ArticlePDF AvailableLiterature Review

The Cognitive-Interpersonal Maintenance Model of Anorexia Nervosa Revisited: A summary of the evidence for cognitive, socio-emotional and interpersonal predisposing and perpetuating factors

Authors:

Abstract and Figures

To describe the evidence base relating to the Cognitive-Interpersonal Maintenance Model for anorexia nervosa (AN). A Cognitive-Interpersonal Maintenance Model maintenance model for anorexia nervosa was described in 2006. This model proposed that cognitive, socio-emotional and interpersonal elements acted together to both cause and maintain eating disorders. A review of the empirical literature relating to the key constructs of the model (cognitive, socio-emotional, interpersonal) risk and maintaining factors for anorexia nervosa was conducted. Set shifting and weak central coherence (associated with obsessive compulsive traits) have been widely studied. There is some evidence to suggest that a strong eye for detail and weak set shifting are inherited vulnerabilities to AN. Set shifting and global integration are impaired in the ill state and contribute to weak central coherence. In addition, there are wide-ranging impairments in socio-emotional processing including: an automatic bias in attention towards critical and domineering faces and away from compassionate faces; impaired signalling of, interpretation and regulation of emotions. Difficulties in social cognition may in part be a consequence of starvation but inherited vulnerabilities may also contribute to these traits. The shared familial traits may accentuate family members’ tendency to react to the frustrating and frightening symptoms of AN with high expressed emotion (criticism, hostility, overprotection), and inadvertently perpetuate the problem. The cognitive interpersonal model is supported by accumulating evidence. The model is complex in that cognitive and socio-emotional factors both predispose to the illness and are exaggerated in the ill state. Furthermore, some of the traits are inherited vulnerabilities and are present in family members. The clinical formulations from the model are described as are new possibilities for targeted treatment.
Content may be subject to copyright.
R E V I E W Open Access
The cognitive-interpersonal maintenance model
of anorexia nervosa revisited: a summary of the
evidence for cognitive, socio-emotional and
interpersonal predisposing and perpetuating
factors
Janet Treasure
*
and Ulrike Schmidt
Abstract
Aim: To describe the evidence base relating to the Cognitive-Interpersonal Maintenance Model for anorexia
nervosa (AN).
Background: A Cognitive-Interpersonal Maintenance Model maintenance model for anorexia nervosa was
described in 2006. This model proposed that cognitive, socio-emotional and interpersonal elements acted together
to both cause and maintain eating disorders.
Method: A review of the empirical literature relating to the key constructs of the model (cognitive, socio-emotional,
interpersonal) risk and maintaining factors for anorexia nervosa was conducted.
Results: Set shifting and weak central coherence (associated with obsessive compulsive traits) have been widely
studied. There is some evidence to suggest that a strong eye for detail and weak set shifting are inherited
vulnerabilities to AN. Set shifting and global integration are impaired in the ill state and contribute to weak central
coherence. In addition, there are wide-ranging impairments in socio-emotional processing including: an automatic
bias in attention towards critical and domineering faces and away from compassionate faces; impaired signalling of,
interpretation and regulation of emotions. Difficulties in social cognition may in part be a consequence of
starvation but inherited vulnerabilities may also contribute to these traits. The shared familial traits may accentuate
family memberstendency to react to the frustrating and frightening symptoms of AN with high expressed
emotion (criticism, hostility, overprotection), and inadvertently perpetuate the problem.
Conclusion: The cognitive interpersonal model is supported by accumulating evidence. The model is complex in
that cognitive and socio-emotional factors both predispose to the illness and are exaggerated in the ill state.
Furthermore, some of the traits are inherited vulnerabilities and are present in family members. The clinical
formulations from the model are described as are new possibilities for targeted treatment.
Keywords: Anorexia nervosa, Model, Complex intervention, Eating disorder
* Correspondence: janet.treasure@kcl.ac.uk
Department of Psychological Medicine, Kings College London, Institute of
Psychiatry, The Basement, P059, 103 Denmark Hill, London SE5 8AF, UK
© 2013 Treasure and Schmidt; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the
Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use,
distribution, and reproduction in any medium, provided the original work is properly cited.
Treasure and Schmidt Journal of Eating Disorders 2013, 1:13
http://www.jeatdisord.com/content/1/1/13
Background
Treatment for anorexia nervosa (AN) has focused on
remediating the eating and weight symptoms. Historic-
ally, inpatient care was used but the NICE guidelines
recommended outpatient care in the first instance. In
the early phase of adolescent AN, mobilising the parents
to restore a normal eating pattern is effective [1-3].
Nevertheless a sizeable proportion of patients (30-60%)
fail to change their behaviour. In adult patients, particu-
larly if the duration of illness has lasted over 3 years,
change is more difficult [4].
Premorbid vulnerabilities contribute to a poor response
to treatment. Cognitive rigidity and obsessive compulsive
traits [5] and social communication difficulties are associ-
ated with a poorer outcome from AN [6]. Furthermore,
secondary consequences of malnutrition that accumulate
over time contribute to treatment resistance. A starved
brain, for instance, is less plastic and hence responds less
well to talking treatments which require changes to be
made in reflective cognitive functions.
Features such as these led us to develop a cognitive-
interpersonal maintenance model for AN. The essential
features of this model were that there were predisposing
factors such as obsessive compulsive features and anxious
avoidance (particularly of close relationships) increased
the vulnerability to AN and that these contributed also to
the maintenance of the disorder because they fostered pro
anorexia nervosa beliefs and behaviours. These traits cause
problems relating to others and, in addition, the highly vis-
ible eating disorders (ED) symptoms and behaviors have a
profound effect on other people and lead them to react in
ways which in turn serve to maintain the disorder. Thus,
interpersonal relationships become entangled with the
disorder in a complex manner.
The predictions from this model were that obsessive
compulsive and anxious avoidant traits would be inter-
mediate phenotypes increasing the risk of the disorder de-
veloping and that social processing and interpersonal
interactions might be problematic. It follows that treat-
ment for AN would therefore need to be a complex form
of intervention with multiple interacting components. The
Medical Research Council (MRC) has developed guide-
lines on the development of complex interventions as it is
acknowledged that they entail unique challenges [7]. A
key step is to develop a strong theoretical understanding
in order to target the processes and outcomes that are
integral to recovery. Developing the theoretical framework
is an ongoing process and the model may need to be
adjusted as new evidence emerges.
The aim of this paper is to examine the evidence relat-
ing to the cognitive interpersonal model. First, we scru-
tinise and synthesise the literature on genes, molecules,
cells, circuits, physiology, behavior and self report mea-
sures relating to the cognitive phenotype (OCPD traits)
and the anxious, avoidant, social emotional phenotype.
We then summarise the evidence relating interpersonal
aspects of the illness. Lastly, we describe how clinical
formulations and treatments follow from the model.
Premorbid traits
In the original model, obsessive compulsive traits (OCP)
traits were considered to be a key vulnerability factor [8]
[9] contributing to maintenance through pro anorexia
nervosa beliefs and behaviours. Cognitive processing
styles such as set shifting and central coherence [10-12]
underpin these traits and have been the subject of highly
active examination.
Set shifting
Behavioural studies
People with EDs (AN and BN) have moderate to large
sized problems with set shifting in a range of tasks (as
summarised in a systematic review see [13]). After re-
covery, these inefficiencies remain in an attenuated form
[14,15]. Adolescents with anorexia nervosa are also less
impaired [16-19]. This suggests that set shifting may be
accentuated as a consequence of the illness. The alterna-
tive explanation is that individuals with less pronounced
problems in this area are more likely to recover and that
these serve as moderating factors. First degree relatives
(sisters, twins, parents) of people with eating disorders
also perform poorly on some tasks (WCST) [15,20].
Furthermore, in a study by Kothari et al., (2012), chil-
dren (aged 8) of women with EDs perform poorly on a
set shifting task [21]. In summary reduced set shifting is
a feature of AN in the acute state. Furthermore, this trait
is also present in first degree relatives which suggests
that it might be an inherited vulnerability for AN. It is
less pronounced after recovery (see Figure 1) suggesting
that it is accentuated by starvation.
What do we know about the underpinning biology of set
shifting?
Set shifting tasks involve increased frontal and parietal
and decreased striatal activation in AN [22] and BN
[23]. One interpretation is that these tasks may involve
more cognitive effort in people with EDs.
Set shifting difficulties are a generic risk factor for
other forms of psychopathology. It appears to result
from a biological vulnerability in corticostriatal circuits.
Set shifting in rodents [24] and in primates is associated
with frontal lobe function [25]. An inbred mouse model
(BTBR) has problems in set shifting [26,27], Thus, set
shifting inefficiencies seen in EDs may be linked to gen-
etic factors that control brain development.
