Cognitive Behaviour Therapy For Eating Disorders

Cognitive behaviour therapy for eating disorders: a
“transdiagnostic” theory and treatment􏰀

Christopher G. Fairburn ∗, Zafra Cooper, Roz Shafran Oxford University Department of
Psychiatry, Warneford Hospital, Oxford OX3 7JX, UK Received 28 March 2002; received in revised form 27 May 2002;
accepted 27 May 2002
This paper is concerned with the psychopathological processes that account for the persistence of severe eating
disorders. Two separate but interrelated lines of argument are developed. One is that the leading evidence-based
theory of the maintenance of eating disorders, the cognitive behavioural theory of bulimia nervosa, should be
extended in its focus to embrace four additional maintaining mechanisms. Specifically, we propose that in
certain patients one or more of four additional maintaining processes interact with the core eating disorder
maintaining mechanisms and that when this occurs it is an obstacle to change. The additional maintaining
processes concern the influence of clinical perfectionism, core low self-esteem, mood intolerance and
interpersonal difficulties. The second line of argument is that in the case of eating disorders shared, but
distinctive, clinical features tend to be maintained by similar psychopathological processes. Accordingly, we
suggest that common mechanisms are involved in the persistence of bulimia nervosa, anorexia nervosa and the
atypical eating disorders. Together, these two lines of argument lead us to propose a new transdiagnostic theory
of the maintenance of the full range of eating disorders, a theory which embraces a broader range of maintaining
mechanisms than the current theory concerning bulimia nervosa. In the final sections of the paper we describe a
transdiagnostic treatment derived from the new theory, and we consider in principle the broader relevance of
transdiagnostic theories of maintenance.
2003 Elsevier Science Ltd. All rights reserved.

Keywords: Eating disorders; Bulimia nervosa; Anorexia nervosa; Diagnosis; Theory; Cognitive behaviour therapy
∗
Corresponding author. Tel.: 44-1865-226479; fax: 44-1865-226244. E-mail address: credo@medicine.ox.ac.uk (C.G. Fairburn).
􏰀
This paper is based upon a keynote address given by CGF at the Annual Meeting of the British Association for Behavioural and Cognitive
Psychotherapies held in Glasgow in July 2001. The three authors contributed equally to this paper
0005-7967/03/$ - see front matter 2003 Elsevier Science Ltd. All rights reserved. doi:10.1016/S0005-7967(02)00088-8
www.elsevier.com/locate/brat
Abstract
510 C.G. Fairburn et al. / Behaviour Research and Therapy 41 (2003) 509–528
1. Introduction
This paper is concerned with the psychopathological processes that account for the persistence of the
full range of severe eating disorders. For clarity, we take as our starting point bulimia nervosa and its
cognitive behavioural theory and treatment (CBT-BN) since both have been well- specified and
extensively studied. The treatment was first described by Fairburn in 1981 (Fairburn, 1981). Several
years later further procedural details were described (Fairburn, 1985) together with a more complete
exposition of the theory upon which it was based (Fairburn, Cooper, & Cooper, 1986). A full
treatment manual was published in 1993 (Fairburn, Marcus, & Wilson, 1993b) and this has been
widely used in subsequent treatment trials (e.g., Agras et al., 2000a; Agras, Walsh, Fairburn, Wilson,
& Kraemer, 2000b; Fairburn, Jones, Peveler, Hope, & O’Connor, 1993a). As a result of further
experience across different treatment centres, a supplement to the manual was published in 1997 in
which aspects of its implementation were discussed (Wilson, Fairburn, & Agras, 1997). The theory
was elaborated in the same year (Fairburn, 1997a).
2. Cognitive behaviour therapy for bulimia nervosa

