controls They found a 17% reduced SERT availability in hypothalamusand thalamus and a similar reduction in striatal DAT availability In addition, there was anegative correlation between illness duration and SERT availability As with other alter-ations it remains unclear whether reduced SERT availability might be an etiologic defect,adaptive mechanism or an unrelated epiphenomenon of another etiologic lesion

Functional Magnetic Resonance Imaging

fMRI studies offer an important opportunity to look at cognitive processing Ellison et al.(1998) studied cerebral blood oxygenation changes with fMRI in six adult patients withanorexia nervosa and six healthy controls Images were obtained while the participantsviewed a 5-minute videotape that showed pictures of labelled high and low calorie drinks

The group with anorexia nervosa showed more extreme and powerful signal changes inresponse to the contrasting stimuli, especially in the left insula, anterior cingulate gyrus andleft amygdala–hippocampal region Anxiety was also rated and found to be much higher

in the anorexic group when viewing the high calorie drinks The authors suggest that theleft amygdala–hippocampal region may mediate conditioned fear of high calorie foods andthat the insula and anterior cingulate may be involved in autonomic arousal and attentionalprocesses

Magnetic Resonance Spectroscopy

With MRS a wide range of metabolic processes can be studied Roser et al (1999) found thatpatients with anorexia nervosa showed a decrease in myo-inositol (by 15%) and lipid com-pounds (by 50%) within the frontal white matter Interestingly, myo-inositol is a metabolitewhich is found in reduced levels also in patients treated with corticosteroids The concen-tration was further reduced with decreasing BMI Again, the metabolic changes seem to

be a consequence of nutritional deficiency and hormonal changes typical in patients withanorexia nervosa The authors could not find evidence for neuronal degeneration or damage

NEUROTRANSMITTER SYSTEMS

Central Nervous System Serotonin Activity

Brain serotonin (5-HT) systems (Table 5.3) play a role in the modulation of appetite,depression, anxiety, impulse control, obsessionality, and neuroendocrine function Centralserotonin pathways, particularly involving the paraventricular nucleus of the hypothalamus,

Table 5.3 Research methods of assessing serotonin function

Pharmacological challenge strategy

Administration of an agent (e.g mCPP, fenfluramine, L-tryptophan) with serotonin-specificproperties and the subsequent assessment of changes in behavior or hormonal release(e.g prolactin) Measure of hypothalamic–pituitary neuroendocrine responsiveness

Acute tryptophan depletion

Methodology that induces a rapid and substantial lowering of plasma tryptophan levels andmarkedly reduces brain 5-HT synthesis in humans followed by the examination of

behavioral responses (mood, urge to eat, food consumption)

Platelet measures of serotonin function

Peripheral measures of 5-HT activity as an indirect means of assessing central 5-HT function:

3H-imipramine binding, platelet uptake of serotonin, serotonin-amplified platelet

aggregation, serotonin-induced platelet calcium mobilization,3H-LSD binding, plateletMAO activity

Precursor and metabolite studies

Tryptophan levels and plasma TRP/LNAA ratio, CSF concentrations of 5-HIAA, the majormetabolite of serotonin

Treatment trials with serotonergic agents

Serotonin antagonists (cyproheptadine), serotonin agonists (SSRIs)

seems to play a major role in the development of postprandial satiety and the determination

of the amount of food eaten (Blundell, 1991) Treatments which increase intrasynapticserotonin or directly activate serotonin receptors tend to reduce food consumption Thus,

a brain serotonergic dysfunction may contribute to the etiology and/or pathophysiology ofeating disorders

There are studies in symptomatic patients with eating disorders and in women whohave long recovered from anorexia and bulimia nervosa Studies in individuals who haveachieved stable remission from anorexia or bulimia nervosa provide better opportunity toidentify trait-related characteristics that may have constituted a risk factor in the originaldevelopment of the disorder Nevertheless, it is not entirely possible to differentiate if alter-ations of serotonergic activity are the cause of an eating disorder, a reversible consequence

of the eating disorder (which might contribute to the perpetuation of the disorder), or a

