Cognitive Behaviour Therapy

ISSN: 1650-6073 (Print) 1651-2316 (Online) Journal homepage: http://www.tandfonline.com/loi/sbeh20

Meta-analysis of the effects of cognitive-

behavioral therapy on the core eating disorder
maintaining mechanisms: implications for
mechanisms of therapeutic change

Jake Linardon

To cite this article: Jake Linardon (2018) Meta-analysis of the effects of cognitive-
behavioral therapy on the core eating disorder maintaining mechanisms: implications for
mechanisms of therapeutic change, Cognitive Behaviour Therapy, 47:2, 107-125, DOI:
10.1080/16506073.2018.1427785

To link to this article: https://doi.org/10.1080/16506073.2018.1427785

Published online: 30 Jan 2018.

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Cognitive Behaviour Therapy, 2018
VOL. 47, NO. 2, 107–125
https://doi.org/10.1080/16506073.2018.1427785

Meta-analysis of the effects of cognitive-behavioral therapy

on the core eating disorder maintaining mechanisms:
implications for mechanisms of therapeutic change
Jake Linardon
School of Psychology, Deakin University, 221 Burwood Highway, Burwood, VIC 3125, Australia

ABSTRACT ARTICLE HISTORY

The original and enhanced cognitive model of eating disorders Received 2 October 2017
proposes that cognitive-behavioral therapy (CBT) "works" through Accepted 10 January 2018
modifying dietary restraint and dysfunctional attitudes towards
KEYWORDS
shape and weight. However, evidence supporting the validity of CBT; eating disorders;
this model is limited. This meta-analysis examined whether CBT mechanisms; randomized
can effectively modify these proposed maintaining mechanisms. trials; cognitive model
Randomized controlled trials that compared CBT to control
conditions or non-CBT interventions, and reported dietary restraint
and shape and weight concern outcomes were searched. Twenty-
nine trials were included. CBT was superior to control conditions in
reducing shape (g=0.53) and weight (g=0.63) concerns, and dietary
restraint (g=0.36). These effects occurred across all diagnoses and
treatment formats. Improvements in shape and weight concerns
and restraint were also greater in CBT than non-CBT interventions
(g's=0.25, 0.24, 0.31, respectively) at post-treatment and follow-up.
The magnitude of improvement in binge/purge symptoms was
related to the magnitude of improvement in these maintaining
mechanisms. Findings demonstrate that CBT has a specific effect in
targeting the eating disorder maintaining mechanisms, and offers
support to the underlying cognitive model. If changes in these
variables during treatment are shown to be causal mechanisms, then
these findings show that CBT, relative to non-CBT interventions, is
better able to modify these mechanisms.

The specific manualized versions of cognitive-behavioral therapy (CBT) developed by

Fairburn and colleagues (Fairburn, 2008; Fairburn, Marcus, & Wilson, 1993) are effica-
cious treatments for a range of eating disorder presentations. This treatment was originally
designed specifically for bulimia nervosa (BN), and was known as CBT-BN (Fairburn et
al., 1993). Fairburn, Cooper, and Shafran (2003) then devised a transdiagnostic theory of
eating disorders, in which an enhanced version of CBT-BN (known as CBT-E), suitable for
any eating disorder subgroup, was developed and manualized (Fairburn, 2008). Data from
numerous randomized controlled trials (RCTs) have demonstrated that both CBT-BN and
CBT-E are associated with large and long-lasting symptom improvement in individuals with

CONTACT Jake Linardon Jake.linardon@deakin.edu.au School of Psychology, Deakin University, 221 Burwood
Highway, Burwood VIC 3125, Australia.
© 2018 Swedish Association for Behaviour Therapy
108  J. LINARDON