Treasure and Schmidt Journal of Eating Disorders 2013, 1:13 Page 2 of 10
http://www.jeatdisord.com/content/1/1/13
Central coherence
Weak central coherence (an inability to see the forest for
the trees) is thought to arise from an imbalance between
global and detail processing and is common in people
with EDs. People with EDs have a moderate to large
superiority in detail processing tasks in the acute state
[15,28] and after recovery [11,15,29,30]. Superior detail
processing is also found to a degree in first degree rela-
tives (sisters) [11,15,31]. This suggests that a strong focus
on detail might be an inherited vulnerability of AN.
Global integration is poor in acute AN, and it may be
a consequence of low weight [29]. Therefore, with
starvation the balance between global and detail process-
ing which contributes to central coherence is reduced
(Figure 1). Moreover, the accentuated set shifting prob-
lems in the acute state reduce the flexible switching
between the global/detail processing. Thus, weak central
coherence may be a secondary consequence of the ill-
ness contributing to the maintenance of the illness by
impeding adaptation to environmental demands.
Clinical formulation relating to obsessive compulsive traits
A causal and maintenance model derived from the evi-
dence described above is shown in Figure 2. Although
people with EDs, in general, have good cognitive abilities
with superior attention to detail they show problems in
set shifting. Both of these appear to be an inherited
traits. These traits in the child make them more suscep-
tible to societal rules and their eye for detail makes as-
pects of appearance more salient. The traits mean that
once dieting behaviour is started (triggered by stress for
example), it is undertaken meticulously and the rules
and rituals become embedded as rigid habits. Attention
Figure 1 Obsessive compulsive personality traits. Legend A
diagrammatic representation of traits related to obsessive compulsive
personality disorder (OCPD) in eating disorders . Those that are mainly
present in the acute, starved state are shown in italics.
Figure 2 A diagrammatic formulation of obsessive compulsive personality disorder (OCPD) traits. Legend. A diagrammatic formulation of
obsessive compulsive personality disorder (OCPD) traits showing how they predispose to, and increase, the vulnerability to precipitating factors
and also perpetuate the disorder. The grey box indicates how shared familial traits may contribute to the perpetuation of the problem.
Treasure and Schmidt Journal of Eating Disorders 2013, 1:13 Page 3 of 10
http://www.jeatdisord.com/content/1/1/13
to the detail of weight control rules and inflexibility
leads to success in the goal of weight loss. This, because
of starvation, in turn, impacts on brain function redu-
cing global integration and central coherence and so the
focus is further narrowed to the dieting behaviour which
become even more habitual. A vicious circle which
maintains the disorder develops.
Parents and other family members may share some of
these obsessive compulsive traits. These may lead to
over controlling parenting (Corfield et al. submitted)
which can increase risk particularly in those with the ss
form of the serotonin transporter gene [32,33]. Also
these traits in parents and other family members may
make the process of adjustment and management of the
ED behaviours more difficult. A battle for control can
ensue as both sides defend their rules, often losing sight
of the bigger picture and the longer view of life. This un-
helpful reaction inhibits flexible adjustment and serves
to maintain ED behaviours.
Anxiety, avoidance (social and emotional) behaviours
Anxious avoidance of emotions, in particular those
aroused by social encounters, insecure attachments, was
the second feature within the model considered to be
present before the illness. Social avoidance can be a core
feature of people with EDs. For example, a personal ac-
count of the illness by a medical practitioner described the
illness in one word: isolation[34]. Difficulties relating to
others predate the onset of the illness, can be accentuated
by the illness and sometimes persist despite recovery.
People with AN are more likely than controls to report
an impoverished social network before the onset of the
illness (e.g. having no close friends in childhood; [33,35]
fewer social activities [36] and less social support [37]).
In part, this relates to temperamental characteristics, as
people with EDs are inhibited and shy with internalising
problems [38]. Loneliness, feelings of inferiority and high
levels of social anxiety [39] are also reported.
In cases ascertained in adolescence, social problems
predated the illness in 20% of cases and informed the
prognosis, such that cases with social deficits prior to on-
set at age 15, were found to be impaired 18 years later at
follow-up [6,40]. Experiences of teasing, bullying and criti-
cism, often pertaining to weight/shape and eating, are
found before the illness [41]. During the illness social net-
works are often reduced [42,43]. In addition, a sense of in-
feriority in relationship to others can persist post recovery
[44]. Thus, a wide variety of behavioural features support
the model, in that an avoidant social phenotype is of rele-
vance to the onset and prognosis. In the next section we
examine the form of this social phenotype in more detail.
A variety of experimental paradigms have been used to
examine factors that may underpin social avoidance in
people with EDs, [45] including attention, emotional ex-
pression and interpretation and theory of mind.
Attentional mechanisms
People with AN differ from healthy controls in that they
have an attentional bias towards negative facial expres-
sions such as anger [46-48] criticism [49] and domin-
ance (Cardi et al. submitted) but not towards positive
facial expressions such as happiness [46] and compas-
sion [49]. Also, people with AN have been found to dir-
ect their gaze less at the face and eyes [50]. These traits
remain present, albeit in an attenuated form, in the re-
covered state and in first degree relatives (twins, parents)
(Kanakam et al. submitted Goddard et al. submitted).
These findings suggest that there is increased attention
to social threat and a decreased attention to social re-
ward and that this may be an inherited vulnerability.
Interpretation of social signals
Accurate reading of the intentions and emotions of
others is necessary for effective social communication.
People with AN have impairments in this domain. A sys-
tematic review and meta analysis concluded that people
with AN have impairments in recognizing facial emo-
tions, [51]. In contrast, people with BN have little or no
impairment in facial emotion recognition [52], and may
be better than healthy controls at recognizing negative
emotions [53]. In AN, interpreting emotional meaning
from the voice [54,55], body movement [56] and from
films [54] is also impaired. For the most part, these im-
pairments are less marked after recovery, suggesting that
they may be starvation, state effects. There is little evi-
dence that these traits are part of an inherited vulner-
ability as they are not present in first degree relatives
(twins, parents) (Kanakam et al. submitted Goddard
et al. submitted).
Signaling emotions
The ability to signal ones own intentions and emotions
to others is an important component of effective social
communication and people with AN also have impair-
ments in this domain. In a study that examined emo-
tional expression and experience of people with AN, it
was found that when watching sad or funny films,
people with AN expressed little facial emotional expres-
sion and were also less attentive, e.g. turning away more,
when watching sad films. This lack of reciprocity and at-
tention contrasts with their self reported emotional reac-
tions which were intense [57]. Also, when people with
AN were engaged in a therapeutic emotional skills train-
ing video game, they had minimal facial displays of anger
and yet on self report measures they had high levels of
anger [58]. This suggests that there is inhibited emo-
tional expression and reduced mirroring of emotion.
Treasure and Schmidt Journal of Eating Disorders 2013, 1:13 Page 4 of 10
http://www.jeatdisord.com/content/1/1/13
This has not been examined after recovery and in family
members.
Understanding the mind of another
The most sophisticated aspect of social communication
is the ability to understand the mental processes of other
people, so called theory of mind. A proportion of
people with AN have problems with theory of mind
tasks such as cartoons, which require understanding of
implicit thoughts rather than explicit words spoken
[59,60]. This has not been examined after recovery and
in family members.
A related concept is that of social perception, which
denotes a persons ability to ascertain social cues from
behaviour provided in a social context, which includes,
but is not limited to, emotion cues. Social perception
abilities are preserved in ED patients, but those with
restricting AN have difficulty in identifying degree of in-
timacy in social relationships (Renwick et al., submitted).
Understanding the self
Finally the perception and understanding of self is an
additional component of the social cognition domain
that has found to be disturbed in anorexia nervosa. The
most widely studied concept in this domain is alexithymia.
Sisters of people with anorexia nervosa also have problems
in this area which suggests that it might be an additional
endophenotype [61]. Abnormalities in other paradigms
which measure aspects of interoception such as the rubber
hand illusion have also been found [62].
The traits relating to social processing are displayed in
Figure 3.
What do we know about the underpinning biology of social
processes
Brain activation during social processing in AN differs
from that seen in the comparison population. The
evoked potential to faces (implicitly and explicitly
presented) was reduced both in the acute state and after
weight restoration [63]. Two groups have used a task
in which moving shapes representing social or non-
social/mechanical interactions are shown. Adults (par-
tially recovered) [64] and adolescents (in both the acute
phase of AN and after weight restoration (> 100 days
treatment)) did not show the expected increase in acti-
vation in social processing circuits. On the other hand
there was normal activation to emotional faces after re-
covery AN [65]. Thus, it is possible that some of the
anomalies in the brain response to social processing
tasks in AN, result from the illness state and are re-
solved with full recovery but this needs further study.