2.1. The cognitive behavioural theory
The theory that underpins CBT-BN is primarily concerned with the processes which maintain bulimia
nervosa, although it is also of relevance to the development of the disorder. According to the theory,
central to the maintenance of bulimia nervosa is a dysfunctional system for evaluating self-worth.
Whereas most people evaluate themselves on the basis of their perceived performance in a variety of
domains of life (e.g., the quality of their relationships, work, parenting, sporting ability, etc), people
with eating disorders judge themselves largely, or even exclusively, in terms of their eating habits,
shape or weight (and often all three) and their ability to control them. As a result, their lives become
focused on their eating, shape and weight, with dietary control, thinness and weight loss being
actively pursued whilst overeating, ‘fatness’ and weight gain are assiduously avoided. These
distinctive, and highly characteristic, behavioural and attitudi- nal features are prominent and well-
recognised, as is the dysfunctional system for evaluating self- worth (e.g., American Psychiatric
Association, 2000).
According to the cognitive behavioural theory of the maintenance of bulimia nervosa, this over-
evaluation of eating, shape and weight and their control is of primary importance in maintaining the
disorder. Most of the other clinical features can be understood as stemming directly from this ‘core
psychopathology’, including the extreme weight-control behaviour (viz., the persistent attempts to
restrict food intake (dietary restraint), the self-induced vomiting, misuse of laxatives and diuretics,
and the over-exercising), the various forms of body checking and avoidance, and the preoccupation
with thoughts about eating, shape and weight. Fig. 1 provides a schematic representation of the main
processes involved.
The only feature that is not obviously a direct expression of the core psychopathology is these
patients’ ‘binge eating’ (episodes of uncontrolled overeating). The cognitive behavioural theory
proposes that binge eating is largely a product of the particular way that these patients attempt to
restrict their eating (i.e., their form of dietary restraint), whether or not there is an actual energy
C.G. Fairburn et al. / Behaviour Research and Therapy 41 (2003) 509–528 511
Fig. 1. A schematic representation of the cognitive behavioural theory of the maintenance of bulimia nervosa (modified from
Fairburn, Marcus, & Wilson, 1993b).
deficit. Rather than adopting general guidelines about how they should eat, they try to adhere to
multiple extreme, and highly specific, dietary rules. Accompanying these dietary rules is a tendency
to react negatively to the (almost inevitable) breaking of them with even minor dietary slips being
interpreted as evidence of their lack of self-control, the result being that they respond by temporarily
abandoning their efforts to restrict their eating. Patient reports indicate that this is a major trigger of
binge eating. The consequence is a highly distinctive pattern of eating in which sustained dietary
restraint is repeatedly punctuated by episodes of binge eating. This binge eating in turn maintains the
core psychopathology by magnifying patients’ concerns about their ability to control their eating,
shape and weight. This encourages yet greater dietary restraint, thereby further increasing the risk of
binge eating.
In the original cognitive behavioural formulation (Fairburn, Cooper & Cooper, 1986), it was noted
that these patients’ dietary slips and binges do not happen at random; rather, they are particularly
likely to occur in response to acute changes in mood (typically adverse mood states) since these
appear to interfere with the ability to maintain dietary restraint. However, since binge eating can have
the effect of temporarily neutralising such states, and distracting patients from life difficulties, the
result is that it is reinforced (as discussed later).
A further process maintains binge eating amongst those patients who practise compensatory ‘purging’
(i.e., those who induce vomiting or take laxatives in response to specific episodes of binge eating).
These patients’ faith in the ability of such purging to minimise weight gain results in a major deterrent
against binge eating being undermined1.
One other maintaining process has been highlighted in more recent accounts of the theory (Fairburn,
Marcus & Wilson, 1993b; Fairburn, 1997a). These patients tend to be extremely self- critical. They
set themselves demanding standards in terms of their eating, shape and weight, and their control, and
when they cannot meet them, they see themselves as being at fault rather than
1
This view is mistaken since vomiting only retrieves part of what has been eaten, and laxatives have little or no effect on energy absorption
(see Fairburn, 1995, pp. 48–54).
their standards as being too harsh. The result is secondary negative self-evaluation. This too maintains
the eating disorder since it leads patients to strive even harder to achieve ‘success’ in the area of life
that is most important to them; that is, controlling their eating, shape and weight. In this way a further
vicious circle serves to maintain the eating disorder.
2.1.1. Evidence supporting the theory
This cognitive behavioural theory is supported by variety of lines of evidence:
1. Indirect support comes from the large body of research indicating that CBT-BN, a treatment
that is targeted at these specific maintaining mechanisms, is effective in many cases and is
superior to comparison treatments that control for the non-specific effects of psychological
treatment and to pharmacotherapy (see below). This is not to say that CBT-BN could not be
more effective.
2. Also consistent with the theory is the finding from one study that, among patients who made a
full response to treatment, those with the highest residual level of over-evaluation of shape
and weight were most prone to relapse (Fairburn, Peveler, Jones, Hope, & Doll, 1993c),
although another study failed to replicate this finding (Cooper & Steere, 1995).
3. Additional support comes from a study of mediators of response to CBT-BN which found that
a decrease in dietary restraint mediated the treatment’s effect on binge eating (Wilson,
Fairburn, Agras, Walsh, & Kraemer, 2002).
4. Further support comes from two treatment trials in which largely behavioural versions of the
treatment (which did not address the over-evaluation of eating, shape and weight) were found
to be associated with an increased risk of relapse compared to the full treatment (Cooper &
Steere, 1995; Fairburn, Jones, Peveler, Hope & O’Connor, 1993a).
5. Many of the main predictions of the theory were supported by the findings from a cross-
sectional structural equation modeling study which examined the relevant psychopathological
relationships, although its findings concerning binge eating and purging are difficult to
interpret as a result of the specific assessment measures used (Byrne & McLean, 2002).
6. Support also comes from the findings from a prospective study of the natural course of
bulimia nervosa in which it was found that the baseline level of over-evaluation of shape and
weight predicted persistence of binge eating (over 15 months), and that the degree of dietary
restraint partially mediated this relationship (Fairburn et al., in press).
2.2. The cognitive behavioural treatment
The cognitive behavioural theory of the maintenance of bulimia nervosa has clear implications for
treatment. Specifically, it suggests that the focus of treatment should not solely be on these patients’
binge eating, despite the fact that binge eating is often their primary (and sometimes only) complaint.
Rather, it suggests that to achieve a full and lasting response, these patients’ dietary restraint also
needs to be addressed, as does their response to adverse mood states and their over-evaluation of
eating, shape and weight and their control.
The cognitive behavioural treatment for bulimia nervosa stems from this theory. It is designed to
address each of the maintaining processes outlined above. The treatment is outpatient-based and, as
evaluated in treatment trials, involves 15–20 sessions over approximately five months. A
range of cognitive behavioural procedures are used with its cornerstone being a specific sequence of
cognitive behavioural tasks and “experiments” set within the context of a personalised version of the
cognitive behavioural theory of maintenance (Fairburn, Marcus & Wilson, 1993b).
2.2.1. Evidence supporting the treatment
Given that bulimia nervosa was first described relatively recently (American Psychiatric Associ-
ation, 1980; Russell, 1979), there has been a remarkable amount of research on its treatment. Over 50
randomised controlled trials have been completed and there have been over 20 studies of CBT-BN.
Although almost all of these studies have been “efficacy” rather than “effectiveness” trials, there are
good reasons to think that their findings are relevant to everyday patient care (see Wilson, 1998a;
Wilson & Fairburn, 2002), not least because the patients have closely resembled those seen in routine
clinical practice (Wilson, 1998b).
The main findings of relevance may be summarised as follows (see Wilson and Fairburn, 2002) for a
more detailed review of the findings)2:
 􏰂 CBT-BN has a substantial effect on the frequency of binge eating and purging, and the full
range of the psychopathology of bulimia nervosa. Among treatment completers (typically 80
to 85%), between 40–50% cease binge eating and purging altogether. These patients generally
improve in all respects, and it seems that most remain well in the long-term (e.g., Fairburn et
al., 1995). The remaining patients range in outcome from substantially improved to not
improved at all.
 􏰂 CBT-BN is more effective than both delayed treatment and pharmacotherapy.
 􏰂 CBT-BN has been compared with a wide range of psychological treatments including
supportive psychotherapy, focal psychotherapy, supportive-expressive psychotherapy,
interpersonal psychotherapy (IPT), hypnobehavioural treatment, stress management,
nutritional counselling, behavioral versions of CBT-BN, and various forms of exposure with
response prevention (see Wilson & Fairburn, 2002). It has proved as effective as, or more
effective than, all these treatments. The leading alternative treatment is IPT which, in
statistical terms, is comparable in its eventual effects but much slower to act (Agras, Walsh,
Fairburn, Wilson & Kraemer,
2000b; Fairburn, Jones, Peveler, Hope & O’Connor, 1993a).
 􏰂 Consistent predictors of response to CBT-BN have been difficult to find but there is
emerging
evidence that the most powerful and consistent predictors are the frequency of binge eating
and purging at the start of treatment (the higher the frequency, the worse the prognosis) and,
most especially, the extent of their reduction over the initial weeks of treatment (Agras et al.,
2000a)3. As Wilson (1999a) has highlighted, the predictive utility of early response to CBT is
a phenomenon not confined to bulimia nervosa but has been reported in other disorders
including depression, alcohol abuse and obesity.
Therefore, two clear findings emerge from this large body of research. The first is that CBT-
2
The findings of the Cochrane systematic review of studies of the treatment of bulimia nervosa (Hay & Bacaltchuk, 2000) are
impossible to interpret because the review conflates studies of binge eating disorder with those of bulimia nervosa.
3
This finding has been replicated using data from the Stanford-Oxford-Columbia CBT-IPT trial. (See Agras and colleagues (2000b) for
details of this study.).
BN is an effective treatment for bulimia nervosa: indeed, given the quantity, quality and breadth of
the research evidence, bulimia nervosa is one of the clearest indications for CBT. The second finding
is that CBT-BN is not effective enough: at best, only half the patients make a full and lasting response.
This raises the important question “Why aren’t more people getting better?”
2.3. Why aren’t more people getting better?
In principle, four main explanations may be proposed as to why the response to CBT-BN is not
greater than it is.
2.3.1. The theory upon which CBT-BN is based is incorrect, and therefore the targeted maintaining
mechanisms are the wrong ones
As outlined above, there are strong grounds for thinking that this is not the case. This is not to say that
the theory is a complete account of the processes that maintain bulimia nervosa.
2.3.2. CBT-BN has not been implemented optimally in the research trials
This seems unlikely since the larger and most influential trials have been conducted at major research
centres with principal investigators who are experts in psychological treatment research. Furthermore,
quality control measures were in place. Having said this, adherence findings have yet to be published.
It might be argued that the response rates would have been higher had the treatment not had to
conform to a research protocol (e.g., being restricted to a fixed number of sessions over a
predetermined time period) and a specific treatment manual (Fairburn, Marcus & Wilson, 1993b). The
former point is a reasonable one but the latter neglects the clinical flexibility inherent within such
manuals and the arguments and evidence supporting manual-based treatment in general (see Wilson,
1996, 1998a).
2.3.3. While the theory underpinning CBT-BN is valid and the focus of treatment is therefore
appropriate, the existing treatment procedures are not sufficiently potent
Clinical experience suggests that this is undoubtedly true in some cases. Even when the treatment is
well implemented, the targeted psychopathology can prove resistant to change.
There are a number of ways in which the effectiveness of CBT-BN might be improved without
shifting its focus from the maintaining mechanisms specified above. First, new generic cognitive
behavioural procedures have been developed since CBT-BN was first devised and these could be
capitalised upon (for example, see Beck, 1995; Greenberger and Padesky, 1995; Padesky and
Greenberger, 1995; Segal, Williams, & Teasdale, 2002). Second, certain aspects of the core psy-
chopathology have received insufficient attention in CBT-BN yet accumulating clinical experience
suggests that they may play an important role in maintaining the disorder. For example, it has only
recently been appreciated that many patients repeatedly check aspects of their body in highly
idiosyncratic ways, and that their means of doing so is likely to intensify their concerns and
dissatisfaction (Fairburn, Shafran, & Cooper, 1999; Rosen, 1997). The treatment procedures for
addressing body checking therefore need to be enhanced (Rosen, 1996; Wilson, 1999b). Indeed, it is
our view that the entire strategy for addressing the over-evaluation of eating, shape and weight, and its
various expressions, needs to be reformulated, and that greater emphasis needs to be placed on it. A
third way of possibly improving CBT-BN stems from the finding that the
magnitude of initial behavioural response is a powerful predictor of outcome. This suggests that
increasing the proportion of patients who do well early on in treatment might increase the overall
response rate. For example, benefits might come from reverting to the original CBT-BN strategy of
seeing patients twice a week for the initial four weeks (Fairburn, 1985), rather than for just two weeks
as in recent research protocols, since in our experience doing so results in greater behaviour change. It
is also our view that effort should be made to ensure that the momentum of treatment is not
interrupted, particularly in the early stages, since even quite short breaks can result in substantial
setbacks.
2.3.4. The theory is valid but it needs to be extended to embrace additional maintaining mechanisms
Several authors have suggested that the existing theory is too narrowly focused in that it concen-
trates primarily on the “specific psychopathology” of eating disorders (i.e., clinical features pecul- iar
to eating disorders) (e.g., Hollon & Beck, 1993; Meyer, Waller, & Waters, 1998). We too think that
there is a need for a revised conceptualisation of the processes that maintain bulimia nervosa.
Accordingly, we have developed one and it is described below.
3. A new cognitive behavioural theory of the maintenance of bulimia nervosa
The new theory represents an extension of the original theory illustrated in Fig. 1. Specifically, it is
proposed that in certain patients one or more of four additional maintaining processes interact with
the core eating disorder maintaining mechanisms shown in Fig. 1 and that when this occurs it is an
obstacle to change. The first of these additional maintaining mechanisms concerns the influence of
severe perfectionism (“clinical perfectionism”); the second concerns the impact of unconditional and
pervasive low self-esteem (“core low self-esteem”); the third concerns difficulty coping with intense
mood states (“mood intolerance”); and the fourth is interpersonal and developmental in character
(“interpersonal difficulties”). Thus this new cognitive behavioural theory is broader in its scope than
the original more focused one. However, it must be stressed that this theory is not intended to replace
the former one—this would make little sense given the weight of evidence supporting it. Rather, the
new theory is designed to supplement it. This point is illustrated in Fig. 2 which shows in schematic
form some of the main hypothesised maintaining mechanisms. These will now be described.
3.1. Clinical perfectionism
Although the notion of perfectionism is widely used, there have been few attempts to define and
characterise it. We have recently provided a cognitive behavioural analysis of what we term “clinical
perfectionism”—that is, perfectionism of clinical significance (Shafran, Cooper, & Fair- burn, 2002).
This we define as the over-evaluation of the striving for, and achievement of, person- ally demanding
standards, despite adverse consequences. In other words we suggest that at the heart of the
psychopathology of clinical perfectionism is a system for self-evaluation in which self-worth is
judged largely on the basis of striving to achieve demanding goals and success at meeting them. It
should be evident therefore that we view clinical perfectionism as a form of
Fig. 2. A schematic representation of the extended cognitive behavioural theory of the maintenance of bulimia nervosa.
‘Life’ is shorthand for interpersonal life.
psychopathology that is similar in nature to the “core psychopathology” of eating disorders in that
both are examples of dysfunctional systems for self-evaluation.
Perfectionism is well-known to co-occur with eating disorders (see Wonderlich, 2002; Shafran et al.,
2002). Under these circumstances, there is often an interaction between the two forms of
psychopathology with the patient’s perfectionist standards being applied to the attempts to control
eating, shape and weight, as well as to other aspects of their life (e.g., their performance at work or
sport). As in other expressions of clinical perfectionism (Shafran et al., 2002), there is fear of failure
(i.e., in these patients, fear of overeating, “fatness”, weight gain); frequent and selective attention to
performance (in these patients, repeated calorie-counting, frequent shape and weight checking); and
self-criticism arising from negatively biased appraisals of their performance. The resulting secondary
negative self-evaluation in turn encourages even more determined striving to meet valued goals—
including, in this case, striving to meet goals in the domain of controlling eating, shape and weight—
thereby serving to maintain the eating disorder. Therefore in such patients it may be predicted that
were their clinical perfectionism to be corrected, a potent additional network of maintaining
mechanisms would be removed thereby facilitating change.
3.2. Core low self-esteem