BN (Agras, Walsh, Fairburn, Wilson, & Kraemer, 2000; Poulsen et al., 2014), anorexia ner-
vosa (AN; Byrne et al., 2017), binge eating disorder (Grilo, Masheb, Wilson, Gueorguieva,
& White, 2011), and other specified feeding and eating disorders (Fairburn et al., 2009).
Although the efficacy of these forms of CBT have been established, little is known about
how, why, or through what mechanisms, these treatments achieve their therapeutic effects.
The underlying cognitive maintenance model through which these forms of CBT are
based provides several hypotheses on CBTs likely mechanisms of change (Fairburn et al.,
1993). This cognitive model is now embedded within a transdiagnostic perspective (i.e. an
approach designed to understand all eating disorders outside of the traditional categorical
[diagnostic] conceptualization), such that the hypothesized maintaining mechanisms that
were thought to operate exclusively in BN are now purported to operate in all eating disorder
presentations (Fairburn et al., 2003). According to this model, the core psychopathology
of all eating disorders is a dysfunctional self-evaluative system, where self-worth is judged
largely in terms of weight and shape, and their control. This over-concern with weight and
shape is hypothesized to encourage and maintain inflexible dietary restraint, which includes
strict dietary rules that govern eating behavior. For a small subset of eating disorders (i.e.
AN-restricting type), attempts to restrain eating are relatively successful, which reinforces
and maintains starvation-related symptoms. However, for most eating disorders, such cog-
nitive control of eating is lost, and chaotic dietary habits develop with binge eating and at
times compensatory purging. This binge-purge cycle increases extreme concerns about
weight and shape, thereby reinforcing further dietary restraint and a self-perpetuating cycle
(Fairburn et al., 2003).
Based on this cognitive model, two possible mechanisms have been proposed to explain
the effects of CBT. The first mechanism is reducing dietary restraint. CBT attempts to
normalize an individual’s eating habits, with the hypothesis that the more an individual
engages in a pattern of regular and flexible eating, the less likely they are to binge eat
and purge (Fairburn, 2008). The second hypothesized mechanism of change is reducing
shape and weight concerns. CBT attempts to modify dysfunctional cognitions and beliefs
held toward body weight and shape, with the prediction that changes in shape and weight
over-concern will reduce the desire to diet, which in turn will reduce binge eating and
purging (Fairburn, 2008).
This cognitive model and its hypothesized mechanisms of change are indirectly sup-
ported by a variety of lines of evidence. For example, several cross-sectional studies using
structural equation modeling in both clinical (e.g. individuals with bulimia nervosa) and
non-clinical samples (e.g. undergraduate women) have found support for most of psycho-
pathological relationships specified in the cognitive model (Hoiles, Egan, & Kane, 2012;
Lampard, Byrne, McLean, & Fursland, 2011; Lampard, Tasca, Balfour, & Bissada, 2013;
Schnitzler, von Ranson, & Wallace, 2012). Additionally, laboratory-based experimental
studies in non-eating disordered individuals have also provided important insights toward
the causal relationship between certain pathways in this model. For instance, some studies
have shown that experimentally inducing a dietary transgression (i.e. forced consumption
of a forbidden food) in restrained eaters has been causally linked to overeating in the labo-
ratory (see Jansen, 2016; Knight & Boland, 1989). Finally, RCTs showing that CBT is more
effective than no treatment provides some support for the underlying cognitive model and
its hypothesized mechanisms of change. However, all these lines of evidence (cross-sectional
 COGNITIVE BEHAVIOUR THERAPY  109