It is not surprising that social cognition is impaired in
the acute state, as this form of cognition requires higher
levels of processing. An illustration of this is the social
brain hypothesis of Dunbar and colleagues. This theory
is based on the observations that throughout the animal
and bird kingdoms, social complexity is related to brain
size [66,67]. The shrunken, starved brain of AN may not
have the functional capacity to optimally participate in
the sophisticated communication developed in humans
[68]. Moreover, oxytocin functioning, a hormone which
is central to aspects of social communication, appears to
be disturbed in AN. In the acute state, oxytocin is re-
duced both peripherally [69] and in the brain [70]. Even
after recovery, however, oxytocin released after a test
meal is reduced [71].
Clinical formulation
The balance of evidence is that there are both predispos-
ing inefficiencies in this system and secondary problems
acquired as a consequence of the illness. A causal and
maintenance model derived from the evidence described
above is shown in Figure 4.
Negative self evaluation, internalising strategies and re-
duced social processing skills predispose to the develop-
ment of the illness. This is perhaps due to an increased
sensitivity to social hierarchies and to negative judg-
ments from others (particularly teasing and criticism
about shape, weight or eating) or by the desire to belong
and be accepted by attaining social norms (internalisa-
tion of thinness). By starving the brain and reducing
high level brain function, the symptoms themselves de-
crease social processing abilities which leads to further
withdrawal from social pursuits and poor confidence in
situations that require social problem solving abilities
[72]. This allows the ED thoughts and behaviours, used
to control the biological homeostatic forces, to dominate
brain function. The ED becomes the only friend and a
vicious circle develops.
Figure 3 Social processing traits. Legend. A diagrammatic
representation of social processing traits in eating disorders. Those that
are mainly present in the acute starved state are shown in italics.
Treasure and Schmidt Journal of Eating Disorders 2013, 1:13 Page 5 of 10
http://www.jeatdisord.com/content/1/1/13
There is a small amount of evidence suggesting that
some of these traits run in families. This may make so-
cial communication in the family more difficult and
allow the isolation of AN to take a greater hold.
Interpersonal relationships
In the initial prototype of the model, the key interper-
sonal maintaining factors were thought to be high
expressed emotion, criticism, hostility and over protec-
tion. Systematic reviews of this concept suggest that
these behaviours are present and impact on the response
to treatment and outcome [73] ( Duclos in press). Ac-
commodating and enabling behaviours [74-78] have
been added as behavioural reactions that maintain the
illness, another vicious circle.
A formulation for carers showing the interface with
eating disorder symptoms is shown in Figure 5. There
may be shared OCPD and anxiety traits which become
pronounced in the face of the symptoms of anorexia
nervosa. This may lead to high expressed emotion (criti-
cism, over protection) and accommodating behaviour
which fuels further symptoms.
Adaptations to the model on the basis of new evidence
The new clinical and behavioural evidence has clarified
the model. Although the original key concepts remain,
the model has become somewhat more complex as some
of the risk factors (strong detail, set shifting and social
communication difficulties) appear to be familial vulner-
ability traits and so have a wider effect by causing a
maladaptive response by family members. Also social
communication deficits develop or are accentuated as a
result of starvation which means that interpersonal rela-
tionships become more difficult. Thus, three interlocking
formulations relating to cognitive, emotional and inter-
personal style may be needed to encapsulate the illness
and plan treatment.
Translational treatment implications
Psycho education
This model is a useful heuristic to help patients and
their families understand the illness, the role that they
can play in causing the illness to persist and how treat-
ment can be managed and directed. Firstly, patients and
their families can be helped to understand the many fac-
tors that contribute to the illness and which become
entwined in a complex manner when the symptoms
themselves either alter brain function and so make the
individual less capable of change or cause others to react
in ways that maybe unhelpful.
Patients and family members may find it helpful to
know that the strength in detail, can become problem-
atic when combined with weakened set shifting in the ill
state. Also, when patients and families understand how
their automatic attention and interpretation mode is
biased towards the negative, they can appreciate that
Figure 4 A diagrammatic formulation of social processing traits. Legend. A diagrammatic formulation of social processing traits showing
how they predispose to and increase the vulnerability to precipitating factors and also perpetuate the disorder. The grey box indicates how
shared familial traits may contribute to the perpetuation of the problem.
Treasure and Schmidt Journal of Eating Disorders 2013, 1:13 Page 6 of 10
http://www.jeatdisord.com/content/1/1/13
their judgments about themselves and the world may be
skewed. Furthermore, painful miscommunication can
occur because social communication is attenuated by star-
vation induced, inefficient brain function. Thus their abil-
ity to have a balanced appraisal of the emotional state and
intentions of themselves and others is weakened.
Therapeutic relationship
A common ingredient of many forms of psychotherapy
used to treat people with EDs, is the development of a
good working alliance and reflective listening to help the
individual obtain a more realistic and holistic view of the
world and themselves. However, one or three hours a
week of therapy is a minimal input compared to the 20
hours a week or more of contact time that most par-
ents/carers have with their offspring [79]. Thus, if fam-
ilies can be helped to develop more effective forms of
social communication, this may help them facilitate a
restoration of nutritional balance.
In our experience families and therapists find that this
conceptualization and explanation of the brain based
factors underpinning ED behaviours with an emphasis
on the cognitive and social facets of the illness, rather
than food alone, can build a more collaborative, inclusive
approach. This serves as the rationale to explain why it
is helpful to reduce the critical and dominating commu-
nication style, which is an understandable reaction to
the frustrations of the illness, and instead use a style
which elicits a positive self concept by increasing
warmth and listening and selectively attending to healthy
behaviours rather than anorexia talk. Teaching parents
the basic skills of motivational interviewing (MI), such
as reflective listening with affirmations and differential
attention to change talkfosters this communication
style. The complex reflections, which are a key part of
MI, are a form of theory of mind intervention, in that
they seek to encapsulate the gist of the other persons
beliefs motivations and drives. Carers (professional and
family members) can model high quality listening and
communication. Affirmations serve to allow the individual
with an ED to have a positive self image in mind. Improv-
ing communication within the family can be generalised
to a wider social network. We have found that it is pos-
sible for carers to develop high levels of these skills.
Specific interventions
We have developed a talking therapy (Maudsley Model of
Anorexia Nervosa, MANTRA) based on the cognitive-
interpersonal model of AN. This manual-based treatment
has been pilot-tested in a case series [80] and a small ran-
domized controlled trial [81]. However, like all forms of
talking treatments MANTRA targets complex aspects of
brain function which are impaired with a severe and /or
chronic form of illness. To improve outcomes further, ad-
junctive strategies may be needed which use interventions
that target some of these brain mechanisms more directly.
Examples of these include attention training protocols that
have been used to modify threat-related attentional biases
in anxiety disorders [82,83] (Renwick et al., in press). The
use of pharmacological approaches to supplement psycho-
logical interventions for EDs may be of value. For ex-
ample, oxytocin may enhance the effectiveness of social
interventions [84] and promote affiliation and the forma-
tion of positive bonding. Finally, neuromodulatory treat-
ments which improve focal brain activation may also have
potential [85].
Conclusion
We have summarised and evaluated the new evidence re-
lating to the cognitive interpersonal model of AN. The key
concepts of the model have been clarified and the
constructs relating to cognitive, socio-emotional and inter-
personal relationships have been more clearly defined,
including aspects that pertain to all ED and those that are
specific to AN. Primary strengths in detail and vulnerabil-
ities in social and emotional processing may increase the
potency of social pressures during adolescence a critical
Figure 5 A diagrammatic formulation of carers involvement
within the maintenance of an eating disorder. Legend. A
diagrammatic formulation of how carers own vulnerabilities,
insecure attachment, anxiety and OCPD traits predispose to more
difficulties coping with the eating disorder leading to anxiety and
distress which in turn are associated with high expressed emotion,
or accommodation to eating disorder symptoms which act to
maintain the disorder.
Treasure and Schmidt Journal of Eating Disorders 2013, 1:13 Page 7 of 10
http://www.jeatdisord.com/content/1/1/13
stages of development. These in combination with
reduced set shifting allow the illness to take a hold. The
secondary consequences of the illness (intra and interper-
sonal) accentuate these difficulties and cause the illness to
persist. There are three sub formulations within the model
which can be used to guide treatment. Involving close
others, irrespective of individuals age, is helpful as social
and interpersonal reactions are central to the model. New
treatments specifically targeted to aspects of the model
may improve outcomes.
Competing interests
The authors declare that they have no competing interests.
Authorscontribution
Both authors have contributed to the manuscript and have read and
approved the final draft.
Received: 21 December 2012 Accepted: 3 February 2013
Published: 15 April 2013
References
1. Fisher CA, Hetrick SE, Rushford N: Family therapy for anorexia nervosa.
Cochrane Database Syst Rev 2010(4):CD004780. Epub 2010/04/16.
2. Lock J, Le Grange D, Agras WS, Moye A, Bryson SW, Jo B: Randomized
clinical trial comparing family-based treatment with adolescent-focused
individual therapy for adolescents with anorexia nervosa. Arch Gen
Psychiatry 2010, 67(10):10251032. Epub 2010/10/06.