‘scar’ caused by the abnormal eating behavior which persists after recovery

In addition to affecting eating behavior directly, alterations in CNS serotonin functioncould contribute to other psychological symptoms associated with eating disorders Thediminished CNS serotonin could play a role in the high prevalence of depressive disorders

in patients with bulimia nervosa An impulsive-aggressive behavioral style which is quently seen in bulimic patients may also be associated with diminished CNS serotoninfunction Consequently, altered central serotonin function may reflect a shared neurobio-logical diathesis across several psychiatric disorders

In most studies anorexic patients have a significant blunting of plasma prolactin response

to drugs with serotonin activity (Brewerton & Jimerson, 1996; Hadigan et al., 1995;Monteleone et al., 1998b) There is some evidence that reduced brain serotonin activitypersists after short-term weight recovery (Frank et al., 2001) However, in long-term weight-recovered patients with a history of anorexia nervosa this blunted response could no longer

be found (O’Dwyer et al., 1996; Ward et al., 1998) In the study of Ward et al (1998)the recovered group showed diminished responses to the appetite-suppressant effects ofd-fenfluramine relative to the control subjects Consequently, it cannot be ruled out thatthe appetitive and neuroendocrine responses are mediated by different serotonin systems

It must be kept in mind that there are multiple brain 5-HT pathways and several subtypes

of 5-HT receptors

Human platelets are a model for studying serotonergic systems because of similarities

to those in the central nervous system Anorexic patients have been found to have reduced

3H-imipramine binding, but normal serotonin uptake in platelets (Weizman et al., 1986;Zemishlany et al., 1987).

Together these findings suggest that CNS serotonergic responsiveness is substantiallyreduced in low-weight patients with anorexia nervosa and increases toward normal withweight restoration

There is evidence that the serotonin/histamine antagonist cyproheptadine has a tic benefit in hospitalised patients with anorexia nervosa Halmi et al (1986) found thatcyproheptadine hydrochloride, at a dose of 32 mg/day, had a small but significant effect

therapeu-in accelerattherapeu-ing weight gatherapeu-in therapeu-in restricttherapeu-ing anorexic patients, but not therapeu-in bulimic anorexicpatients, when compared to treatment with amitriptyline Antidepressants are modestly if

at all effective in severely weight reduced AN patients (Attia et al., 1998) However, in

a controlled study Kaye et al (2001) reported that fluoxetine may be effective in weightrestored AN patients in preventing relapse

Bulimia Nervosa

As opposed to anorexia nervosa, normal weight patients with bulimia nervosa had normalCSF 5-HIAA levels compared to healthy controls (Jimerson et al., 1992; Kaye et al., 1990).However, patients with a history of bingeing twice a day had 5-HIAA levels lower thanless symptomatic patients As in anorexia nervosa, long-term recovered bulimic patientsshowed elevated levels of 5-HIAA (Kaye et al., 1998)

Also, the results of pharmacological challenge studies resemble those in anorexia nervosa:blunted prolactin response to serotonin agonists in acutely ill bulimic patients (Goldbloom

et al., 1990; Brewerton et al., 1992; Levitan et al., 1997; Jimerson et al., 1997; McBride

et al., 1991; Monteleone et al., 1998a; Monteleone et al., 2000) and no difference in lactin response between remitted patients and controls (Wolfe et al., 2000; Kaye et al.,1998) Studies have shown an inverse relationship between symptom severity and prolactinresponse to a serotonergic challenge (Monteleone et al., 2000) and there is evidence for

pro-an association between self-destructiveness, a history of sexual abuse, pro-and impulsivity pro-andreduced serotonin function (Steiger et al., 2001a, 2001b, 2001c)

When depleted of tryptophan, bulimic patients showed increased caloric intake (Weltzin

et al., 1994, 1995) and an increased desire to binge (Kaye et al., 2000) Consequently,lowering serotonin function can increase the clinical severity of bulimia nervosa in ac-tively ill subjects In abstinent patients one study found no effect of tryptophan depletion

on food intake (Oldman et al., 1995), although in another study subjects with a history ofbulimia nervosa had significant increases in ratings of body image concern and subjectiveloss of control of eating (Smith et al., 1999) The authors conclude that subjects at risk ofbulimia nervosa might have trait abnormalities in the regulation of brain serotonin func-tion that might make them vulnerable to dieting-induced decreases in plasma tryptophan.Dieting is a common precursor to bulimia nervosa Dieting significantly lowers plasmatryptophan which results in a decreased plasma ratio of tryptophan to large neutral aminoacids (TRP/LNAA) This reduces the availability of tryptophan to the brain and reducedbrain serotonin synthesis Even though a study of baseline measures found no difference