studies, lab-based experiments, pre-post RCTs) only provide indirect support for this cog-
nitive model. In order to provide strong and convincing empirical support for the validity
and specificity of theoretical models of therapeutic change, Lorenzo-Luaces, German, and
DeRubeis (2014) proposed that four distinct yet related questions need to be addressed.
(1) Differential efficacy of CBT on symptoms: does CBT produce greater change in
symptoms (binge/purge behavior) than other psychological therapies?
(2) Differential efficacy of CBT on the proposed mechanisms of action: does CBT produce
greater change in the hypothesized mechanisms of change (dietary restraint and
shape and weight concerns) than other psychological therapies?
(3) The relationship between changes in the proposed mechanisms and changes in symp-
toms: do changes in these hypothesized mechanisms lead to changes in symptoms,
irrespective of the treatment that brought about the changes in these purported
mechanisms?
(4) Cognitive specificity: do changes in the purported mechanisms that occur as a result
of CBT lead to greater changes in symptoms than changes in these mechanisms
resulting from non-CBT approaches?
The current meta-analysis was designed to specifically answer the second question pro-
posed by Lorenzo-Luaces et al. (2014). A focus on the second question was made because (a)
the first question (that CBT is more effective than non-CBT treatments in reducing binge/
purge symptoms) has already been answered in several meta-analyses (Hay, Bacaltchuk,
Stefano, & Kashyap, 2009; Linardon, Wade, de la Piedad Garcia, & Brennan, 2017a, 2017b),
and (b) too few single studies have examined the third or fourth question, so a meta-analytic
review is not yet feasible (for a discussion, see Linardon, Brennan, & de la Piedad Garcia,
2016; Linardon, de la Piedad Garcia, & Brennan, 2016). However, whether CBT is associated
with greater reductions in the core maintaining mechanisms (dietary restraint, and shape
and weight concerns) than non-CBT interventions is not well understood (question 2). More
specifically, some RCTs have shown CBT to lead to greater reductions in these hypothesized
mechanisms than non-CBT interventions (Fairburn et al., 1991), whereas others have not
replicated this (Agras et al., 2000). Currently, no meta-analysis has been conducted to
examine whether CBT results in greater changes in these hypothesized mechanisms than
non-CBT interventions.1 This is an important oversight, because the mixed findings from
RCTs might be due inadequate statistical power to detect differences between active treat-
ments on these variables. Since a meta-analysis aggregates data from multiple trials, it has
greater power to detect group differences, thereby providing more accurate and definitive
answers to the question of differential efficacy of CBT on the purported mechanisms of
action (Cuijpers, Donker, van Straten, Li, & Andersson, 2010).
For these reasons, the objective of the present meta-analysis was designed to gather
another incremental piece of evidence supporting the validity of the cognitive model of
eating disorders, by specifically (1) examining whether manualized CBT for eating disor-
ders, relative to control condition, is efficacious in reducing dietary restraint and shape and
weight concerns at both post-treatment and follow-up; (2) testing whether CBT produces
greater improvements in dietary restraint and shape and weight concerns than non-CBT
interventions at post-treatment and follow-up.
110  J. LINARDON

Method
Identification and selection of studies
This review was conducted in accordance to the Preferred Reporting Items for Systematic
Reviews and Meta-Analyses guidelines (Moher, Liberati, Tetzlaff, & Altman, 2009). To
identify studies for inclusion, five online databases (PsycINFO, Medline, Cochrane Library,
EMBASE, and CINAHL) were searched for all studies that had been published up until June
2017. The following key terms were searched: eating disorder, bulimi*, anorexi*, EDNOS,
OSFED, bing*, AND CBT*, cognitive-behav, cognitive behav*, AND random*, trial*, RCT,
controlled, allocat*, assign*. The reference list of all included studies was also searched.
Relevant reviews were also searched.
Once the output from the five databases were combined, duplicate records were removed.
The title and abstract of each record was screened, and full texts of articles that appeared to
meet inclusion criteria were read in their entirety. Studies were included in this meta-anal-
ysis if they met all of the following inclusion criteria: (a) delivered a CBT protocol that was
based off Fairburn and colleagues (Fairburn, 2008; Fairburn et al., 1993) cognitive model and
treatment manuals; (b) sampled individuals with BN, BED, or related OSFEDs; (c) employed
a RCT; (d) assessed at least one of the purported maintaining mechanisms separately at
post-treatment or follow-up (dietary restraint; over-concern with weight and shape; see
below for how these were operationalized); (d) the study was published in English. Studies
were excluded if they (a) reported data on global measures of eating disorder psychopa-
thology, rather than on the subscales that assess the three specific maintaining mechanisms
(dietary restraint, over-concern with weight, and over-concern with shape); and (b) sam-
pled AN-restricting type,2 because the maintaining mechanisms specified by the cognitive
model are hypothesized to serve a different function in this eating disorder subgroup (e.g.
reinforcing self-starvation).