Whilst most patients with bulimia nervosa are self-critical as a result of their failure to achieve their
goals, a form of negative self-evaluation that generally reverses with successful treatment, there is a
subgroup that has a more global negative view of themselves. Thus, rather than simply thinking
negatively about themselves as a result of their inability to control their eating, shape and weight,
these patients have an unconditional and pervasive negative view of themselves which is seen as part
of their permanent identity. Their negative self-judgements are autonomous and
largely independent of performance: in other words, they are less affected by changes in the state of
the eating disorder.
Such “core low self-esteem” tends to obstruct change in general. This is through two main
mechanisms. First, it creates in patients hopelessness about their capacity to change, thereby
undermining their compliance with treatment; and second, it results in them pursuing, with particular
determination, achievement in their valued domains (in this case the pursuit of control over eating,
shape and weight) thereby making change in these areas all the more difficult. The state is also self-
perpetuating since these patients show particularly pronounced negative cognitive processing biases,
coupled with over-generalisation, with the result that any perceived “failure”is interpreted as
confirmation that they are failures as people thereby reaffirming their overall negative view of
themselves.
Given the many barriers to change that arise as a result of core low self-esteem, it is not surprising
that clinical experience and some research findings suggest that such patients respond particularly
poorly to treatment (Fairburn, Kirk, O’Connor, Anastasiades, & Cooper, 1987, 1993c). On the other
hand, were their core low self-esteem to be corrected, it would be predicted that their outcome would
improve as a result.
3.3. Mood intolerance
It was recognised in the original cognitive behavioural theory that adverse mood states can be a
trigger of binge eating, and it was suggested that their primary effect was to disrupt dietary restraint
(Fairburn, Cooper & Cooper, 1986). It is now clear that in some patients there is a more complex
relationship between emotional states and binge eating (e.g., Meyer, Waller & Waters, 1998; Polivy &
Herman, 1993; Steinberg, Tobin, & Johnson, 1990; Stice, 1994; Waller, 2002).
A subgroup of patients with eating disorders have what may be termed “mood intolerance”. We use
this term to refer to an inability to cope appropriately with certain emotional states. Usually this
intolerance is of adverse mood states, such as anger, anxiety or depression, but in some cases there is
intolerance of all intense mood states including positive ones (e.g., excitement). Instead of accepting
changes in mood and dealing appropriately with them, these patients engage in what may be termed
“dysfunctional mood modulatory behaviour.” This reduces their awareness of the triggering mood
state (and the associated cognitions), and also neutralises it, but at a personal cost. The dysfunctional
mood modulatory behaviour may take the form of self-injury (e.g., cutting, punching or burning
themselves) which has the effect of rapidly dissipat- ing the initial mood state, or it may involve
taking psychoactive substances (e.g., alcohol, tranquillizers) to directly modify how they feel. Both
classes of behaviour are not uncommon among patients with eating disorders (e.g., Claes,
Vandereycken, & Vertommen, 2001; Holder- ness, Brooks-Gunn, & Warren, 1994; Paul, Schroeter,
Dahme, & Nutzinger, 2002). In patients with bulimia nervosa, binge eating, self-induced vomiting
and intense exercising may also be used as forms of mood modulatory behaviour, binge eating most
commonly serving this purpose. Among these patients (i.e., those with an eating disorder and mood
intolerance), such forms of behaviour (i.e., binge eating, vomiting, intense exercising) can become
habitual means of mood modulation.
It is not clear whether these patients actually experience unusually intense mood states or whether
they are especially sensitive to them. Often both appear to be the case. Either way,
cognitive processes commonly contribute to the phenomenon; for example, such patients typically
respond to incipient mood change by thinking that they will not be able to cope with the resulting
feelings and thoughts, a reaction that can amplify the mood state.
3.4. Interpersonal difficulties
The original cognitive behavioural account of the maintenance of bulimia nervosa existed in
something of a vacuum in that it paid little attention to patients’ circumstances—other than
acknowledging that the proximal triggers of binge eating were commonly interpersonal in nature. The
need to broaden this focus has been made especially clear by the research on IPT. This indicates that
an exclusively interpersonal form of this treatment is about as effective as cognitive behaviour therapy
in the longer-term (Agras, Walsh, Fairburn, Wilson & Kraemer, 2000b; Fair- burn, Jones, Peveler,
Hope & O’Connor, 1993a, 1995) despite the fact that it does not directly address any of the
maintaining mechanisms identified by the cognitive behavioural theory (Fairburn, 1997b).
There can be no doubt that interpersonal processes contribute in a variety of ways to the mainte-
nance of eating disorders. Four examples may be used to illustrate this point. First, in younger
patients, family tensions often intensify resistance to eating. It can be argued that this reflects a short-
term intensification of their need for a sense of “control”, a need which is displaced onto dietary self-
control (Fairburn, Shafran & Cooper, 1999). Second, it is obvious that certain interpersonal
environments magnify concerns about controlling eating, shape and weight. These include families in
which there are other members with an eating disorder, and occupations in which there is pressure to
be slim. Third, as already noted, adverse interpersonal events commonly precipitate episodes of binge
eating, and there is evidence that patients with bulimia nervosa may be especially sensitive to social
interactions (Steiger, Gauvin, Jabalpurwala, Seguin, & Stotland, 1999). Fourth, long-term
interpersonal difficulties undermine self-esteem which, as noted earlier, is prone to result in patients
striving even harder to achieve valued goals, such as success at controlling eating, shape and weight.
It is also relevant that there is evidence that disturbed interpersonal functioning predicts a poor
response to treatment (Agras et al., 2000a; Steiger, Leung, & Thibaudeau, 1993).
Having said this, it is not known how IPT achieves its beneficial effects. It is likely to be through
several mechanisms (Fairburn, 1997b). First, it is clear from clinical experience that it succeeds in
helping many patients overcome ongoing interpersonal difficulties, ones which may have been
longstanding. For example, one of its foci is on interpersonal “role transitions” (see Klerman,
Weissman, Rounsaville, & Chevron, 1984). This is especially pertinent to those patients who have
missed out on the interpersonal challenges of late adolescence and early adulthood as a result of being
immersed in their eating disorder. Second, it is our observation that IPT can also open up new
interpersonal opportunities (“fresh start events”; Brown, Adler, & Bifulco, 1988) which may
themselves have positive effects (Fairburn, 1997b). When this happens interpersonal aspects of life
start to occupy a greater place in these patients’ system for self-evaluation which, in turn, reduces the
importance that they attach to eating, shape and weight and their control. Third, IPT can give patients
a sense that they are capable of influencing their interpersonal lives (in some cases for the first time)
which may also lessen their need to control their eating, shape and weight.
In summary, there are good reasons to think that interpersonal difficulties can perpetuate eating
disorders, and there is evidence that their resolution facilitates change.
4. A transdiagnostic perspective
We now turn to our second line of argument, that concerning transdiagnostic maintaining mech-
anisms, starting with anorexia nervosa.
4.1. Anorexia nervosa
Anorexia nervosa is the other main eating disorder recognised by the leading classificatory systems in
psychiatry. Anorexia nervosa and bulimia nervosa have much in common. They share essentially the
same core psychopathology with both groups of patients over-evaluating eating, shape and weight and
their control4, and this psychopathology is expressed in similar attitudes and behaviour. Thus patients
with anorexia nervosa restrict their food intake in the same rigid and extreme way as patients with
bulimia nervosa, and they too may vomit, misuse laxatives or diuretics, and over-exercise. In those
anorectic patients who over-evaluate controlling their shape and weight as well as their eating (see
footnote 4), there are the same forms of body checking as in bulimia nervosa, and both groups of
patients complain of preoccupation with thoughts about eating, shape and weight. Nor does binge
eating distinguish the two disorders, for in a subgroup of patients with anorexia nervosa binge eating
(with or without compensatory purging) is also present (Casper, Eckert, Halmi, Goldberg, & Davis,
1980; Garfinkel, Moldofsky, & Garner, 1980). Thus anorexia nervosa and bulimia nervosa share the
same distinctive and characteristic clinical features. The major difference between the two disorders
lies in the relative balance of the under- eating and over-eating, and its effect on body weight. In
bulimia nervosa the two forms of behaviour tend to cancel each other out with the result that body
weight is usually unremarkable, whereas in anorexia nervosa under-eating predominates—indeed,
there may be no binge eating at all—with the result that body weight is extremely low, and symptoms
of starvation are prominent (see Garner, 1997).
If the commonalities between the two disorders are obvious when they are viewed cross-section- ally,
they become even more evident when a longitudinal perspective is taken. In patients who do not
recover from anorexia nervosa, cross-over to bulimia nervosa is a frequent occurrence (e.g., Sullivan,
Bulik, Fear, & Pickering, 1998), the result being that about a quarter of patients with bulimia nervosa
have had anorexia nervosa in the past (e.g., Agras, Walsh, Fairburn, Wil- son & Kraemer, 2000b).
This movement across from anorexia nervosa to bulimia nervosa reflects a shift in the balance of
under-eating and over-eating with the former ceasing to be dominant in its influence on body weight.
Generally other aspects of the psychopathology remain much the same but with the starvation
symptoms fading as weight increases and with the fears of fatness being intensified by the episodes of
binge eating.
4
If there is a difference in their core psychopathology, it is that in some patients with anorexia nervosa the primary focus is on controlling
eating per se, rather than on shape and weight and their control. In our experience, this tends to be especially true of younger cases of short
duration. (See Fairburn et al., 1999 for discussion of the issue of control in anorexia nervosa.)
4.2. Atypical eating disorders or EDNOS
Although the concept of an “eating disorder” tends to be equated with anorexia nervosa and bulimia
nervosa, both the leading classificatory systems in psychiatry recognise a third residual category of
eating disorder. These “atypical eating disorders” (Fairburn & Walsh, 2002)—the DSM-IV term is “
eating disorder not otherwise specified”or EDNOS (American Psychiatric Association, 1994)—are
“eating disorders” of clinical severity that do not meet the specific criteria for anorexia nervosa or
bulimia nervosa. They are at least as prevalent as anorexia nervosa and bulimia nervosa, if not more
so (e.g., Millar, 1998; Ricca et al., 2001), and they too have much in common with bulimia nervosa
(and, indeed, anorexia nervosa). Some resemble the full syndromes of anorexia nervosa or bulimia
nervosa but do not quite meet their diagnostic criteria, whereas in others the characteristic
psychopathological features are combined in a somewhat different way. In our clinical experience
rigid and extreme dietary restraint is prominent in most atypical eating disorders and sometimes it is
accompanied by self-induced vomiting, over-exercising or laxative misuse. Binge eating (objective
or subjective) is also a common feature, and in the majority of cases there is the over-evaluation of
eating, shape and weight and their control that is the hallmark of the two prototypic eating disorders.
As with the comparison of anorexia nervosa and bulimia nervosa, cross-diagnostic commonalities
become even more obvious when a longitudinal perspective is taken. For example, an atypical eating
disorder is a common outcome of anorexia nervosa (e.g., Sullivan, Bulik, Fear & Pickering, 1998);
bulimia nervosa typically starts as anorexia nervosa or an atypical eating disorder; and a particularly
common outcome of bulimia nervosa is a chronic atypical eating disorder (e.g., Fair- burn et al.,
1995).
The significance of this migration of patients across the diagnostic categories of anorexia nervosa,
bulimia nervosa and the atypical eating disorders has received surprisingly little attention. It is far
from random and its basis is not understood. Age and/or duration of disorder appear to be relevant, the
two being difficult to disentangle. The eating disorders of mid-adolescence typically take the form of
anorexia nervosa or an anorexia nervosa-like state, whereas a bulimia nervosa-like picture is more
typical of those of late adolescence or early adulthood. Thus disorders which persist from adolescence
to adulthood commonly change in form from a restricting anorexia nervosa-like picture to one more
typical of bulimia nervosa. Indeed, this transition is so common that it has recently been suggested
that the restricting form of anorexia nervosa (i.e., one in which there is no regular binge eating or
purging) should merely be viewed as a “phase” in the course of the eating disorder (Eddy et al., 2002).
The phenomenon has encouraged us to take a transdiagnostic perspective on the maintenance of
eating disorders.
4.3. Implications of the transdiagnostic perspective for the maintenance of eating disorders
In summary, anorexia nervosa, bulimia nervosa and the atypical eating disorders share the same
distinctive psychopathology, and patients move between these diagnostic states over time. These two
characteristics, together with the clinical observation that shared clinical features tend to be
maintained by similar psychopathological processes, suggest that common mechanisms are involved
in the persistence of bulimia nervosa, anorexia nervosa and the atypical eating disorders. This is
illustrated in principle in Fig. 3 (left-hand figure) in which the focused cognitive behav-
Fig. 3. A schematic representation of the maintenance of anorexia nervosa. The left-hand figure represents the ‘restricting
type’ and the right-hand figure represents the ‘binge-eating/purging type’.
ioural formulation of bulimia nervosa has been modified to represent the main processes maintaining
anorexia nervosa (restricting type). As can be seen, the binge eating and compensatory purging have
been replaced by a box labelled “starvation syndrome” since, as Garner and others (e.g., Fairburn,
Shafran & Cooper, 1999; Garner, Rockert, Olmsted, Johnson & Coscina, 1985; Garner, 1997) have
argued, various aspects of the starvation syndrome appear to maintain anorexia nervosa. Particularly
important in our view is the pronounced social withdrawal seen in starvation since it has the effect of
encouraging self-absorption whilst also isolating patients from external influences that might diminish
their over-evaluation of eating, shape and weight and their control. In the binge-eating/purging type of
anorexia nervosa both the starvation syndrome and the binge eating contribute to the maintenance of
the eating disorder (see Fig. 3, right-hand figure), possibly explaining the relatively poor prognosis of
such patients (Steinhausen, 1991). In our experience, equivalent processes serve to maintain the
various forms of atypical eating disorder.
This transdiagnostic line of argument applies equally to the new broader conceptualisation of bulimia
nervosa. Its cross-diagnostic relevance may be best illustrated with reference to anorexia nervosa
since this disorder’s clinical features are more consistent and better established than those of the
atypical eating disorders. First, with respect to clinical perfectionism, the mechanisms that were
specified as operating in some cases of bulimia nervosa also operate in certain cases of anorexia
nervosa: indeed, clinical perfectionism is more prominent in anorexia nervosa than bulimia nervosa
which may partly account for these patients success at restricting their eating. Core low self-esteem
also occurs in anorexia nervosa especially in more chronic cases where it appears to be an important
maintaining factor. In contrast, mood intolerance (as defined above) is less typical of patients with
anorexia nervosa, although it is seen among some of those with the binge eating/purging form of the
disorder. Lastly, interpersonal difficulties are frequently present in anorexia nervosa, both with the
patient’s family and with his or her peers, hence the
widespread use of family therapy (Dare & Eisler, 2002) and the recent interest in IPT (McIntosh,
Bulik, McKenzie, Luty & Jordan, 2000). Thus, each of the four additional sets of maintaining
processes specified in the broader conceptualisation of bulimia nervosa is also likely to operate among
subgroups of patients with anorexia nervosa. And again, in our experience, the same applies in
precisely the same way to subgroups of patients with atypical eating disorders 5.
It is important to note that this broader conceptualisation of the maintenance of eating disorders is
consistent with other accounts, particularly cognitive behavioural accounts of anorexia nervosa: for
example, Garner, Vitousek/Bemis and Pike have particularly stressed the contribution of low self-
esteem (e.g., Garner & Bemis, 1982, 1985; Garner, Vitousek, & Pike, 1997; Pike, Loeb, & Vitousek,
1996). It should also be noted that the emphasis on interpersonal processes is consistent with family
therapy (Dare and Eisler, 2002; Lock, le Grange, Agras, & Dare, 2001) and IPT perspectives
(Fairburn, 1997b; McIntosh, Bulik, McKenzie, Luty & Jordan, 2000). What is distinctive about the
present theory is its transdiagnostic scope, its specificity and its clear implications for treatment.
5. The transdiagnostic treatment
In this paper we have proposed that a network of inter-related maintaining mechanisms accounts for
the persistence of anorexia nervosa, bulimia nervosa and the atypical eating disorders. This network is
illustrated in schematic form in Fig. 4. More specifically, we have suggested that in the great majority
of cases there is a central cognitive disturbance characterised by the over- evaluation eating, shape
and weight and their control, and that in subgroups of these patients one or more of four additional
mechanisms also serve to maintain the eating disorder. We have not proposed that these additional
mechanisms necessarily operate simultaneously, nor have we suggested that they are active in every
case. Indeed, their partial independence may account in part for the varied and fluid form of these
disorders. Rather, we have suggested that in individual patients they contribute to the maintenance of
the eating disorder and that, under such circumstances, unless they are successfully corrected,
treatment is not likely to result in full and lasting recovery.
On the basis of this cognitive behavioural theory, we have developed a new transdiagnostic treatment
(Fairburn, Cooper, & Shafran, 2002). Its main characteristics are as follows:
1. The treatment has been designed to be suitable for all forms of clinical eating disorder so long as
outpatient management is appropriate. In our experience this is true of the great majority of cases.
2. The patient’s specific eating disorder diagnosis is not of relevance to the treatment. Rather, its
5
In the subtype of EDNOS termed “binge eating disorder”, binge eating occurs in the absence of extreme weight-control behaviour
(American Psychiatric Association, 2000; Grilo, 2002). Here the primary maintaining process appears to be the mood-modulatory effect of
binge eating. Thus a relatively circumscribed maintaining mechanism is operating. This might account for the disorder’s tendency to remit
in the absence of treatment (Fairburn, Cooper, Doll, Norman, and O’Connor, 2000) and its responsiveness to a variety of interventions
(Wilson & Fairburn, 2000).
Fig. 4. A schematic representation of the ‘transdiagnostic’ theory of the maintenance of eating disorders. ‘Life’ is shorthand
for interpersonal life.
content is dictated by the particular psychopathological features present and the processes that
appear to be maintaining them.
3. The treatment has been designed to be practicable under normal outpatient conditions. Thus it
can be provided by male or female therapists (unlike those treatments which involve in-
session mirror exposure), and it is not unduly labour-intensive when compared with existing
treatments. No special facilities are required.
4. As operationalised for an ongoing research trial, the treatment is provided in two versions, a
20-session treatment for the majority of patients, and a 40-session treatment for patients who
are significantly underweight (defined as a BMI 􏰁17.5). The two forms of the treatment are
delivered over 20 and 40 weeks respectively with the initial sessions being twice-weekly. The
style and content of the two versions are essentially the same except that the longer treatment
also includes procedures designed to help patients regain weight. The optimal length of treat-
ment and number of sessions remains to be determined.
5. The treatment is provided on a one-to-one basis. We believe that this is likely to be the best
way of delivering the treatment given its idiographic nature.
6. The treatment has four stages:
o 􏰂 Stage One is an intensive initial stage which lasts four weeks, the focus being on
engaging
and educating the patient, creating an initial personalised formulation, and obtaining
maximal
early behaviour change.
o 􏰂 In Stage Two (which occupies one to three sessions) there is a detailed review of
progress
so far, as well as the characterisation of any barriers to change. In addition, there is a