in the TRP/LNAA ratio between patients with bulimia nervosa and normal control jects (Lydiard et al., 1988), patients who fail to exhibit an increase in the TRP/LNAA ratio

sub-during bingeing may experience prolongation of the binge–purge cycle (Kaye et al., 1988b)suggesting a self-medicating model of restoration of 5-HT activity.

With regard to platelet measures, high platelet 5-HT uptake, which may reflect creased 5-HT uptake at central nervous system synapses (Goldbloom et al., 1990) anddecreased platelet3H-imipramine binding have been reported (Marazziti et al 1988) Othersfound evidence of an increased sensitivity of 5-HT2areceptor activity (platelet aggregation,calcium mobilization) in patients with bulimia but not with anorexia (McBride et al., 1991;Okamoto et al., 1995) However, this might be related more to difficulty with impulse control

in-in general rather than with bulimic attitudes specifically (Okamoto et al., 1999) In tion, platelet MAO activity was significantly lower in bulimic patients and was inverselycorrelated with scores on impulsivity (Carrasco et al., 2000)

addi-Further support for the serotonergic hypothesis of BN comes from evidence of asatisfactory response to treatment with SSRIs in these patients Most double-blind,placebo-controlled studies of medications that have actions on serotonin are efficacious

in reducing symptoms in bulimia nervosa (FBNC Study Group, 1992; Goldstein et al.,1995; Wood, 1993)

The available data do not indicate whether disturbances of serotonergic function as scribed above predate the onset of bulimic symptoms or result from dietary abnormalities

de-or other changes characteristic of the disde-order Disde-ordered eating behavide-or could producealterations in serotonin function Alternatively, patients with bulimia nervosa could engage

in abnormal eating behavior to ‘treat’ an intrinsic defect in serotonergic activity Studies ofunaffected first-degree relatives of eating disorder patients and other high-risk individualsprior to the development of an eating disorder may be clarifying

Central Nervous System Activity of Other Neurochemicals

However strong the link between eating disorders and serotonin seems to be, it is unlikelythat a specific dysfunction of one neurotransmitter system can fully explain the pathogenesis

of anorexia nervosa and bulimia nervosa Preclinical studies indicate that other icals are involved in the initiation, continuation, and termination of a meal CNS nore-pinephrine and neuropeptide Y contribute to enhanced food intake, possibly by increasinghunger Dopamine and endogenous opiates are likely to play a role in food reward Chole-cystokinin, like serotonin, appears to contribute to post-ingestive satiety Leptin is thought

neurochem-to serve as a metabolic signal for decreased food intake and increased energy metabolism.Finally, ghrelin, a recently discovered gastric peptide, has been demonstrated to increaseappetite and food intake in humans Fasting plasma levels of ghrelin have been found to

be elevated in patients diagnosed with anorexia nervosa (Otto et al., 2001)

Homovanillic acid (HVA), the major metabolite of dopamine, was decreased in CSF

of underweight anorexic subjects (Kaye et al., 1984) and in bulimic patients who had ahigh binge frequency (Kaye et al., 1990; Jimerson et al., 1992) Kaye et al (1999) studiedwomen who had recovered from anorexia and bulimia nervosa and compared them to healthycontrols CSF HVA was significantly lower in former restricting-type anorexic women com-pared to bulimia nervosa, bulimic-type anorexic women and control women CSF MHPG,

a norepinephrine metabolite, showed similar values in all groups Consequently, a related disturbance of dopamine metabolism may contribute to a vulnerability to developrestricting-type anorexia nervosa

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Attachment and Childhood

et al (1997) meanwhile showed that dieting and exercise were used to control weight in

as many as 29% of boys and 41% of girls aged 8–10 years Clearly the seeds for thedevelopment of the typical concerns of eating disorders are sown early In this chapter

we explore some of the early biological and family factors which shape personality andfuture human relationships and which may subsequently confer a vulnerability to theirdevelopment