3. Stiles-Shields C, Hoste RR, Doyle PM, Le Grange D: A review of family-
based treatment for adolescents with eating disorders. RRCT 2012,
7(2):133140. Epub 2012/02/23.
4. Treasure J, Russell G: The case for early intervention in anorexia nervosa:
theoretical exploration of maintaining factors. Br. J. Psychiatry: J Ment Sci.
2011, 199(1):57. Epub 2011/07/02.
5. Crane AM, Roberts ME, Treasure J: Are obsessive-compulsive personality
traits associated with a poor outcome in anorexia nervosa? A systematic
review of randomized controlled trials and naturalistic outcome studies.
Int J Eat Disorder 2007, 40(7):581588. Epub 2007/07/04.
6. Anckarsater H, Hofvander B, Billstedt E, Gillberg IC, Gillberg C, Wentz E, et al:
The sociocommunicative deficit subgroup in anorexia nervosa: autism
spectrum disorders and neurocognition in a community-based,
longitudinal study. Psychol Med 2012, 42(9):19571967. Epub 2011/12/22.
7. Craig P, Dieppe P, Macintyre S, Michie S, Nazareth I, Petticrew M:
Developing and evaluating complex interventions: the new Medical
Research Council guidance. BMJ 2008, 337:a1655. Epub 2008/10/01.
8. Anderluh MB, Tchanturia K, Rabe-Hesketh S, Treasure J: Childhood
obsessive-compulsive personality traits in adult women with eating
disorders: defining a broader eating disorder phenotype. Am. J. Psych
2003, 160(2):242247. Epub 2003/02/04.
9. Jacobi C, Hayward C, De Zwaan M, Kraemer HC, Agras W: Coming to Terms
With Risk Factors for Eating Disorders: Application of Risk Terminology
and Suggestions for a General Taxonomy. Psychol Bull 2004, 130(1):1965.
10. Roberts ME, Tchanturia K, Treasure JL: Exploring the neurocognitive
signature of poor set-shifting in anorexia and bulimia nervosa. J Psychiatr
Res 2010, 44(14):964970.
11. Roberts ME, Tchanturia K, Treasure JL: Is attention to detail a similarly
strong candidate endophenotype for anorexia nervosa and bulimia
nervosa? World J Biol Psychiat: J World Federation Soc Bio Psyc 2012.
Epub 2012/01/24.
12. Kanakam N, Treasure J: A review of cognitive neuropsychiatry in the
taxonomy of eating disorders: State, trait, or genetic? Cogn
Neuropsychiatry 2012. Epub 2012/09/22.
13. Alexander-Bloch A, Lambiotte R, Roberts B, Giedd J, Gogtay N, Bullmore E:
The discovery of population differences in network community
structure: new methods and applications to brain functional networks in
schizophrenia. Neuroimage 2012, 59(4):3889900. Epub 2011/11/29.
14. Tchanturia K, Davies H, Roberts M, Harrison A, Nakazato M, Schmidt U, et al:
Poor cognitive flexibility in eating disorders: examining the evidence
using the Wisconsin Card Sorting Task. PLoS One 2012, 7(1):e28331.
Epub 2012/01/19.
15. Tenconi E, Santonastaso P, Degortes D, Bosello R, Titton F, Mapelli D, et al:
Set-shifting abilities, central coherence, and handedness in anorexia
nervosa patients, their unaffected siblings and healthy controls:
exploring putative endophenotypes. J World Federation Soc Bio Psyc 2010,
11(6):81323. Epub 2010/05/22.
16. McAnarney ER, Zarcone J, Singh P, Michels J, Welsh S, Litteer T, et al:
Restrictive anorexia nervosa and set-shifting in adolescents: a
biobehavioral interface. J Adolescent Health: Pub Soc Adolescent Med 2011,
49(1). Epub 2011/06/28.
17. Buhren K, Mainz V, Herpertz-Dahlmann B, Schafer K, Kahraman-Lanzerath B,
Lente C, et al:Cognitive flexibility in juvenile anorexia nervosa patients
before and after weight recovery. J Neural Transm 2012. Epub 2012/05/31.
18. Stedal K, Rose M, Frampton I, Landro NI, Lask B: The neuropsychological
profile of children, adolescents, and young adults with anorexia nervosa.
Arch Clin Neuropsych: J Nat Acad Neuropsych 2012, 27(3):32937. Epub 2012/
03/15.
19. Shott ME, Filoteo JV, Bhatnagar KA, Peak NJ, Hagman JO, Rockwell R, et al:
Cognitive Set-Shifting in Anorexia Nervosa. Eur Eat Disord Rev: J Eating
Disorders Assoc 2012. Epub 2012/04/12.
20. Holliday J, Tchanturia K, Landau S, Collier D, Treasure J: Is impaired
set-shifting an endophenotype of anorexia nervosa? Am J Psychiatry 2005,
162:22692275.
21. Kothari R, Solmi F, Treasure J, Micali N: The neuropsychological profile of
children at high risk of developing an eating disorder. Psychol Med
2012:112. Epub 2012/10/02.
22. Zastrow A, Kaiser S, Stippich C, Walther S, Herzog W, Tchanturia K, et al:
Neural correlates of impaired cognitive-behavioral flexibility in anorexia
nervosa. Am. J. Psych 2009, 166(5):60816. Epub 2009/02/19.
23. Marsh R, Steinglass JE, Gerber AJ, Graziano OLeary K, Wang Z, Murphy D, et
al:Deficient activity in the neural systems that mediate self-regulatory
control in bulimia nervosa. Arch Gen Psychiatr 2009, 66(1):5163. Epub
2009/01/07.
24. Chase EA, Tait DS, Brown VJ: Lesions of the orbital prefrontal cortex
impair the formation of attentional set in rats. Eur J Neurosci 2012,
36(3):236875. Epub 2012/06/08.
25. Stoet G, Snyder LH: Neural correlates of executive control functions in the
monkey. Trends Cogn Sci 2009, 13(5):22834. Epub 2009/04/14.
26. Meyza KZ, Defensor EB, Jensen AL, Corley MJ, Pearson BL, Pobbe RL, et al:
The BTBR T(+)tf/J mouse model for autism spectrum disorders-in search
of biomarkers. Behav Brain Res 2012. Epub 2012/09/11.
27. Amodeo DA, Jones JH, Sweeney JA, Ragozzino ME: Differen ces in BT BR T + tf/
J and C57BL/6J mice on probabilistic reversal learning and stereotyped
behaviors. Behav Brain Res 2012, 227(1):6472. Epub 2011/11/08.
28. Lopez C, Tchanturia K, Stahl D, Booth R, Holliday J, Treasure J: An examination
of the concept of central coherence in women with anorexia nervosa.
Int J Eating Disorders 2008, 41(2):14352. Epub 2007/10/17.
29. Harrison A, Tchanturia K, Naumann U, Treasure J: Social emotional
functioning and cognitive styles in eating disorders. Br J Clin Psychol
2012, 51(3):26179. Epub 2012/07/19.
30. Lopez C, Tchanturia K, Stahl D, Treasure J: Weak central coherence in
eating disorders: a step towards looking for an endophenotype of
eating disorders. J Clin Exp Neuropsyc 2009, 31(1):11725.
Epub 2008/07/09.
31. Kanakam N, Raoult C, Collier D, Treasure J: Set shifting and central
coherence as neurocognitive endophenotypes in eating disorders: A
preliminary investigation in twins. World J Biol Psychia: J World Federation
Soc Bio Psych 2012. Epub 2012/05/29.
32. Karwautz A, Wagner G, Waldherr K, Nader I, Fernandez-Aranda F, Estivill X,
et al:Gene-environment interaction in anorexia nervosa: Relevance of
non-shared environment and the serotonin transporter gene. Mol Psych
2011, 16(6):5902.
33. Fairburn CG, Cooper Z, Doll HA, Welch SL: Risk factors for anorexia
nervosa: three integrated casecontrol comparisons. Arc Gen Psych 1999,
56(5):46876. Epub 1999/05/08.
34. McKnight R, Boughton N: A patients journey. Anorexia nervosa. BMJ 2009,
339:b3800. Epub 2009/09/26.
35. Karwautz A, Rabe-Hesketh S, Hu X, Zhao J, Sham P, Collier DA, et al:Individual-
specific risk factors for anorexia nervosa: a pilot study using a discordant
sister-pair design. Psych Med 2001, 31(2):31729. Epub 2001/03/10.
Treasure and Schmidt Journal of Eating Disorders 2013, 1:13 Page 8 of 10
http://www.jeatdisord.com/content/1/1/13
36. Krug I, Penelo E, Fernandez-Aranda F, Anderluh M, Bellodi L, Cellini E, et al:
Low social interactions in eating disorder patients in childhood and
adulthood: A multi-centre European case control study. J Health Psych
2012, 2012:2012. Epub 2012/04/12.