formal
524
C.G. Fairburn et al. / Behaviour Research and Therapy 41 (2003) 509–528
assessment of the likely contribution of each of the four additional maintaining mechanisms specified
above. The resulting information is used to create, jointly with the patient, a revised and extended
formulation.
Stage Three occupies the largest part of the treatment and its content is dictated by the revised
formulation. It always includes emphasis on modifying the patient’s eating disorder psychopathology
(for example, the over-evaluation of eating, shape and weight and their control, and its various
expressions), but it also involves addressing those additional processes identified in the revised
formulation. To this end there are treatment “modules” focused on clinical perfectionism, core low
self-esteem, mood intolerance and interpersonal difficulties. These are deployed as indicated.
The final stage in treatment, Stage Four, is similar to the final stage in CBT-BN (Fairburn, Marcus &
Wilson, 1993b), although it is broader in scope. The emphasis is on ensuring that progress is
maintained after treatment ends. Sessions are fortnightly by this stage.
We have evolved this new transdiagnostic treatment over the past three years selecting patients of a
type that do not typically respond well to a more focused style of approach (as exemplified by CBT-
BN). The results have been sufficiently encouraging for us to embark on a transdiagnostic treatment
trial designed to test not only the new treatment, but also the theory upon which it is based.
6. Broader implications
It has not escaped our attention that this transdiagnostic approach to theory and treatment has
implications beyond the field of eating disorders6. We therefore close this paper by addressing the
circumstances under which such a strategy is likely to be of value.
In principle, transdiagnostic conceptualisation and treatment is relevant when major clinical features
shared by two or more diagnostic states are maintained by common pathological processes. We
propose that the presence of either of the following two characteristics is suggestive of the operation
of common maintaining processes, but that neither is sufficient:
􏰂 shared distinctive clinical features