It is widely accepted that parent–child relationships play a central role in children’spsychological development and so we will focus largely on these The quality and form

of these relationships are thought to predict later interpersonal relationships and have aprofound influence on personality development and related psychological functioning, such

as in the areas of self-esteem and social confidence Surprisingly, there has been untilrelatively recently, only a small body of good empirical evidence to support the importance ofthese relationships in development It is largely within the area of attachment that a lucid andcomprehensive theory of early relationships has evolved The grounds for attachment theory

Handbook of Eating Disorders Edited by J Treasure, U Schmidt and E van Furth.

were laid by Bowlby from the late 1950s (Bowlby, 1958, 1969, 1973, 1980) However, it onlyformally emerged as a scientific discipline in the 1980s with the development of appropriateresearch instruments A means of assessing individual differences in attachment behaviourwas later developed through the work of Mary Ainsworth (Ainsworth et al., 1978) This hasbeen enormously helpful in enabling intensive, ongoing attempts to assess the psychologicaleffects of early relationships on development.

We will begin then by reviewing the major influences on child development starting withattachment theory and then examine the research evidence for their role in the developmentand maintenance of eating disorders

ATTACHMENT

Origins of Attachment Theory

Bowlby’s early theories were influenced by ethology, attachment behaviour being seen as

a ‘safety regulating system’ to protect against predators In this formulation attachment isseen as protective, in as much as children need protection from disease, injury and at timeshuman predation and thus their distress at separation is viewed as adaptive Attachment

is seen as a feature of a relationship and not a characteristic of the infant alone; it ops as a function of a caregiver’s general sensitivity to an infant’s signals Thus Bowlbysuggested, the child learns about the caregivers emotional and physical availability andresponds accordingly Bringing together elements from cognitive psychology and objectrelations theory, Bowlby proposed that children internalise their experience with attach-

devel-ment figures to form internal working models of the relationships between themselves and

others

Responsive parenting and sensitivity to infant and child signals is thought within thistheory to have an important impact on one’s sense of self-efficacy, that is the child’s beliefthat they have control over life events Children who have experienced caring and responsivecaregiving, generally see others as caring and reliable and themselves as lovable and worthy

of care If they have been ignored or rejected they may grow to see others as uncaring andunreliable and themselves as unworthy or unlovable

Many of the first attempts to study the impact of early care and relationships on velopment focused on the consequences of poor or inconsistent care Children raised inorphanages, without consistent caregivers were found to suffer developmental delays andalso displayed unusual social and emotional behaviour They seemed unable to form closerelationships and were sometimes indiscriminately friendly to strangers Initially these

de-deficits were ascribed to ‘maternal deprivation’ but subsequent research has drawn

atten-tion to the role of fathers, siblings and family life as well as the opportunities for healthyattachment and subsequent social development offered by substitute care-givers providedthey are consistent and offer quality one-to-one relationships

A scheme for measuring attachment was developed by Ainsworth who classified theresponses of infants to separation from mothers, followed by reunion in a laboratory set-ting (the so-called Strange Situation) Thus attachments could be rated secure, avoidant orresistant, and ambivalent denoted by the letters B, A and C Furthermore, this classificationwas found to be a marker for behaviour in the home More recently a fourth category ofdisorganised/disorientated attachment has been added to the scheme

Influences on Attachment

Early relationships play such a crucial part in a child’s early years that it is difficult toseparate influences on attachment from other influences on development Similarly, whileattachment relationships depend on the interaction between parent and child, factors in thechild, in the parent and issues outside the relationship will have a bearing on their quality

Factors in the Child

Temperament

Most parents who have brought up more than one child will say that they noticed differencesbetween them right from the beginning These early infant characteristics include suchfactors as activity level, predominant mood, readiness to approach new experiences andsleep pattern, often referred to as temperamental factors On the one hand temperamenttheory provides a challenge to attachment theory as an explanation for the quality of parent–child relationships, but on the other can be seen as an influence on it Thomas et al (1968)were responsible for initiating much temperament research and in an attempt to reduce theblame on parents for children’s behavioural disorders, suggested that some children weremuch harder to parent than others