37. Kim Y-R, Heo SY, Kang H: Song Kj, Treasure J. Childhood risk factors in
Korean women with anorexia nervosa: Two sets of casecontrol studies
with retrospective comparisons. Int J Eating Disorders. 2010, 43(7):58995.
38. Adambegan M, Wagner G, Nader IW, Fernandez-Aranda F, Treasure J,
Karwautz A: Internalizing and externalizing behaviour problems in
childhood contribute to the development of anorexia and bulimia
nervosa-a study comparing sister pairs. Eu Eating Disorders Rev: J Eating
Disorders Assoc 2012, 20(2):11620. Epub 2011/08/10.
39. Swinbourne J, Hunt C, Abbott M, Russell J, St Clare T, Touyz S: The
comorbidity between eating disorders and anxiety disorders: prevalence
in an eating disorder sample and anxiety disorder sample. Aust Nz J
Psychia 2012, 46(2):11831. Epub 2012/02/09.
40. Wentz E, Gillberg IC, Anckarsater H, Gillberg C, Rastam M: Adolescent-onset
anorexia nervosa: 18-year outcome. Br. J. Psychiatry: J Men Sci 2009,
194(2):16874. Epub 2009/02/03.
41. Menzel JE, Schaefer LM, Burke NL, Mayhew LL, Brannick MT, Thompson JK:
Appearance-related teasing, body dissatisfaction, and disordered eating:
A meta-analysis. Body Image 2010, 7(4):26170. Epub 2010/07/27.
42. Adenzato M, Todisco P, Ardito RB: Social cognition in anorexia nervosa:
evidence of preserved theory of mind and impaired emotional
functioning. PLoS One 2012, 7(8):e44414. Epub 2012/09/07.
43. Tiller JM, Sloane G, Schmidt U, Troop N, Power M, Treasure JL: Social
support in patients with anorexia nervosa and bulimia nervosa. Int J
Eating disorders 1997, 21(1):318. Epub 1997/01/01.
44. Oldershaw A, Dejong H, Hambrook D, Broadbent H, Tchanturia K, Treasure J,
et al:Emotional Processing Following Recovery from Anorexia Nervosa.
Eu Eating Disorders Rev: J Eating Disorders Assoc 2012. Epub 2012/01/14.
45. Zucker NL, Losh M, Bulik CM, LaBar KS, Piven J, Pelphrey KA: Anorexia
nervosa and autism spectrum disorders: guided investigation of social
cognitive endophenotypes. Psychol Bull 2007, 133(6):9761006.
Epub 2007/10/31.
46. Cserjesi R, Vermeulen N, Lenard L, Luminet O: Reduced capacity in
automatic processing of facial expression in restrictive anorexia nervosa
and obesity. Psychia Res 2011, 188(2):2537. Epub 2011/01/07.
47. Harrison A, Sullivan S, Tchanturia K, Treasure J: Attentional bias, emotion
recognition and emotion regulation in anorexia: state or trait? Bio Psychia
2010, 68(8):75561.
48. Harrison A, Sullivan S, Tchanturia K, Treasure J: Emotional functioning in
eating disorders: attentional bias, emotion recognition and emotion
regulation. Psychol Med 2010, 40(11):188797. Epub 2010/01/28.
49. Cardi V, Matteo RD, Corfield F, Treasure J: Social reward and rejection
sensitivity in eating disorders: An investigation of attentional bias and
early experiences. World J Biol Psychia: J World Federation Soc Bio Psychia
2012. Epub 2012/03/20.
50. Watson KK, Werling DM, Zucker NL, Platt ML: Altered social reward and
attention in anorexia nervosa. Front Psychol 2010, 1:36. Epub 2010/01/01.
51. Oldershaw A, Hambrook D, Stahl D, Tchanturia K, Treasure J, Schmidt U: The
socio-emotional processing stream in Anorexia Nervosa. Neurosci
Biobehav Rev 2011, 35(3):97088. Epub 2010/11/13.
52. Dejong H, Van den Eynde F, Broadbent H, Kenyon MD, Lavender A, Startup
H, et al:Social cognition in bulimia nervosa: A systematic review.
Eu Psychia: J Assoc Eu Psychia 2011. Epub 2011/09/17.
53. Kenyon M, Samarawickrema N, Dejong H, Van den Eynde F, Startup H,
Lavender A, et al:Theory of mind in bulimia nervosa. Int J Eating Disorders.
2012, 45(3):37784. Epub 2012/01/04.
54. Oldershaw A, Hambrook D, Tchanturia K, Treasure J, Schmidt U: Emotional
theory of mind and emotional awareness in recovered anorexia nervosa
patients. Psychosom Med 2010, 72(1):739. Epub 2009/12/10.
55. Kucharska-Pietura K, Nikolaou V, Masiak M, Treasure J: The recognition of
emotion in the faces and voice of anorexia nervosa. Int J Eating Disorders.
2004, 35(1):427. Epub 2004/01/06.
56. Zucker N, Moskovich A, Bulik CM, Merwin R, Gaddis K, Losh M, et al:
Perception of affect in biological motion cues in anorexia nervosa.
Int J Eating Disorders. 2012. Epub 2012/10/31.
57. Davies H, Schmidt U, Stahl D, Tchanturia K: Evoked facial emotional
expression and emotional experience in people with anorexia nervosa.
Int J Eating Disorders. 2011, 44(6):5319. Epub 2010/10/20.
58. Claes L, Jimenez-Murcia S, Santamaria JJ, Moussa MB, Sanchez I, Forcano L,
et al:The facial and subjective emotional reaction in response to a video
game designed to train emotional regulation (playmancer). Eu Eating
Disorders Rev: J Eating Disorders Assoc 2012, 20(6):4849. Epub 2012/10/26.
59. Russell TA, Schmidt U, Doherty L, Young V, Tchanturia K: Aspects of social
cognition in anorexia nervosa: affective and cognitive theory of mind.
Psychiatry Res 2009, 168(3):1815. Epub 2009/05/27.
60. Gillberg IC, Billstedt E, Wentz E, Anckarsater H, Rastam M, Gillberg C:
Attention, executive functions, and mentalizing in anorexia nervosa
eighteen years after onset of eating disorder. J Clin Exp Neuropsychol
2010, 32(4):35865. Epub 2009/10/27.
61. Rozenstein MH, Latzer Y, Stein D, Eviatar Z: Perception of emotion and
bilateral advantage in women with eating disorders, their healthy sisters,
and nonrelated healthy controls. J Affect Disorder 2011, 134(13):38695.
Epub 2011/07/16.
62. Eshkevari E, Rieger E, Longo MR, Haggard P, Treasure J: Increased plasticity
of the bodily self in eating disorders. Psych Med 2012, 42(4):81928.
Epub 2011/10/25.
63. Hatch A, Madden S, Kohn MR, Clarke S, Touyz S, Gordon E, et al:EEG in
adolescent anorexia nervosa: impact of refeeding and weight gain.
Int J Eating Disorders 2011, 44(1):6575. Epub 2010/01/12.
64. McAdams CJ, Krawczyk DC: Impaired neural processing of social
attribution in anorexia nervosa. Psychia Res 2011, 194(1):5463.
Epub 2011/08/30.
65. Cowdrey FA, Harmer CJ, Park RJ, McCabe C: Neural responses to emotional
faces in women recovered from anorexia nervosa. Psychia Res 2012,
201(3):1905. Epub 2012/04/03.
66. Powell J, Lewis PA, Roberts N, Garcia-Finana M, Dunbar RI: Orbital
prefrontal cortex volume predicts social network size: an imaging study
of individual differences in humans. Proc Bio Sci/Royal Soc 2012, 279(1736):
215762. Epub 2012/02/03.
67. Dunbar R: Psychology. Evolution of the social brain. Science 2003,
302(5648):11601. Epub 2003/11/15.
68. Freeberg TM, Dunbar RI, Ord TJ: Social complexity as a proximate and
ultimate factor in communicative complexity. Philos Trans R Soc Lond B
Biol Sci London Series B, Biol Sci 2012, 367(1597):1785801.
Epub 2012/05/30.
69. Lawson EA, Donoho DA, Blum JI, Meenaghan EM, Misra M, Herzog DB, et al:
Decreased nocturnal oxytocin levels in anorexia nervosa are associated
with low bone mineral density and fat mass. J Clin Psychia 2011,
72(11):154651. Epub 2011/09/10.
70. Demitrack MA, Lesem MD, Listwak SJ, Brandt HA, Jimerson DC, Gold PW:
CSF oxytocin in anorexia nervosa and bulimia nervosa: clinical and
pathophysiologic considerations. Am J Psychia 1990, 147(7):8826.
Epub 1990/07/01.
71. Lawson EA, Holsen LM, Santin M, Meenaghan E, Eddy KT, Becker AE, et al:
Oxytocin secretion is associated with severity of disordered eating
psychopathology and insular cortex hypoactivation in anorexia nervosa.
J Clin Endocrinol Metab 2012, 97(10):E1898908. Epub 2012/08/09.