Quality assessment
The validity of trials was assessed using the four criteria of the Cochrane Collaboration
Risk of Bias tool (Higgins & Green, 2011). This risk of bias tool assesses potential sources
of biases in RCTs, such as the adequate generation of allocation sequence, the concealment
of allocation to treatment conditions, blinding of outcome assessors or the use of self-re-
port questionnaires, and dealing with incomplete data. Dealing with incomplete data was
assessed as low risk when intention to treat analyses were conducted. Quality assessments
were performed by the study author and an independent research assistant. Ratings were
cross-checked, and any discrepancies were resolved by discussion.

Meta-analysis
For each comparison between CBT and the control/ non-CBT psychological comparison
treatment, the effect size (d) was calculated by dividing the difference between the CBT
group mean and the comparison group mean by the pooled standard deviation. If means and
standard deviations were not reported, d was calculated using conversion equations from
significance tests (Borenstein, Hedges, Higgins, & Rothstein, 2009). To correct for potential
small-sample biases, d was converted to Hedges g. To calculate a pooled effect size, each
 COGNITIVE BEHAVIOUR THERAPY  111

study’s overall effect size was weighted by its inverse variance. A positive g indicates that the
CBT group had lower scores on the outcome than the comparison group. A small (g = .02),
medium (g = .05), and large (g = .08) effect size was specified (Lipsey & Wilson, 2001).
The following variables were analyzed as outcomes. For the maintaining mechanisms,
an a priori decision was made to analyze the three subscales from the self-report or inter-
view-based Eating Disorder Examination (EDE; Fairburn & Beglin, 1994). Specifically,
over-concern with weight and shape was assessed via the five and eight item weight and
shape concern subscale, respectively, and dietary restraint was assessed via the five-item
dietary restraint subscale.3 The frequency of binge eating and/or purging at post-treatment
was also analyzed as an outcome, purely to test whether there were relationships between the
effect sizes for the maintaining mechanisms and the effect sizes for binge/purge symptoms
(see meta-regressions below). If trials reported both binge eating and purging frequency, the
mean of both effect sizes was calculated, so that each comparison yielded only one binge/
purge frequency effect size.
All analyses were computed using Comprehensive Meta-Analysis (Borenstein et al.,
2009). Since considerable heterogeneity was expected, a random effects model was used.
Heterogeneity was assessed using the I2 statistic. The I2 statistic assesses the degree of het-
erogeneity, where a value of 0% indicates no heterogeneity, 25% low heterogeneity, 50%
moderate heterogeneity, and 75% as high heterogeneity (Higgins & Thompson, 2002).
Subgroup analyses and meta-regressions were also performed to examine possible
sources of heterogeneity. In the subgroup analyses, a mixed effects model was used, which
pools studies within a subgroup using a random effects model, but tests for significant
differences between subgroups using a fixed effects model. Meta-regression analyses were
also performed to examine whether there was a significant relationship between continuous
predictors and the effect size for the selected dependent variable, as indicated by a Z-value
and an associated p-value.
Publication bias was also examined. Publication bias was tested via inspecting the funnel
plots of each meta-analysis and by Duval and Tweedie’s trim and fill procedure (Duval &
Tweedie, 2000). If funnel plots indicated the presence of publication bias, the trim and fill
procedure was used. This procedure produces an estimate of the effect size after publication
bias has been taken into account (or corrected for), by calculating adjusted values of the
pooled effect sizes and 95% CIs.

Results
Study characteristics
Figure 1 presents a flowchart describing the literature search and inclusion process. Twenty-
nine RCTs met full inclusion criteria. The characteristics of the 29 RCTs are presented in
Table 1. Thirteen trials sampled BN. Of the BN trials, three compared CBT (all self-help-
based) to a control condition-two used a wait-list and one used a pill-placebo. Eleven
BN trials compared CBT to an active psychological comparison treatment (see Table 1).4
Of these eleven trials, eight delivered individual CBT, one delivered group CBT, and two
delivered self-help-based CBT. In terms of the CBT protocols delivered in all BN trials, five
trials delivered the original manualized CBT-BN, two delivered CBT-E (focused version),
and six trials used adapted or abbreviated versions of CBT-BN or CBT-E.
112  J. LINARDON

Records identified through database Additional unpublished identified

searching through other sources
(n = 1971 ) (n =1)

Records after duplicates removed

(n =713 )

Records screened Records excluded

(n = 713) (n =592 )

Full-text articles assessed for

eligibility Full-text articles excluded, with
(n =121 ) reasons
(n = 92)

CBT v pharmacotherapy only (n=5)

Compared variants of CBT (n=17)

Studies included in Psychoeducation only (n=1)

quantitative synthesis (meta-
No data to calculate effect size (n=3)
analysis)
(n = 29) No measure of mechanisms (n=42)

CBT not based on Fairburn’s

manuals (n=22)

Secondary data analysis (n=2)

Figure 1. PRISMA flowchart of literature search.