􏰂 movement of patients between the diagnostic states
To establish the operation of transdiagnostic pathological processes there would need to be direct
clinical and research evidence that the processes maintaining the diagnostic states do indeed over- lap
(for example, by identifying common distinctive obstacles to change or by developing common
distinctive methods of achieving change).
We leave readers to consider the frequency with which these conditions apply within psychiatry.
6
Those familiar with the origins of behaviour therapy will recognise in our strategy the focus on individualised case formulation rather than
psychiatric diagnosis, and the theory-driven design of patient-specific treatment.
Acknowledgements
All three authors are supported by the Wellcome Trust: CGF is supported by a Principal Research
Fellowship (046386); ZC is supported by a programme grant (046386); and RS is supported by a
Research Career Development award (063209). Without the Wellcome Trust’s sustained support this
work would not have been possible. The ongoing transdiagnostic trial is being conducted in
collaboration with Dr Robert Palmer of the University of Leicester. This trial is funded by the
programme grant from the Wellcome Trust.
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Patterns of 'Abnormal' Illness
Behavior among Healthy
Individuals
Kirsty N Prior 1, Malcolm J Bond
Affiliations expand
 PMID: 28452690
 DOI: 10.5993/AJHB.41.2.4
Abstract
Objectives: We extend the seminal work of Professor Issy Pilowsky by presenting a
contemporary re-conceptualization of abnormal illness behavior (AIB) as a general
psychological phenomenon evident among healthy community members.
Methods: Participants (N = 344) completed a self- report questionnaire comprising health

information and well-validated psychological measures from the field of somatization (eg,
AIB, attributional style for physical symptoms, cognitive distortion of somatic information,
illness likelihood, maladaptive coping).
Results: Cluster analysis of illness behavior responses resulted in 3 unique groupings

distinguished by key health and psychological variables. Cluster 1 reflected 'normal'
responses, Cluster 2 'atypical' and Cluster 3 'maladaptive'. Cluster 3 may represent a
personality attribute indicative of a general style of interpreting illness in a more extreme way
(trait AIB) whereas Cluster 2 may reflect a transient response to a specific illness event (state
AIB).
Conclusions: The construct of 'abnormal' illness behavior may usefully be extended to

include individual differences in responses regardless of current health status. Furthermore,
the potential to further characterize illness behavior as either dispositional (trait) or situational
(state) emerges as a fruitful area for future analyses. Specifically, longitudinal studies are
recommended to determine the causal links between health events and illness behavior
profiles.
Patterns of 'Abnormal' Illness

Behavior among Healthy
Individuals
Kirsty N Prior 1, Malcolm J Bond
The Unifying Concept of Illness Behavior

Laura Sirria Giovanni A. Favaa, c Nicoletta Soninob, c
a
Laboratory of Psychosomatics and Clinimetrics, Department of Psychology, University of Bologna, Bologna, and
b
Department of Statistical Sciences, University of Padova, Padova, Italy; cDepartment of Psychiatry, State University of New
York at Buffalo, Buffalo, N.Y., USA
Key Words
Clinimetrics 􏰀 Delay in seeking treatment 􏰀 Frequent attenders 􏰀 Health care-seeking behavior 􏰀 Illness
behavior 􏰀 Illness perception 􏰀 Treatment adherence 􏰀 Treatment-seeking behavior
Abstract
The concept of illness behavior was introduced to indicate the ways in which given symptoms may be
perceived, evaluated and acted upon at an individual level. Illness behavior may vary greatly according to
illness-related, patient-related and doctor-related variables and their complex interactions. In the past decades,
important lines of research have been concerned with illness perception, frequent attendance at medical
facilities, health care-seeking behavior, treatment- seeking behavior, delay in seeking treatment, and treatment
adherence. They have, however, mostly investigated single aspects separately. In this concise review, we
suggest that the concept of illness behavior may provide a unifying framework and useful insights to
observations and findings that would otherwise remain scattered and unrelated in the medical literature. The
wide range of expressions of illness behavior is likely to affect the presentation of any disease and its
identification, course and treatment. Assessing illness
behavior and devising appropriate responses by health care providers may contribute to the improvement of
final outcomes. Copyright © 2012 S. Karger AG, Basel
The disease model is still considered the basis for optimal identification of treatments for patients.
However, it does not take into consideration that behavioral responses to a medical condition vary
widely among subjects facing the same illness. When patient behaviors dif- fer from those expected
or recommended by physicians, the greater this discrepancy, the less likely the course of a disease will
be predicted solely by biomedical factors [1–3]. Therefore, the disease model cannot explain how
recognition, presentation and outcome of a disease may be largely influenced by individual responses
to symptoms [4].
The concept of illness behavior provides an explana- tory model for clinical phenomena that do not
find room in customary taxonomy [1, 2, 5]. It was based on the early work of Sigerist [6] and
Parsons [7], who suggested that each disorder cannot be ascribed only to pathophysiolog- ical
mechanisms but also entails both psychological and social dimensions. In 1929, the Swiss medical
historian
Laura Sirri, PhD