Developmental Maturity

The ability of a child to develop social relationships including attachment relationships willdepend on its developmental maturity Usually social maturity equates broadly to generalmaturity but in certain disorders such as autism, social maturity may be specifically retarded

Health

Certain physical disorders may adversely affect the child’s ability to respond to signalsput out by caregivers; this will particularly be the case for deficits in hearing or vision.Disfiguring conditions meanwhile, particularly those affecting the child’s face, such ascleft palate or port-wine stain may also affect parental bonding Life-threatening conditions

in infancy may influence attachment because of their influence on the parents’ ability tomaintain physical closeness, if the child is for example nursed in an incubator or subject tomultiple surgical procedures Alternatively, the fear of the potential loss of the child mayinhibit the parents’ willingness to allow themselves to engage in an intimate relationship

On occasions the child’s ill-health may promote a ‘high concern’ or overprotective style ofparenting, which may continue after the health problem has been resolved

Factors in Parents

Attitudes towards the child develop from the point of conception, through fantasies aboutthe sex, appearance and personality of the child At the point of birth, the feelings towardsthe child, particularly from the mother, will generally be positive, but ambivalent or negative

feelings may predominate, particularly if the pregnancy was unwanted or if the relationshipwith the father is poor.

Parental high concern or an overprotective style of parenting may result from parentalanxiety or a perceived physical or psychological weakness in the child irrespective ofobjective evidence of the child’s vulnerability (Shoebridge & Gowers, 2000)

Parental Health and Personality

Parental anxiety may be a constitutional trait or arise from a specific child-related antecedentsuch as a problematic past obstetric history The index child may be born after a period ofinfertility or the loss of an earlier child

Parental ill-health can have an effect on the quality of attachment through a number ofroutes The parent may be unavailable either physically or emotionally and the relationshipmay suffer frequent disruptions Where disruptions occur without warning, for example

as a result of emergency hospitalisation, they are likely to be particularly bewildering,while children’s ability to understand the implications of ill-health will be governed bytheir developmental maturity Serious ill-health in one parent may be compensated for by

a good quality relationship with the other, or a substitute caregiver, but healthy parents arelikely in turn to be adversely affected in terms of their physical availability and their ownpsychological adjustment to their spouse’s illness

Mental ill-health in a parent poses particular challenges for the relationship with thechild and his or her psychological development A parent who is anxious or fearful of theworld may transmit such attitudes, while depressive mood will have an impact on emo-tional responsiveness and availability and may present a gloomy outlook on life Psychoticdisorders may confront a child with both disturbances of behaviour and belief For an olderchild a negative effect on peer relationships may ensue, with the child being reluctant tobring friends home, he or she may suffer bullying

Eating disorders provide a good example of the effects of the interplay between parentalattitudes and behaviours (in themselves and directed to the child) Mothers who diet orhave weight concerns themselves are more likely to bottle feed (Crisp, 1969) The mother’sattitude to feeding is likely to be a more important influence than the direct effect of bottlefeeding on infant growth

Children’s perceptions of their parents’ health in turn impact on their feelings of securityand their view of their own health and resilience The development of an external locus ofcontrol or a feeling of personal ineffectiveness may be particularly potent as risk factors foreating disorders

Parental Attachment Status

There are good grounds for supposing that parents’ own experiences of being parented andtheir attachment relationships in their families of origin will predict the quality of theirown children’s attachments Until recently there were few ways of linking intergenerationalattachment representations

The Adult Attachment Interview (AAI; George et al., 1984) is a semi-structured based measure for adults which enables evaluation of the quality of past attachments inchildhood It is designed to assess the adults ‘state of mind’ with respect to attachment, byenquiring about relationships in childhood and evaluating the coherence of their accounts

interview-It is concerned not so much with what happened as what the subject feels about what pened and whether what the subject says is backed up by evidence The general quality

hap-of child–caregiver relationships is probed, together with experiences hap-of early separation,illnesses, losses, rejection, and maltreatment; the interviewer probes for specific memories

to illustrate general statements There are three main categories in this classification tem: Free-autonomous (F), Dismissive (D), and Preoccupied (E) Secure adults categorised(F) are said to value intimate relationships, and acknowledge their effects In addition,some interviews are characterised by an apparent failure to resolve mourning over loss