Eight trials sampled BED. Five trials compared CBT (one individual, one group, and one
self-help format) to a control condition-four used a wait-list and one used a pill-placebo
control. Three trials compared CBT to an active intervention (behavioral weight loss or
self-monitoring-only condition), of which one used guided self-help CBT, and two used
group-based CBT. In terms of CBT protocols delivered, one used manualized CBT-BN and
the others used an adapted or abbreviated (self-help book) version of CBT-BN.
Eight trials sampled mixed diagnoses. None of these trials included individuals with
AN-restricting type. Three trials compared CBT (two delivered guided self-help and one
delivered individual treatment) to a control (all wait-lists) condition. Five trials compared
CBT to an active non-CBT psychological intervention. Two delivered individual CBT and
three delivered CBT guided self-help. Most trials (k = 6) delivered an adapted or abbreviated
version of CBT-BN or CBT-E, two trials delivered the CBT-E focused version and one trial
delivered the CBT-E broad version.
 COGNITIVE BEHAVIOUR THERAPY  113

Table 1. Characteristics of all included randomized controlled trials.

Mechanisms
Study Sample Conditions n Format reported Quality
Agras et al. (2000) BN CBT-BN 65 Individual Restraint
IPT 64 SC
WC +++−
Banasiak, Paxton, BN CBT-Ab 54 GSH Restraint
and Hay (2005) WL 55 SC
WC ++++
Carrard et al. (2011) BED CBT-Ab 37 GSH Restraint
WL 37 SC +−SR+
Carter and Fairburn BED CBT-Ab 34 GSH Restraint
(1998) WL 24 SC
WC ++++
Carter et al. (2003) BN CBT-Ab 28 PSH Restraint
NSST 28 SC
WL 29 WC ++++
Cooper and Steere BN CBT-Ad 13 Individual Restraint
(1995) BT 14 SC
WC ??+−
DeBar et al. (2011) BN + BED + EDNOS CBT-Ab 81 GSH Restraint
TAU 79 SC
WC +?SR+
DeBar et al. (2013) BN + BED + EDNOS CBT-Ab 13 GSH Restraint
TAU 13 SC
WC ??++
Durand and King BN CBT-Ab 34 GSH Restraint
(2003) TAU 34 SC
WC ++–
Fairburn et al. (2015) BN + BED + EDNOS CBT-E 58 Individual Restraint
IPT 60 SC
WC +?+−
Fairburn et al. (2009) BN + EDNOS CBT-Eb 53 Individual Restraint
CBT-EfWL 50 Individual SC
51 WC +?++
Fairburn et al. (1991) BN CBT-BN 21 Individual Restraint
BT 19 SC
IPT 22 WC ??+−
Garner et al. (1993) BN CBT-BN 25 Individual Restraint
SET 25 SC
WC +−?−
Grilo and Masheb BED CBT-Ab 38 GSH Restraint
(2005) BWL 37 SC
Self-mon 15 WC ++SR+
Grilo, Masheb, and BED CBT-BN 28 Individual Restraint
Wilson (2005) Placebo 27 SC
WC ++SR+
Grilo et al. (2011) BED CBT-BN 45 Group Restraint
BWL 45 SC
WC +??+
Lavender et al. BN CBT-Ad 23 Group Restraint
(2012) ESMT 21 SC
WC +?++
Ljotsson et al. (2007) BED + BN CBT-Ab 33 GSH Restraint
WL 34 SC
WC +??−
McIntosh et al. BN + BED CBT-Ad 38 Individual Restraint
(2016) CBT-A 36 SC
ST 38 WC ++++
Munsch et al. (2007) BED CBT-Ad 25 Group Restraint
BWL 23 SC
WC ++++
Poulsen et al. (2014) BN CBT-E 36 Individual Restraint
Psychoanalysis 34 SC
WC ++++