Department of Psychology
University of Bologna
viale Berti Pichat 5, IT–40127 Bologna (Italy) E-Mail laurasirri @ libero.it
Fax +41 61 306 12 34 E-Mail karger@karger.ch www.karger.com
© 2012 S. Karger AG, Basel 0033–3190/13/0822–0074$38.00/0
Accessible online at: www.karger.com/pps
Henry Sigerist [6] noted how different societies have rec- ognized a specific social status to sick
persons characterized by privileges and obligations. Two decades later, the American sociologist
Talcott Parsons [7] introduced the term ‘sick role’, which allows the privilege to sick persons to be
exempt from normal responsibilities and social du- ties, such as work, but includes the obligations to
try to get well and, thus, to seek qualified help and to cooperate in recovering. In 1960, Mechanic and
Volkart [5] investigated the different ways people react to physical symptoms and the psychosocial
and cultural factors affecting such reactions. They defined illness behavior as ‘the ways in which
given symptoms may be differentially perceived, evaluated, and acted (or not acted) upon by different
kinds of persons’. Subsequently, Mechanic [8] provided the following specification: ‘Illness behavior
refers to the varying ways individuals respond to bodily indications, how they monitor internal states,
define and interpret symptoms, make attributions, take remedial actions and utilize various sources of
informal and formal care’.
Important lines of research have been concerned with illness perception, health care-seeking behavior,
frequent attendance at medical facilities, treatment-seeking behavior, delay in seeking treatment, and
treatment adherence. Different investigations, however, dealt with single aspects separately. In this
concise review, we suggest that the concept of illness behavior may provide a unifying framework
and useful insights. A discussion of issues related to abnormal illness behavior [4, 9, 10] is beyond
the aim of this paper.
Clinical Implications of Illness Behavior
As stated by Mechanic [8], illness behavior ‘shapes the recognition of illness, the selection of patients
into care, the degree of compatibility between patient and physician attributions, patterns of health
practice and adherence with medical advice, and the course of illness and the treatment process’.
The simple fact that, in the presence of certain physical symptoms (e.g. chest pain), some persons
immediately seek medical help while others wait a long time before consulting a physician determines
the likelihood of early recognition of a life-threatening disease and its prompt treatment and
prognosis. Indeed, delay in seeking medical attention may be crucial for the subsequent length of
survival of the patient. In a community-based population aged 55 years or older, attention to
symptoms suggestive of cancer and intention to seek timely medical help were inadequate on average
[11]. In
cardiology settings, less than 10% of patients actively sought professional help as the first response to
acute myocardial infarction symptoms, the most frequent initial responses being ‘to try to relax’
(30.7% of subjects) and ‘to hope or pray symptoms would disappear’ (21.7%) [12]. Prehospital delay
was found to significantly predict increased mortality risk [13].
Illness behavior of patients may widely influence health care costs and the workload of physicians.
The phenomenon of frequent attendance at primary care health services is emblematic. A great
amount of the work of primary-care physicians is concerned with a small per- centage of their patients
[14, 15]. However, both subjects who seem to overuse health care services and subjects who tend to
self-medicate determine significant reper- cussions for their own health and public welfare. Com-
munity-based studies found that up to 50% of subjects with severe musculoskeletal pain do not seek
medical help [16]. Major consequences include persistence and progression of functional disability,
diminished quality of life, increased risk of psychological distress and sleep problems. Furthermore,
many individuals who do not seek professional help turn to self-medication, with subsequent risks of
complications [16].
The diffusion of chronic medical conditions further highlights how patients themselves determine the
course of illness through treatment adherence and daily self- management behaviors, such as glucose
testing in diabetes. Inadequate adherence, which also includes overcom- pliance, may be
conceptualized as a variance between treatment-related behaviors displayed by patients and those
expected by their physicians [17, 18].
Illness behavior may be a source of research bias in clinical trials. Studies on patients recruited in
clinical settings may be representative only of those, sometimes the minority, who seek medical help
for a certain illness. Thus, findings about medical and psychosocial characteristics as well as
response to treatments may pertain to those who adopt the sick role rather than to all the subjects
with that illness [8]. Illness behavior may thus affect the recruitment process [19] and account for
variations and discrepancies in the results of clinical trials [20]. This is an aspect that deserves
attention.
Determinants of Illness Behavior
As a major component of clinical encounters, illness behavior involves several variables related to
health care efficacy and outcomes (fig. 1).
Illness Behavior
Psychother Psychosom 2013;82:74–81 75
ILLNESS-RELATED VARIABLES
Use of health care services
PATIENT-RELATED VARIABLES
ILLNESS BEHAVIOR
Adherence to medical regimens
DOCTOR-RELATED VARIABLES
Response to preventive screenings
Fig. 1. Main determinants and consequences of illness behavior.
Illness-Related Variables
According to Mechanic and Volkart [5], the way persons react to an illness may depend on four
characteristics of that illness: (1) frequency in the population, (2) familiarity of the symptoms to the
average member of the population, (3) predictability of the outcome and (4) degree of threat and
loss.
Pain severity and physical disability were frequently reported as reasons for seeking medical help by
subjects with chronic pain [16]. Frequency and severity of abdominal pain predicted health care-
seeking behavior among subjects with functional gastrointestinal disorders [21].
A rapid onset, together with intensity and persistence of symptoms, were significantly associated with
less delay in seeking medical help for chest pain suggestive of a heart attack [22]. On the other hand,
subjects with angina could delay seeking help because of an exaggerated sense of control due to
previous experiences of chest pain end- ing with self-help strategies such as resting [22]. Further-
more, diabetic patients may find it more difficult to recognize symptoms of myocardial infarction
because of diabetes-related alterations of pain receptors [22, 23].
Persistence of frequent attendance during a two-year follow-up was significantly related both to a
higher number of chronic conditions (in particular diabetes) and to medically unexplained symptoms
[24].
Patient-Related Variables
Demographic Variables
Studies examining the relationship between demographic characteristics and illness behavior
frequently
yielded conflicting results. In subjects with functional gastrointestinal disorders, older age was an
independent predictor of health care-seeking behavior. Female gender also seemed to be associated
with a higher likelihood of seeking help, but the relationship reached significance only for globus
[21].
In subjects with chronic pain, help-seeking behavior seemed to be restrained by masculinity, to