72. Sternheim L, Startup H, Pretorius N, Johnson-Sabine E, Schmidt U, Channon
S: An experimental exploration of social problem solving and its
associated processes in anorexia nervosa. Psychia Res 2012,
200(23):5249. Epub 2012/07/20.
73. Zabala MJ, Macdonald P, Treasure J: Appraisal of caregiving burden,
expressed emotion and psychological distress in families of people with
eating disorders: a systematic review. Eu Eating Disorders Rev: J Eating
Disorders Assoc 2009, 17(5):33849. Epub 2009/04/16.
74. Treasure J, Sepulveda AR, MacDonald P, Whitaker W, Lopez C, Zabala M,
et al:The assessment of the family of people with eating disorders.
Eu Eating Disorders Rev: J Eating Disorders Assoc 2008, 16(4):24755.
Epub 2008/02/02.
75. Sepulveda AR, Kyriacou O, Treasure J: Development and validation of the
accommodation and enabling scale for eating disorders (AESED) for
caregivers in eating disorders. BMC Health Services Res 2009, 9:171.
Epub 2009/09/25.
76. Grover M, Naumann U, Mohammad-Dar L, Glennon D, Ringwood S, Eisler I,
et al:A randomized controlled trial of an Internet-based cognitive-
behavioural skills package for carers of people with anorexia nervosa.
Psych Med 2011:111. Epub 2011/07/08.
77. Grover M, Williams C, Eisler I, Fairbairn P, McCloskey C, Smith G, et al:An
off-line pilot evaluation of a web-based systemic cognitive-behavioral
Treasure and Schmidt Journal of Eating Disorders 2013, 1:13 Page 9 of 10
http://www.jeatdisord.com/content/1/1/13
intervention for carers of people with anorexia nervosa. Int J Eating
Disorders 2011, 44(8):70815. Epub 2011/11/11.
78. Goddard E, Macdonald P, Sepulveda AR, Naumann U, Landau S, Schmidt U,
et al:Cognitive interpersonal maintenance model of eating disorders:
intervention for carers. Brit J Psychia: J Men Sci 2011, 199(3):22531.
Epub 2011/07/06.
79. Raenker S, Hibbs R, Goddard E, Naumann U, Arcelus J, Ayton A, et al:
Caregiving and coping in carers of people with anorexia nervosa
admitted for intensive hospital care. Int J Eating Disorders 2012.
Epub 2012/10/31.
80. Wade TD, Treasure J, Schmidt U: A case series evaluation of the Maudsley
Model for treatment of adults with anorexia nervosa. Eu Eating Disorders
Rev: J Eating Disorders Assoc 2011. Epub 2011/02/01.
81. Schmidt U, Oldershaw A, Jichi F, Sternheim L, Startup H, McIntosh V, et al:
Out-patient psychological therapies for adults with anorexia nervosa:
randomised controlled trial. Brit J Psychiat: J Men Sci 2012, 201:3929.
Epub 2012/09/22.
82. MacLeod C, Mathews A: Cognitive bias modification approaches to
anxiety. Annu Rev Clin Psycho 2012, 8:189217. Epub 2011/11/01.
83. Beard C, Sawyer AT, Hofmann SG: Efficacy of attention bias modification
using threat and appetitive stimuli: a meta-analytic review. Behav Ther
2012, 43(4):72440. Epub 2012/10/11.
84. Meyer-Lindenberg A, Domes G, Kirsch P, Heinrichs M: Oxytocin and
vasopressin in the human brain: social neuropeptides for translational
medicine. Nat Rev Neurosci 2011, 12(9):52438. Epub 2011/08/20.
85. Van den Eynde F, Guillaume S, Broadbent H, Campbell IC, Schmidt U:
Repetitive transcranial magnetic stimulation in anorexia nervosa: A pilot
study. Eu Psychiat: J Assoc Eu Psychiat 2011. Epub 2011/09/02.
doi:10.1186/2050-2974-1-13
Cite this article as: Treasure and Schmidt: The cognitive-interpersonal
maintenance model of anorexia nervosa revisited: a summary of the
evidence for cognitive, socio-emotional and interpersonal predisposing
and perpetuating factors. Journal of Eating Disorders 2013 1:13.
Submit your next manuscript to BioMed Central
and take full advantage of:
Convenient online submission
Thorough peer review
No space constraints or color figure charges
Immediate publication on acceptance
Inclusion in PubMed, CAS, Scopus and Google Scholar
Research which is freely available for redistribution
Submit your manuscript at
www.biomedcentral.com/submit
Treasure and Schmidt Journal of Eating Disorders 2013, 1:13 Page 10 of 10
http://www.jeatdisord.com/content/1/1/13
... Other studies suggested that dietary restriction and excessive physical activity in AN could have the function of reducing guilt [37] and that both shame and guilt could elicit bingepurging symptoms [38,39]. Moreover, the impairments in social interactions experienced by individuals with AN [40,41] could be related to the crucial role of SCE in interpersonal contact [26]. Furthermore, there is a lack of studies in the ED field that addresses shame and guilt together, and no study has yet controlled for guilt when measuring shame or vice versa [4]. ...
... This finding leads us to conclude that individuals with AN could be better characterized by shame than by heightened concerns regarding their self-images in their internal and social worlds. This conceptualization seems to be in line with theories that claim that the core problem in AN is the inner experience of incompetence and indignity rather than the judgment based on body shape observation [41,66]. Indeed, differences in proneness to shame between individuals with AN and HCs remained significant even when we considered the potential influence of public and private self-consciousness. ...
Article
Full-text available
Background: the role of self-conscious emotions (SCE) such as shame and guilt in eating disorders (ED) has been systematically studied only in recent years, but it is still debated. This study aims to investigate the role of SCE in anorexia nervosa (AN), evaluating the role of self-consciousness. Methods: fifty-five individuals with AN and seventy-four healthy controls (HC) were enrolled and completed a battery of tests evaluating the proneness to feel shame and guilt, as well as comparing self-consciousness, eating, and general psychopathology. Results: individuals with AN showed a higher proneness to shame. Shame was correlated with body dissatisfaction and drive for thinness, which are core symptoms in AN, after controlling for scores of depression and anxiety. Proneness to guilt seemed to be less correlated with eating and body symptomatology, but it appeared to have a negative correlation with binge-purging symptoms. Furthermore, proneness to shame was independent of guilt or self-consciousness and the two groups did not differ regarding public and private self-consciousness. Conclusions: shame is an important and independent factor in AN. Future research may offer progress in the development of shame-focused therapies.
... Difficulties in the social domain play key roles as maintenance factors in a number of models of ED development/ maintenance, e.g., Transdiagnostic Cognitive Behavioral Model [11,12], Cognitive Interpersonal Maintenance Model [13,14], and Interpersonal Psychotherapy-Eating Disorders [15]. In all, interpersonal difficulties, deficits in social cognition, negative evaluations by others, and avoidance of social interactions are highlighted as factors contributing to the development and maintenance of EDs. ...
Article
Full-text available
Purpose of Review Social and environmental factors have been related to both symptom expression of disordered eating in individuals and changes in the prevalence of eating disorders (EDs) in populations. Neural differences in processing social information may contribute to EDs. This review assesses the evidence for aberrant neural responses during social processing in EDs. Recent Findings This review examines how constructs within the social processing domain have been evaluated by neuroimaging paradigms in EDs, including communication, affiliation, and understanding of both oneself and others. Summary Differences related to social processing in EDs include altered processing for self-relevant stimuli, in the context of identity, valence, expectations, and affiliative relationships. Future work is needed to integrate how differences in processing social stimuli relate to alterations in cognitive control and reward as well as specific disordered eating symptoms.
... Furthermore, they have difficulties in decision making (Guillaume et al., 2015) and show a more pronounced inhibitory control as compared to healthy controls, patients with bulimia nervosa, or patients with binge eating disorder (Bartholdy et al., 2017), and have increased attention to detail (weak central coherence; Lang et al., 2016). Moreover, impaired cognitive flexibility and weak central coherence are considered an essential AN-related neurocognitive endophenotype (Treasure & Schmidt, 2013). Recently, a meta-analysis underlined the evidence that patients with AN show a moderate deficit in overall neuropsychological functioning . ...