(Continued)
114  J. LINARDON

Table 1. (Continued).
Mechanisms
Study Sample Conditions n Format reported Quality
Schlup, Munsch, BED CBT-Ad 18 Group Restraint +?SR+
Meyer, Margraf, WL 18 SC
and Wilhelm WC
(2009)
Stefini et al. (2017) BN CBT-Ad 39 Individual Restraint
Psychodynamic 42 SC
WC ++++
Striegel-Moore et al. BED + BN CBT-Ab 59 GSH Restraint
(2010) TAU 64 SC
WC +?++
Traviss, Heywood-Ev- BED + BN + EDNOS CBT-Ab 37 GSH Restraint
erett, and Hill WL 31 SC
(2011) WC +?++
Wagner et al. (2016) BN CBT-Ab 69 GSH Restraint
WL 70 SC
WC +?SR+
Walsh, Fairburn, BN CBT-Ab 25 GSH Restraint
Mickley, Sysko, and Placebo
Parides (2004) 22 ???+
Walsh et al. (1997) BN CBT-BN 25 Individual Restraint
NSST 22 SC
WC ??++
Wonderlich et al. BN CBT-E 40 Individual Restraint +?++
(2014) ICAT 40 SC
WC
Note: For the quality column a positive sign (low risk), a “?” (unclear), or a negative sign (high risk) is given for the four items
of risk of bias: allocation sequence; concealment of allocation to conditions; blinding of assessors; and intention-to treat
analyses. For Blinding of assessor we reported “SR” when only self-report outcome measures were used; CBT-Ab = ab-
breviated version of Fairburn’s CBT; CBT-Ad = adapted version of Fairburn’s CBT; TAU = treatment as usual; BT = be-
haviour therapy; GSH = guided self-help; BWL = behavioural weight loss; ICAT = integrative affect cognitive therapy;
NSST = non-specific supportive therapy; ESMT = emotion social mind training; SC = Shape concern; WC = Weight concern.

Quality assessment
The quality ratings of included studies can also be seen in Table 1. Twenty-four studies
reported an adequate sequence generation. Only 12 studies reported adequate allocation
concealment, 24 studies reported blinding of outcome assessors or used self-report out-
comes, and 22 studies conducted ITT analyses. Nine studies met all four quality criteria,
10 met three criteria, five met two criteria, and five met one criteria.

CBT versus control groups

The overall pooled effect sizes are based on all eating disorder presentations. This decision
was made for two reasons. First, the maintaining mechanisms outlined by Fairburn and
colleagues (Fairburn, 2008; Fairburn et al., 1993) are hypothesized to operate in all eating
disorders. Second, unlike some CBT protocols, particularly for BED, which aim to induce
some of these maintaining mechanisms (e.g. dietary restraint; Agras et al., 1994), all included
trials aimed to reduce or eliminate these maintaining mechanisms. Note that diagnosis is
tested as a moderator in subgroup analyses.
 COGNITIVE BEHAVIOUR THERAPY  115

Shape concerns
The overall effect of CBT on shape concerns (Ncomp = 11) compared with control conditions
for all diagnoses combined at post-treatment was g = .53 (95% CI = .32, .74, p < .001). There
was moderate heterogeneity (I2 = 57%). The effect size was slightly larger, yet still statistically
significant when adjusting for publication bias (g = .59, 95% CI = .36, .83).
Table 2 also presents the results from the subgroup analyses on post-treatment shape
concerns. There was no evidence that the following study characteristics were significantly
associated with the effect size for post-treatment shape concerns: sample diagnosis (BN vs.
BED vs. mixed samples; CBT format (clinician-led vs. guided self-help CBT); CBT type
(treatment based on CBT-E or CBT-BN); and study quality (high quality vs. lower quality
studies).