increase with aging and to diminish after a certain peak age [16]. Female gender and older age were
also significantly associated with frequent attendance in primary care [14, 25]. Inter- estingly, older
patients, females and racial minorities may be at increased risk of longer prehospital delay after acute
myocardial infarction because of ‘atypical’ presentation of symptoms that make it more difficult to
connect symptoms with a heart attack [22]. Among individuals aged 55 years or older, women paid
significantly more attention than men to symptoms suggestive of cancer [11].
Cognitive Representations of Illness
Lipowski [26] described eight most frequent meanings given by individuals to their illness: challenge,
enemy, punishment, weakness, relief, strategy in interpersonal relations, irreparable loss or damage,
and value. The interpretation of symptoms influences the likelihood to adequately recognize an
underlying disease and to prompt- ly seek medical care. Cognitive representations of illness may also
determine the adoption of preventive behaviors. If a certain disease is considered unavoidable and
depen- dent on factors outside of personal control (e.g. genetics), it is unlikely that preventive
measures (e.g. healthy life- style and/or regular screening visits) will be adopted. Sub- jects with
chronic pain were less likely to seek medical treatment if they attributed pain to the unavoidable pro-
cess of aging [27].
According to the self-regulatory model of Leventhal et al. [28, 29], representations of subjects of their
own illnesses determine the coping behaviors adopted and, con- sequently, the illness outcome.
Experience of symptoms different from those considered by the individual as typical of a given
disease may influence illness behavior, e.g. at the onset of a first myocardial infarction this
mismatch was significantly related to longer delay in seeking medical help [30].
Illness perception, which derives from the self-regulatory model [28], is a useful construct to
describe the main representations of illness. Dimensions of illness perception were found to
significantly predict several features of illness behavior as well as functional recovery [31]. Per-
ception of control over one’s own illness was significant-
76 Psychother Psychosom 2013;82:74–81
Sirri/Fava/Sonino
ly related to higher attendance at cardiac rehabilitation programs after myocardial infarction [32] and
better adherence to medications and self-management recom- mendations in patients with
hypertension [33]. Longitu- dinal assessment of illness perception after myocardial infarction by the
use of patients’ drawings found a significant positive relationship between the size of the heart in the
drawing and health care utilization [34]. In chronic diseases, many patients engage in a subjective
cost-ben- efit analysis in which beliefs about the benefits of prescribed medications are weighed
against their potential adverse effects, and these beliefs are related to adherence to treatment [35].
Psychological Distress and Psychiatric Disorders
Feelings of anxiety and depression may frequently result in both increased attention to and
pessimistic interpretation of bodily sensations [36]. Patients who suffer from depression and/or
anxiety tend to display more worries about illness, concerns about pain and bodily preoccupations
than those who are not depressed or anx- ious. The treatment of depression and anxiety leads to an
improvement in such fears [36–38].
Frequent attenders in general medical practice showed significantly higher levels of psychological
distress and more psychiatric disorders than routine attenders [14, 15, 39]. The prevalence of
psychiatric comorbidity among frequent attenders was found to vary from 26.7 to 54%, with
depressive and somatoform disorders as the most frequent diagnoses [39, 40]. The reduction of
psychological distress through psychotherapy resulted in a significant decrease of health care use
and costs [41, 42].
In functional gastrointestinal disorders, anxiety and depressive symptoms were significantly higher in
health care consulters than nonconsulters, and anxiety independently predicted health care-seeking
behavior [21]. In patients with unexplained abdominal pain, worry about abdominal problems
significantly predicted increased frequency of medical visits over a 12-month period [43].
In a qualitative synthesis, fear was found to be a major barrier to timely seeking medical help for
symptoms suggestive of cancer [44]. Fear was concerned with the consequences of cancer, such as
treatment effects, as well as with being labeled as a time waster or a neurotic, and, especially for
men, with being embarrassed by physical ex- aminations of sexual or private body areas [44].
Personality
The role of alexithymia (a personality construct characterized by difficulties in identifying and
describing
feelings) and emotional inhibition on illness behavior is controversial [45–48]. A positive relationship
between alexithymia and frequent attendance at health care services was found, but it was mediated
by psychological distress [45] and limited to male gender [46].
Type D personality (a combination between negative affectivity and social inhibition) was
significantly associated with increased health care utilization both in the general population [49] and
in cancer survivors [50].
Among the personality dimensions identified by the Big Five model [51], neuroticism was
significantly associated with low adherence to medical treatments [52, 53].
Childhood Adversities
Childhood maltreatment, especially sexual abuse, was found to significantly predict frequent health
care utilization during adulthood [54, 55]. Women with both physical and sexual childhood abuse
were at particularly high risk for overuse of medical services. They also had higher annual health care
costs than women who did not report any abuse [56].
Frequent attendance among general practice patients was significantly related also to other childhood
adversities, including absence of confiding relationships and parental antipathy or neglect [57].
Further, attendance at general practitioners was independently predicted by childhood exposure to
experiences concerning death and illnesses, such as death of a family member, serious illness in the
subject or in a sibling, maternal physical illness, and paternal psychiatric illness [57, 58].
Social Support
Living alone, unemployment and divorce were significantly related to frequent attendance in general
medical practice [14]. Nonetheless, subjects were more likely to seek medical care for symptoms
suggestive of severe diseases or chronic pain when encouraged by family members or friends [16,
22, 59].
Social support is generally associated with better adherence to medical regimens. However, social
environ- ment may also exert a negative effect on illness behavior, when significant others provide
overoptimistic reassurance and discourage professional help seeking [59]. Sub- jects were also less
likely to adhere to treatments if their families were characterized by conflicts and poor cohe- sion
[60].
Illness behavior may thus ensue from the interaction between the specific challenges of a disease and
the social, cultural and psychological background of the patient.
Illness Behavior
Table 1. Instruments for assessing illness behavior
Instrument Author(s) Description
Illness Behaviour Questionnaire (IBQ)
Illness Attitude Scales (IAS)
Symptom Response Questionnaire (SRQ)
Illness Cognition Questionnaire (ICQ)
Scale for the Assessment of Illness Behaviour (SAIB)
Behavioural Responses to Illness Questionnaire (BRIQ)
Brief Illness Perception Questionnaire (Brief IPQ)
Illness Cognitions Scale (ICS)
Diagnostic Criteria for Psychosomatic Research (DCPR)
Doctor-Related Variables
Pilowsky and Spence [69], 1975
Kellner [36], 1986 Sirri et al. [37], 2008
Egan and Beaton [70], 1987
Evers et al. [71], 2001

Rief et al. [72], 2003
Spence et al. [73], 2005
Broadbent et al. [74], 2006
Berk et al. [75], 2012
Fava et al. [76], 1995 Porcelli and Sonino [77], 2007
A 62-item self-rating questionnaire consisting of 7 scales: ‘general hypochondriasis’, ‘disease conviction’,

‘psychological versus somatic focusing’, ‘affective inhibition’, ‘affective disturbance’, ‘denial’, ‘irritability’
A 27-item self-rating instrument made of 9 scales: ‘worry about illness’, ‘concerns about pain’, ‘health habits’,
‘hypochondriacal beliefs’, ‘thanatophobia’, ‘disease phobia’, ‘bodily preoccupations’, ‘treatment experience’,
‘effects of symptoms’
A self-rating instrument which asks subjects to check off what behavioral responses, among a list of 12, they
would be likely to display when facing 13 common illness or pain symptoms
An 18-item self-rating instrument made of 3 scales, each concerning a specific illness cognition, namely
helplessness, acceptance and perceived benefits
A 25-item self-rating instrument with 5 subscales: ‘verification of diagnosis’, ‘expression of symptoms’,

‘medication/treatment’, ‘consequences of illness’, ‘scanning’
A self-rating instrument examining the frequency with which subjects display 21 behaviors in response to the
acute phase of an illness. Four factorial subscales were found: ‘all-or-nothing behavior’, ‘limiting behavior’,
‘emotional support seeking’, ‘practical support seeking’
It includes 9 self-rating items. The first 8 items are scored on a continuous linear scale ranging from 0 to 10 and
assess: ‘consequences’, ‘timeline’, ‘personal control’, ‘treatment control’, ‘identity’, ‘concern’, ‘illness
comprehensibility’, ‘emotions’; the last item is an open question which asks to list the three most important
perceived causes of one’s own illness
A 17-item self-rating scale assessing illness cognitions and behaviors dealing with investment in the sick role
A structured interview containing 58 items for the identification of health anxiety, disease phobia,
thanatophobia, illness denial, functional somatic symptoms secondary to a psychiatric disorder, persistent
somatization, conversion symptoms, anniversary reaction, type A behavior, irritable mood, demoralization,
alexithymia
There are different skills of the physician that may en- hance the adherence to treatments of the
patient, including a clear explanation of the treatment rationale, information about benefits and
potential adverse effects, choice of regimens least complex as possible and follow- up visits [17, 18].
Indeed, an empathetic and communica- tive physician-patient relationship was found to be sig-
nificantly associated with better adherence to medical regimens [61]. Asking patients about their
beliefs on illness and its treatment may be crucial to correct inadequate expectations and
convictions that may result in poor adherence [32, 33]. While female gender of the phy-
sician was related to shorter patient delay in seeking help for symptoms suggestive of cancer,
physician seniority, workload, job satisfaction and burnout did not significantly predict a delay in
cancer diagnosis [62].
Kellner [36] reviewed the attitudes of physicians that were found to favorably affect illness behavior
in controlled studies concerned with functional medical disorders, which he synthesized in an
approach defined as ‘ex- planatory’. It consisted of providing accurate information, reassurance,
clarification, repetition, and teaching the principles of selective perception (attention focused on one
part of the body makes the patient more aware of sensations in that part of the body than in other
parts)
78 Psychother Psychosom 2013;82:74–81
Sirri/Fava/Sonino
[36]. In patients undergoing surgery, Egbert et al. [63] found that the provision of instruction,
encouragement and suggestions by physicians had a beneficial effect on postoperative pain and length
of hospital stay.
Overall, the role of the physician seems to influence and modulate both illness-related and patient-
related characteristics.
Assessment
Patterns of illness behavior may emerge from the medical interview and interaction between patient
and physician [64]. Important correlations have been found with psychosocial variables such as life
stress, affective distur- bances, personality and quality of life, which suggests the need for a broad
evaluation [3, 4, 65–68].
When particular situations occur, such as delay in undergoing preventive screening tests or in
seeking help, inadequate treatment adherence and overuse of health care services, a more systematic
investigation is warranted.
A number of instruments have been developed for identifying the features of illness behavior. The
most representative examples are displayed in table 1. Self-rating scales provide dimensional
measurements of behavior, perception and cognitive representations of illness [37, 69–75]; they allow
a direct appraisal of the patient’s subjective views [64–66]. Structured research interviews [65, 76,
77] make full use of the clinical experience and skills of the interviewer and allow a categorical
definition of the phenomena under observation.
A thorough assessment of illness behavior may thus identify issues that can be addressed by the
physician. In most cases, problem areas may be amenable to improvement through the provision of
medical information and explanation (e.g. in relation to the beliefs of patients about their illness) or
managed by structured interventions
such as psychotherapy (e.g. in case of psychological distress) [65-68]. As to the high prevalence of
medically unexplained symptoms, it has been suggested that it is not that certain disorders lack an
explanation, but rather it is our assessment that is inadequate in most of the clinical encounters [65].
Conclusions
Once the symptoms of a medical disease are experienced by a person, or he/she has been told by a
doctor that he/she is ill even if symptoms are absent, this disease-related information gives rise to
psychological responses which are likely to influence the course, therapeutic response and outcome
of a given illness episode. Illness behavior is one of the factors that demarcate major prognostic
and therapeutic differences among patients who otherwise seem to be deceptively similar since they
share the same diagnosis. At present, there are several useful tools for assessing illness behavior that
can be incorporated in regular practice whenever problems arise. These tools have partial targets and
should be part of an assessment strategy that includes the variations of illness behavior and their
interactions with life stress, anxiety and depression [4]. For instance, focus on the patient’s cognitive
representations of disease, if not associated with assessment of other determinants of illness
behavior, may yield only partial insights. The concept of illness behavior, as origi- nally formulated
[5, 8], is more timely than ever and provides a useful framework for the large body of research
available, whose results would be otherwise scattered and unrelated in the medical literature. A
systematic appraisal of individual illness behavior and the provision of appropriate responses by
the physician may contribute to improving medical outcomes.
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Abnormal illness behaviour, help seeking and attachment
Developmental vs. maintaining factors
In cognitive theories of psychological disorders, including those of EDs, a distinction is often made
between the factors that maintain a disorder and those that lead to its development. Historically, most
cognitive theories of EDs have been concerned primarily with the constructs that maintain disordered
eating, rather than with those that may have led to its development. It has often been assumed that
understanding the maintenance of an ED is sufficient for effective CT treatment to be developed. This
is particularly true in BN, and might lead to the conclusion that only detailed understanding and
knowledge of maintaining factors is, therefore, theoretically important. However, it is becoming clear
that, in eating disorders, the distinction is not clear cut, and that so-called bdevelopmentalQ factors
are intimately involved in the maintenance of EDs. This complex interrelationship has been outlined
in more detail in recent theoretical developments, and also has some preliminary empirical support.
These developments and their related research findings will be discussed further in the next section of
the paper.
Two theories that attempted to address the problems with existing theories, including the relative
neglect of developmental factors, are those of Cooper, Wells, and Todd (2004), for BN and Waller,
Kennerley, and Ohanian (2004), for eating disorder schema theory. These might be described as
bsecond generationQ theories and are briefly summarised below.
2. Waller et al. (2004)
This theory explains at a schema level why some people develop AN and why others develop BN.
Briefly, AN is characterised by primary avoidance—not eating is a way to prevent distressing
cognitions and emotions from being experienced. BN, however, is characterised by secondary
avoidance—bingeing is an attempt to banish or block the experience of distressing emotions and
cognitions.
Some of the predictions that may be derived from these two theories can be seen in Table 3.
Table 3
Hypotheses derived from Cooper et al.’s BN theory
1. Self-statements or automatic thoughts will include positive and negative thoughts about eating, thoughts of no
control, and permissive thoughts.
2. Core beliefs will reflect global negative evaluation of the self.
3. Schema-driven processes will be evident in areas of core belief concerns.
4. Early experience will be important in the formation of core beliefs.
5. Bingeing will be preceded by negative cognition and emotional distress.
6. Bingeing will be followed by negative cognition and emotional distress.
7. There will be a causal relationship between the different types of automatic thought specified in the model and
binge-eating.
8. Negative thoughts about eating will be causally related to vomiting (or other compensatory behaviour).
9. Positive thoughts about eating will be causally related to binge-eating.
Hypotheses derived from Waller et al.’s schema theory