Article
Background: Patients with Anorexia Nervosa (AN) show a moderate deficit in overall neuropsychological functioning. Since previous studies on memory performance mainly employed cross-sectional designs, the present study aims to investigate changes in verbal memory following weight-gain. Methods: Verbal memory was assessed with the Wechsler Memory Scale-Revised (WMS-R; 'logical memory'-story-recall-subtest) and the California Verbal Learning Test-II (CVLT-II; 'verbal learning'). Included were 31 female patients with AN (18 restricting-, 13 purging-subtype; average disease duration: 5.1 years; average baseline BMI: 14.4 kg/m2 ) and 24 medication-free normal-weight healthy women adjusted for age at baseline (T0). In a post-treatment assessment of approx. 6 weeks with weight increase (T1), 18 patients with AN and 20 healthy women were assessed again. Group differences in verbal memory (i.e., WMS-R, CVLT-II) were assessed for the baseline comparisons with a multivariate ANOVA and longitudinal data were analysed with repeated measures (RM) ANOVAs. Results: At baseline, patients with AN as compared to healthy women displayed deficits in logical memory. In the follow-up assessment, patients with AN improved their logical memory significantly compared to healthy controls (p < 0.006). Furthermore, groups did not differ in verbal learning neither before nor after inpatient treatment. Conclusions: Enhanced logical memory in patients with AN following weight-gain is probably due to the impaired memory as compared to healthy controls at T0. A survivorship bias could explain the improved memory performance in longitudinal data in contrast to cross-sectional studies. Patients with AN with poorer memory performance before inpatient treatment are at higher risk to drop out and need support.
... Moreover, relationships between parents and their children [2] or the communication modalities [50] are closely linked to a better outcome. Treasure et al. developed a model of interpersonal relationships in AN [54]. Parents with predisposing factors (insecure attachment, stress sensitivity) will have more difficulties coping with AN. ...
Article
Full-text available
Background and objectives Anorexia nervosa is a severe and potentially life-threatening disorder. However, although the role of parents in treatment is now clearly recognized and therapeutic groups for parents have been used for years, there are but few existent studies concerning their organisation and effectiveness. The objectives of this study were, on the one hand, to evaluate the parents’ and therapists’ subjective experience of these groups through a systematic review of the literature, and on the other hand, to assess the state of current practices in France using an online questionnaire. Methods The Medline and Web of Science databases were systematically searched. French practices were explored through a questionnaire sent by e-mail to French units treating patients suffering from anorexia nervosa. Results Eleven studies were identified, ten of which used only subjective assessment without a control group. They all converged toward the same conclusion: therapeutic groups are perceived, by parents and therapists, as an interesting option in the treatment of anorexia nervosa. The group process allows parents to gain insight into their family dynamics. Therefore, they were able to replicate at home what they have learned during the sessions. The evaluation of French practices showed that one third of the units used a therapeutic group. The frequency and duration of the sessions were relatively homogenous: 75.7% were held once a month or every two months and the average duration was 90 minutes. Other characteristics of the groups were more heterogeneous. Conclusions While the level of evidence supporting the use of therapeutic groups for parents of patients with anorexia nervosa is low, the perceived effectiveness of these groups is high, both among parents and therapists, and they are commonly used in France. Further research is needed to evaluate their effectiveness.
Article
It remains unexplained why some behaviours persist despite being non-hedonic and ostensibly aversive. This phenomenon is especially baffling when such behaviours are taken to excess in the form of psychopathology. Anorexia nervosa is one psychiatric disorder in which effortful behaviours that most people find unpleasant (such as restrictive eating) are persistently performed. We propose that the social psychology theory of learned industriousness provides a novel mechanistic account for such phenomena. This theory posits that high-effort behaviour can be conditioned to acquire secondary reinforcing properties through repeated pairing with reward. Accordingly, effort sensations become less aversive and more appetitive, increasing willingness to engage in effortful behaviour. In this Perspective, we review pre-clinical behavioural and biological data that support learned industriousness, contrast learned industriousness with other models of non-hedonic persistence (such as habit learning), highlight evidence that supports learned industriousness in individuals with anorexia nervosa and consider implications of the model, including translation to other psychiatric presentations. Individuals with anorexia nervosa persistently exert effortful behaviour such as restrictive eating that most individuals find aversive. In this Perspective, Haynos et al. propose a novel mechanistic account for why such behaviours persist from the social psychology theory of learned industriousness.
Article
Full-text available
Background Difficulties in top-down and bottom-up emotion generation have been proposed to play a key role in the progression of psychiatric disorders. The aim of the current study was to develop more ecologically valid measures of top-down interpretation biases and bottom-up evoked emotional responses. Methods A total of 124 healthy female participants aged 18–25 took part in the study. We evaluated two sets of 18 brief film clips. The first set of film clips presented ambiguous social situations designed to examine interpretation biases. Participants provided written interpretations of each ambiguous film clip which were subjected to sentiment analysis. We compared the films in terms of the valence of participants interpretations. The second set of film clips presented neutral and emotionally provoking social scenarios designed to elicit subjective and facial emotional responses. While viewing these film clips participants mood ratings and facial affect were recorded and analysed using exploratory factor analyses. Results Most of the 18 ambiguous film clips were interpreted in the expected manner while still retaining some ambiguity. However, participants were more attuned to the negative cues in the ambiguous film clips and three film clips were identified as unambiguous. These films clips were deemed unsuitable for assessing interpretation bias. The exploratory factor analyses of participants’ mood ratings and evoked facial affect showed that the positive and negative emotionally provoking film clips formed their own factors as expected. However, there was substantial cross-loading of the neutral film clips when participants’ facial expression data was analysed. Discussion A subset of the film clips from the two tasks could be used to assess top-down interpretation biases and bottom-up evoked emotional responses. Ambiguous negatively valenced film clips should have more subtle negative cues to avoid ceiling effects and to ensure there is enough room for interpretation.
Article
Objective: Interpersonal difficulties are evidenced in Anorexia Nervosa (AN) and are thought to contribute to disease onset and maintenance, however, research in the framework of emotional competence is currently limited. Previous studies have often only used static images for emotion recognition tasks, and evidence is lacking on the relationships between performance-based emotional abilities and self-reported intra- and interpersonal emotional traits. This study aimed to test multimodal dynamic emotion recognition ability in AN and analyze its correlation with the psychometric scores of self- and other-related emotional competence. Method: A total of 268 participants (128 individuals with AN and 140 healthy controls) completed the Geneva Emotion Recognition Test, the Profile of Emotional Competence, the Reading the Mind in the Eyes Test, and measures of general and eating psychopathology. Scores were compared between the two groups. Linear mixed effects models were utilized to examine the relationship between emotion recognition ability and self-reported measures and clinical variables. Results: Individuals with AN showed significantly poorer recognition of emotions of both negative and positive valence and significantly lower scores in all emotional competence dimensions. Beside emotion type and group, linear mixed models evidenced significant effects of interpersonal comprehension on emotion recognition ability. Discussion: Individuals with AN show impairment in multimodal emotion recognition and report their difficulties accordingly. Notably, among all emotional competence dimensions, interpersonal comprehension emerges as a significant correlate to emotion recognition in others, and could represent a specific area of intervention in the treatment of individuals with AN. Public significance: In this study, we evidence that the ability to recognize the emotions displayed by others is related to the level of interpersonal emotional competence reported by individuals with anorexia nervosa. This result helps in understanding the social impairments in people with anorexia nervosa and could contribute to advancements in the application of the training of emotional competence in the treatment of this disorder.
Article
Objective: Improved understanding of adolescent eating disorders (EDs), including identification and refinement of treatment and recovery targets, may help improve clinical outcomes. Interpersonal function is a proposed risk and maintenance factor that may be particularly relevant given the significance of adolescence for both psychosocial development and ED onset. This study examined self-referential thinking in adolescents with EDs compared to healthy adolescents. Method: Twenty-nine adolescents with EDs and 31 healthy controls completed a self-report measure of interpersonal attributions as well as a verbal appraisal task that required conducting direct and indirect evaluations about oneself and direct evaluations about others. Results: The ED group had a more negative self-attribution bias than the control group (p = 0.006) even when controlling for depression severity. Additionally, the ED group exhibited less positive direct self (p < 0.001), direct social (p = 0.015), and social reflected self-appraisals (p = 0.011) than the healthy cohort. After including depression as a covariate in the verbal appraisal model, the model was no longer significant, suggesting group differences related to social appraisals may be mediated by depression. Conclusions: Adolescents with EDs have more negative interpersonal beliefs than comparison adolescents. Future studies are needed to determine how the constructs identified here relate to clinical course.
Article
Objective: This study aimed to investigate whether a computerized cognitive bias modification training delivered remotely would reduce expectations of rejection in adolescents with eating disorders. Method: Sixty-seven adolescents aged 12-18 (99.5% female) with an eating disorder diagnosis (94% anorexia nervosa) and receiving specialist treatment were recruited. Participants were randomized to an intervention condition (n = 37) which included treatment as usual (TAU) supplemented by nine sessions of online cognitive bias modification training for social stimuli (CBMT + TAU), or a control condition (n = 30), which included TAU only. Participants were invited to complete assessments at baseline and post-intervention. Results: In the intervention condition, 22/37 participants completed six or more training sessions and post-intervention measures, the pre-defined criteria to be considered "completers." In the control condition, 28/30 participants completed the post-intervention measures. Participants who completed the intervention displayed a significantly greater reduction in negative interpretations of ambiguous social scenarios, with a medium effect size (p = .048, ηp2 = .090), and eating disorder psychopathology, with a medium effect size (p = .027, ηp2 = .105), compared to participants in the control condition. No significant between-group differences were found on emotional response to criticism, and anxiety and depression symptoms post-intervention (ps > .05; small effect sizes). Discussion: Enhancing treatment as usual with CBMT targeting expectations of social rejection might be feasible and effective to reduce expectations of social rejection and eating disorder psychopathology in adolescents with eating disorders. Training adaptations might be necessary to impact on emotional processing and comorbid psychological distress. Public significance: Adolescents with eating disorders who completed a brief (4-week) online cognitive training intervention, alongside their usual treatment, reported greater reductions in expectations of social rejection and eating disorder psychopathology after the intervention, compared to a separate group of patients who received their usual treatment only. This brief and accessible intervention may be a helpful treatment adjunct for adolescents with eating disorders.