Weight concerns
The overall effect of CBT on weight concerns (Ncomp = 10) compared with control conditions
for all diagnoses combined at post-treatment was g = .63 (95% CI = .36, .89, p < .001). There
was high heterogeneity (I2 = 69%). There was no indication of publication bias. Sample
diagnosis, CBT format, CBT type, and study quality were not significantly associated with
the effect size for post-treatment weight concerns.

Dietary restraint
The overall effect of CBT on dietary restraint (Ncomp = 12) compared with control conditions
for all diagnoses combined at post-treatment was g = .36 (95% CI = .11, .62, p = .005). There
was high heterogeneity (I2 = 72%). There was no indication of publication bias. Sample
diagnosis, CBT format, and study quality were not significantly associated with the effect
size for post-treatment dietary restraint. However, the effect size for trials that delivered a
treatment based on transdiagnostic CBT-E was significantly larger than the effect size for
trials that delivered a treatment based on the original CBT-BN.

Binge/purge frequencies
The overall effect of CBT on binge/purge frequencies (Ncomp = 8) compared with control
conditions for all diagnoses combined at post-treatment was g = .63 (95% CI = .33, .92,
p < .001). There was high heterogeneity (I2 = 65%). The effect size was slightly smaller, yet
still statistically significant when adjusting for publication bias (g = .62, 95% CI = .30, .89).

CBT versus non-CBT psychological treatments

Shape concerns
The overall effect of CBT on shape concerns (Ncomp = 22) compared with non-CBT psycho-
logical treatments for all diagnoses combined at post-treatment was g = .25 (95% CI = .09,
.40, p < .001). There was moderate heterogeneity (I2 = 54%). There were no indications of
publication bias. This difference in shape concerns in favor of CBT was also statistically
significant at follow-up. Only sample diagnosis moderated this effect. Specifically, the effect
size was significantly larger for studies that delivered CBT to a transdiagnostic sample
compared to when studies delivered CBT to a BN or BED-only sample.
Table 2. Results from the meta-analyses on the three maintaining mechanisms.
116

Shape concerns Weight concerns Dietary restraint

Analysis Ncomp g (95%CI) p Qbp Ncomp g (95%CI) p Qbp Ncomp g (95%CI) p Qbp
CBT vs. inactive controlsa
Post-treatment
Sensitivity analysis
 J. LINARDON