1. AN will be associated with bprimary processQ, prevention of affect generated by core beliefs. 2. BN will be associated
with bsecondary processQ, avoidance of affect generated by core beliefs.
526 M.J. Cooper / Clinical Psychology Review 25 (2005) 511–531
As well as incorporating much of the new research on cognition, both the theories outlined by Cooper
and colleagues and Waller and colleagues are consistent with theory development elsewhere in
cognitive therapy, and provide a clear link between cognition, affect and observable behaviours
relevant to eating disorders.
A third theoretical contribution also deserves mention here, although there is currently less empirical
evidence to support its constructs. This is the cognitive model of AN described by Wolff and Serpell
(1998). It shares features of the models described by Cooper and Waller, for example in highlighting
self schema and emotional regulation, and is useful in its identification of specific belief content, and
typical safety behaviours, as well as the importance of rumination or worry about food and eating,
weight and shape—the latter which is often underestimated in its contribution to patient distress.
However, it also adds several important and innovative ideas on cognitive constructs relevant to EDs
that have not yet been adequately addressed elsewhere. These include the beliefs that the patient may
have about her illness, e.g. what it means to her to have AN (as opposed to the characteristic
symptoms). This may include bpro-anorexiaQ and banti-anorexia cognitionsQ, such as bif I didn’t
have anorexia, my whole world would fall apartQ, or banorexia stops me from having a lifeQ.
Positive automatic thoughts are also important, e.g. bI look more attractiveQ, as well as (like Cooper’s
theory) judgements based on interoceptive cues. The extent to which these constructs are also
characteristic of BN is unclear.
Models of schemas in the eating disorders
Drawing upon the existing literature, Waller (2004) has developed a preliminary SFCBT
model of the eating disorders. This model aims to explain the range of phenomena in the
eating disorders, and to account for both the similarity of cognitive content and the
discrepancies in cognitive processing across different types of eating disorders. Waller
suggests that different schema processes are central to the development of restrictive and
bulimic psychopathologies. This model proposes two new constructs to encapsulate the
differences that occur in managing affect, and suggests that those constructs distinguish
bulimic from restrictive pathology. The constructs are primary and secondary avoidance of
affect. Primary avoidance of affect is linked to the process of schema compensation for a
maladaptive schema (e.g., engaging in perfectionist behaviours to mask the belief that one is
a failure). Following such behavioural and cognitive compensation (e.g., manifestations such
as restriction and compulsive behaviours), the maladaptive schema does not get triggered.
Thus, painful affect is avoided entirely. Secondary avoidance of affect is linked to the process
of schema avoidance. When a maladaptive schema is triggered, the resulting negative affect
is dealt with by cognitive and behavioural ‘blocking’ mechanisms (e.g., binge- eating, alcohol
use, self-harm). Evidence to date (Luck et al., 2005) supports this model. Thus, bulimia is
marked by secondary avoidance of affect (schema avoidance), while restrictive pathology is
linked to primary avoidance of affect (schema compensation).

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Cognitive behaviour therapy for eating disorders: a

“transdiagnostic” theory and treatment􏰀

2003 Elsevier Science Ltd. All rights reserved.

2. Cognitive behaviour therapy for bulimia nervosa

2.1.1. Evidence supporting the theory

This cognitive behavioural theory is supported by variety of lines of evidence:

2.2. The cognitive behavioural treatment

2.2.1. Evidence supporting the treatment

2000b; Fairburn, Jones, Peveler, Hope & O’Connor, 1993a).

2.3. Why aren’t more people getting better?

3. A new cognitive behavioural theory of the maintenance of bulimia nervosa

3.1. Clinical perfectionism

3.2. Core low self-esteem

3.3. Mood intolerance

3.4. Interpersonal difficulties

4.1. Anorexia nervosa

4.2. Atypical eating disorders or EDNOS

5. The transdiagnostic treatment

appear to be maintaining them.

early behaviour change.

so far, as well as the characterisation of any barriers to change. In addition, there is a

C.G. Fairburn et al. / Behaviour Research and Therapy 41 (2003) 509–528

􏰂 shared distinctive clinical features

Journal of Psychiatry, 152, 487–498.

International Journal of Eating Disorders, 31, 17–31.

models of maintenance. Behaviour Research and Therapy, 33, 875–885.

of anorexia nervosa subtypes. International Journal of Eating Disorders, 31, 191–201.

behaviour therapy (pp. 209–241). Oxford: Oxford University Press.

anorexia and bulimia (pp. 389–404). New York: Basic Books.

of Oxford unpublished manuscript.

Archives of General Psychiatry, 50, 419–428.

nervosa. British Journal of Clinical Psychology, 26, 223–224.

ment and treatment (pp. 361–404). New York: Guilford Press.

Psychiatry, 52, 304–312.

Research and Therapy, 37, 1–13.

subgroup. Archives of General Psychiatry, 37, 1036–1040.

review of the literature. International Journal of Eating Disorders, 16, 1–34.

depression. New York: Basic Books.

American Journal of Psychiatry, 159, 408–411.

specified. Eating and Weight Disorders, 6, 157–165.

Journal of Eating Disorders, 20, 331–343.

Research and Therapy, 40, 773–791.

International Journal of Eating Disorders, 14, 269–276.

for different subgroups? International Journal of Eating Disorders, 9, 51–55.

Psychological Medicine, 21, 447–454.

mechanisms of action. Clinical Psychology Review, 14, 633–661.

American Journal of Psychiatry, 155, 939–946.

and Therapy, 37, S79–S95.

Methods: Participants (N = 344) completed a self- report questionnaire comprising health

Results: Cluster analysis of illness behavior responses resulted in 3 unique groupings

Conclusions: The construct of 'abnormal' illness behavior may usefully be extended to

Patterns of 'Abnormal' Illness

The Unifying Concept of Illness Behavior

Laura Sirri, PhD

© 2012 S. Karger AG, Basel 0033–3190/13/0822–0074$38.00/0

Accessible online at: www.karger.com/pps

Clinical Implications of Illness Behavior

Determinants of Illness Behavior

Psychother Psychosom 2013;82:74–81 75