Thesis
http://deepblue.lib.umich.edu/bitstream/2027.42/174708/1/mhor.pdf
Article
Full-text available
Background: Very limited evidence is available on how to treat adults with anorexia nervosa and treatment outcomes are poor. Novel treatment approaches are urgently needed. Aims: To evaluate the efficacy and acceptability of a novel psychological therapy for anorexia nervosa (Maudsley Model of Anorexia Nervosa Treatment for Adults, MANTRA) compared with specialist supportive clinical management (SSCM) in a randomised controlled trial. Method: Seventy-two adult out-patients with anorexia nervosa or eating disorder not otherwise specified were recruited from a specialist eating disorder service in the UK. Participants were randomly allocated to 20 once weekly sessions of MANTRA or SSCM and optional additional sessions depending on severity and clinical need (trial registration: ISRCTN62920529). The primary outcomes were body mass index, weight and global score on the Eating Disorders Examination at end of treatment (6 months) and follow-up (12 months). Secondary outcomes included: depression, anxiety and clinical impairment; neuropsychological outcomes; recovery rates; and additional service utilisation. Results: At baseline, patients randomised to MANTRA were significantly less likely to be in a partner relationship than those receiving SSCM (3/34 v. 10/36; P<0.05). Patients in both treatments improved significantly in terms of eating disorder and other outcomes, with no differences between groups. Strictly defined recovery rates were low. However, MANTRA patients were significantly more likely to require additional in-patient or day-care treatment than those receiving SSCM (7/34 v. 0/37; P = 0.004). Conclusions: Adults with anorexia nervosa are a difficult to treat group. The imbalance between groups in partner relationships may explain differences in service utilisation favouring SSCM. This study confirms SSCM as a useful treatment for out-patients with anorexia nervosa. The novel treatment, MANTRA, designed for this patient group may need adaptations to fully exploit its potential.
Article
Full-text available
BACKGROUND: There is a large body of evidence indicating that eating disorders (EDs) are characterized by particular neuropsychological profiles. We aimed to further explore whether impairments in neuropsychological functioning previously found in ED groups are present prior to onset, or are secondary to the disorder. Method This is the first study to explore neuropsychological functioning in children born to a mother with a lifetime ED, who are therefore at high risk of developing an ED, in a large cohort sample. We investigated intelligence and attention at age 8 years (n = 6201) and working memory (WM) and inhibition at age 10 years (6192) in children who are at high risk of developing an ED, compared to children who are not. RESULTS: The children of women with lifetime anorexia nervosa (AN) showed high full-scale and performance IQ, increased WM capacity, better visuo-spatial functioning, and decreased attentional control. The children of women with lifetime bulimia nervosa (BN) showed comparatively poor visuo-spatial functioning. CONCLUSIONS: Our findings suggest that high intelligence, increased WM capacity and impaired attentional control might be intermediate phenotypes on the pathway between genetic vulnerability and the development of an ED. http://journals.cambridge.org/repo_I89jprWq
Article
Full-text available
Autism spectrum disorders (ASD) form a common group of neurodevelopmental disorders appearing to be under polygenic control, but also strongly influenced by multiple environmental factors. The brain mechanisms responsible for ASD are not understood and animal models paralleling related emotional and cognitive impairments may prove helpful in unraveling them. BTBR T(+)tf/J (BTBR) mice display behaviors consistent with the three diagnostic categories for ASD. They show impaired social interaction and communication as well as increased repetitive behaviors. This review covers much of the data available to date on BTBR behavior, neuroanatomy and physiology in search for candidate biomarkers, which could both serve as diagnostic tools and help to design effective treatments for the behavioral symptoms of ASD.
Article
Rebecca was diagnosed with anorexia nervosa at age 15 but is now a qualified doctor who is able to maintain a healthy weight, manage her workload, and engage in normal relationships
Article
Nonverbal motion cues (a clenched fist) convey essential information about the intentions of the actor. Individuals with anorexia nervosa (AN) have demonstrated impairment in deciphering intention from facial affective cues, but it is unknown whether such deficits extend to deciphering affect from body motion cues. We examined the capacities of adults with AN (n = 21) or those weight restored for ≥12 months (WR; n = 20) to perceive affect in biological motion cues relative to healthy controls (HC; n = 23). Overall, individuals with AN evidenced greater deficit in discriminating affect from biological motion cues than WR or HC. Follow-up analyses showed that individuals with AN differed especially across two of the five conditions—deviating most from normative data when discriminating sadness and more consistently discriminating anger relative to WR or HC. Implications of these findings are discussed in relation to some puzzling interpersonal features of AN. © 2012 by Wiley Periodicals, Inc. (Int J Eat Disord 2013)
Article
The aim of the study was to examine how carers cope practically and emotionally with caring for individuals with anorexia nervosa who require intensive hospital care. This study explores objective burden (time spent with caregiving and number of tasks), subjective burden (psychological distress), and social support in a sample of parents (n = 224) and partners (n = 28) from a consecutive series of patients (n = 178) admitted to inpatient units within the United Kingdom. Most time was spent providing emotional support and less with practical tasks. Time spent with caregiving was associated with carer distress and was fully mediated by carer burden. This was ameliorated by social support. Partners received minimal support from others, and we found similar levels of burden and distress for mothers and partners. The data indicate that professional and social support alleviates carer distress and may be of particular value for partners who are more isolated than parents. The data also suggest that time spent with practical support may be of more value than emotional support. © 2012 by Wiley Periodicals, Inc. (Int J Eat Disord 2013;)
Article
Several aspects of social and emotional functioning are abnormal in people with eating disorders. The aim of the present study was to measure facial emotional expression in patients with eating disorders and healthy controls whilst playing a therapeutic video game (Playmancer) designed to train individuals in emotional regulation. Participants were 23 ED patients (11 AN, 12 BN) and 11 HCs. ED patients self reported more anger at baseline but expressed less facial expression of anger during the Playmancer game. The discrepancy between self-report and non-verbal expression may lead to problems in social communication. Copyright © 2012 John Wiley & Sons, Ltd and Eating Disorders Association.
Article
Attention bias modification (ABM) protocols aim to modify attentional biases underlying many forms of pathology. Our objective was to conduct an effect size analysis of ABM across a wide range of samples and psychological problems. We conducted a literature search using PubMed, PsycInfo, and author searches to identify randomized studies that examined the effects of ABM on attention and subjective experiences. We identified 37 studies (41 experiments) totaling 2,135 participants who were randomized to training toward neutral, positive, threat, or appetitive stimuli or to a control condition. The effect size estimate for changes in attentional bias was large for the neutral versus threat comparisons (g=1.06), neutral versus appetitive (g=1.41), and neutral versus control comparisons (g=0.80), and small for positive versus control (g=0.24). The effects of ABM on attention bias were moderated by stimulus type (words vs. pictures) and sample characteristics (healthy vs. high symptomatology). Effect sizes of ABM on subjective experiences ranged from 0.03 to 0.60 for postchallenge outcomes, -0.31 to 0.51 for posttreatment, and were moderated by number of training sessions, stimulus type, and stimulus orientation (top/bottom vs. left/right). Fail-safe N calculations suggested that the effect size estimates were robust for the training effects on attentional biases, but not for the effect on subjective experiences. ABM studies using threat stimuli produced significant effects on attention bias across comparison conditions, whereas appetitive stimuli produced changes in attention only when comparing appetitive versus neutral conditions. ABM has a moderate and robust effect on attention bias when using threat stimuli. Further studies are needed to determine whether these effects are also robust when using appetitive stimuli and for affecting subjective experiences.
Article
A greater understanding of neuropsychological traits in eating disorders may help to construct a more biologically based taxonomy. The aim of this paper is to review the current evidence base of neuropsychological traits in people with eating disorders. Evidence of difficulties in set shifting, weak central coherence, emotional processing difficulties, and altered reward sensitivity is presented for people both in the acute and recovered phase of the illness. These traits are also seen in first degree relatives. At present there is limited research linking these neuropsychological traits with genetic and neuroanatomical measures. In addition to improving the taxonomy of eating disorders, neuropsychological traits may be of value in producing targeted treatments.