sys-or abuse, and are separately classified as Unresolved (U) Subjects who simultaneouslypossess E and D qualities are described as Cannot Classify (CC) All interviews are rated

on a number of scales concerning ‘Probable Experience’ (of attachment figures) and rent ‘State of Mind’ of the interviewee; these scales contribute to the overall classification(D/E/F/U)

cur-The AAI has been shown to have predictive validity for the quality of infant attachment

in the next generation (van IJzendoorn, 1995), in as much as two-thirds of infant attachments

on the ABCD classification match their parents attachment category on the AAI

Other Influences on Attachment

Genetics

There is a growing body of evidence from twin studies to suggest a significant geneticcontribution to attachment patterns It may be that genetic contributions to the temperamentalcomponent of distress proneness is greater than that for security/insecurity (Goldberg, 2000)

Siblings

Brothers and sisters can facilitate or impair attachment formation in a number of ways.They may display jealousy towards the new child or else their behaviour or temperamentmay influence parental expectations of subsequent infants

Living Conditions

Good quality attachment is likely to occur when the family is not pressed by financialhardship or overcrowding Good quality family relationships can, however, overcome severematerial deprivation

Effects of Attachment beyond Infancy

Bowlby considered attachment to be a feature of significant relationships throughout thelifespan, as early experiences are coded as internal working models, which are then car-ried forward to influence later personality and behaviour These internal models containboth affective and cognitive information Emotional expressions become more complexand subtle as children get older and they learn implicit rules about displaying affect, includ-ing the masking of negative emotions (Lewis & Michalson, 1983) Attachment theory hasbeen concerned with two aspects of emotional development: the way in which attachment

figures respond to affect and the ways in which attachment relationships vary with vidual differences in emotional expression and regulation Attachment relationships arealso thought to influence information processing through their effects on selective attention

indi-and memory By the age of about 6, children develop a ‘theory of mind’, i.e a notion that

they and others have thoughts about the world, which may not be the same and which areindependent of external objects Internal working models of attachment come prominently

to include attributions of key relationships, e.g ‘Mummy likes to bake cakes for me’.Parental (and to a lesser extent, sibling) attitudes to their own body shape may affect chil-dren in two ways (Stein, 1995) Firstly, children model themselves on their same sex parentand elder siblings Secondly, parents with eating disorders may influence their childrenthrough their attitudes to their children’s weight, shape and eating habits and the impor-tance they attach to these Agras et al.’s (1999) controlled, prospective study of 41 motherswith eating disorders and 153 without a history of eating disorder, demonstrated that foodtended to be used for reward or behavioural control more in the former Also the motherswith eating disorders were more concerned about their daughter’s weight from the age of

2 onwards At 5 years, the children of mothers with eating disorders had greater negativeaffect than controls Although most studies have shown that children of eating-disorderedmothers tend to be thinner than controls (Stein et al., 1996), a group of mothers in this studyoverfed their children through a belief that infant weight was an important index of healthand successful parenting

Attachment and Health

The notion that internal working models play a key role in linking early attachment riences to later social and psychological consequences is appealing, but not widely tested

expe-A simple hypothesis might be that insecure attachment increases vulnerability to behaviouralproblems or psychological disorder The second part of this chapter will address the evi-dence for associations between attachment style and the development of eating disorders,followed by a review of non-attachment developmental influences

ATTACHMENT AND EATING DISORDERS

Historical Perspective

Hilde Bruch, writing in the 1970s, linked emergent attachment ideas to her clinical

obser-vations In her seminal work, Eating Disorders: Anorexia Nervosa, Obesity and the Person

Within (1974), she offers an unusual insight into Mary Ainsworth’s thinking, as the precursor

of the Strange Situation appears associated with early mother–infant feeding interactions:

When rated at 12 months, the infants in whom the feeding interaction had been mostappropriate to their needs, permitting them active participation, showed the strongestattachment to their mothers, with a clear-cut tendency to seek her proximity, and toexpress distress at her absence They made active efforts to gain and maintain contactwith her In contrast babies with inappropriate feeding experiences, showed little or

no tendency to seek proximity, interaction, or contact with the mother and little or notendency to cling when picked up or to resist being released They tended either to