  One ES per study (largest) 10 .55 (.31, .78) <.001 9 .65 (.36, .90) <.001 11 .32 (.05, .59) .019
  One ES per study (smallest) 10 .53 (.29, .76) <.001 9 .59 (.30, .89) <.001 11 .30 (.06, .55) .017
Subgroup analysis
  Diagnosis
   BN 4 .33 (.01, .65) .043 4 .41 (.01, .48) .046 5 .35 (−.07, .78) .105
   BED 5 .61 (.30, .90) <.001 4 .71 (.28, 1.14) .001 5 .34 (−.09, .78) .127
   Transdiagnostic 2 .81 (.32, 1.13) .001 2 .93 (.33, 1.53) .002 2 .39 (−.28, 1.08) .256
.216 .320 .991
  CBT format
   Clinician-led 4 .41 (.05, .76) .026 4 .51 (.07, .95) .021 4 .45 (.00, .90) .050
   Guided self-help 7 .60 (.34, .87) <.001 6 .69 (.34, 1.05) <.001 8 .32 (.01, .63) .047
.391 .535 .643
  CBT type
   Based on CBT-BN 8 .54 (.24, .84) <.001 7 .62 (.24, 1.01) .001 9 .22 (−.06, .51) .126
   Based on CBT-E 3 .48 (.24, .72) <.001 3 .61 (.32, .90) <.001 3 .73 (.47, 1.05) <.001
.750 .950 .009
  Study quality
   High quality (>2 criteria) 10 .48 (.27, .69) <.001 9 .56 (.29, .82) <.001 10 .43 (.15, 3.09) .002
    Lower quality (≤2 criteria) 1 1.05 (.36, 1.75) .003 1 1.28 (.47, 2.10) .002 2 .02 (−.60, .65) .940
.124 .095 .257
CBT vs. other treatments
Post-treatment
Sensitivity analysis
  One ES per study (largest) 20 .26 (.09, .42) .002 20 .26 (.09, .44) .003 20 .32 (.16, .50) <.001
  One ES per study (smallest) 20 .25 (.09, .42) .002 20 .25 (.08, .43) .004 20 .33 (.16, .51) <.001
Subgroup analysis
  Diagnosis
   BN 12 .16 (−.03, .34) .096 12 .21 (.01, .41) .040 12 .27 (.05, .49) .016
   BED 4 .07 (−.25, .38) .682 4 −.04 (−.38, .28) .783 4 .18 (−.19, .55) .350
   Transdiagnostic 6 .50 (.26, .74) <.001 6 .48 (.22, .74) <.001 6 .47 (.02, .76) .001
.041 .043 .410
  CBT format
(Continued)
Table 2. (Continued).
Shape concerns Weight concerns Dietary restraint
Analysis Ncomp g (95%CI) p Qbp Ncomp g (95%CI) p Qbp Ncomp g (95%CI) p Qbp
   Clinician-led 15 .18 (.01, .35) .045 15 .20 (.01, .39) .039 15 .33 (.12, .53) .001
   Guided self-help 7 .39 (.14, .65) .002 7 .34 (.06, .62) .017 7 .28 (−.01, .57) .060
.172 .427 .791
  CBT type
   Based on CBT-BN 17 .25 (.08, .41) .003 17 .23 (.05, .40) .011 17 .27 (.11, .44) .001
   Based on CBT-E 5 .28 (−.12, .68) .177 5 .33 (−.07, .74) .110 5 .45 (−.00, .90) .051
.905 .636 .470
  Study quality
   High quality 13 .17 (−.01, .36) .078 13 .17 (−.02, .38) .084 13 .28 (.07, .48) .008
   Lower quality 9 .39 (.14, .64) .002 9 .36 (.09, .62) .007 9 .36 (.09, .63) .008
.174 .276 .616
Follow-up 14 .24 (.07, .41) .006 14 .18 (.05, .31) .005 14 .28 (.16, .40) <.001
a
There were not enough studies that compared CBT to inactive controls on the selected outcomes at follow-up, so a meta-analysis was not performed.
COGNITIVE BEHAVIOUR THERAPY 
117
118  J. LINARDON

Weight concerns
The overall effect of CBT on weight concerns (Ncomp = 22) compared with non-CBT psycho-
logical treatments for all diagnoses combined at post-treatment was g = .24 (95% CI = .08,
.41, p = .002). There was moderate heterogeneity (I2 = 58%). There were no indications of
publication bias. This difference in weight concerns in favor of CBT was also statistically
significant at follow-up. Only sample diagnosis moderated this effect. The effect size was
significantly larger for studies that delivered CBT to a transdiagnostic sample compared to
when studies delivered CBT to a BN or BED-only sample.

Dietary restraint
The overall effect of CBT on dietary restraint (Ncomp = 22) compared with non-CBT psycho-
logical treatments for all diagnoses combined at post-treatment was g = .31 (95% CI = .15,
.47, p < .001). There was moderate heterogeneity (I2 = 59%). This difference in dietary
restraint in favor of CBT was also statistically significant at follow-up. The effect size was
slightly larger and still statistically significant after adjusting for publication bias (g = .35,
95% CI = .19, .51). Sample diagnosis, CBT format, CBT type, and study quality were unre-
lated to the overall effect size.

Binge/purge frequencies
The overall effect of CBT on binge/purge frequencies (Ncomp = 18) compared with non-CBT
psychological treatments for all diagnoses combined at post-treatment was g = .29 (95%
CI = .09, .49, p = .004). There was high heterogeneity (I2 = 74%). After adjusting for pub-
lication bias, the effect size was small and non-significant (g = .08, 95% CI = −.13, .31).

Sensitivity analyses
In the previous analyses, there were instances where some trials were included in which
more than one CBT condition was compared with the same comparison group. These com-
parisons were thus not independent of each other, thereby potentially affecting the effect
size estimates. Thus, a series of sensitivity analyses were performed in which the comparison
with the smallest effect size was included in the meta-analysis. This sensitivity analysis was
repeated again for the comparison with the largest effect size. These sensitivity analyses
ensured that only one comparison per study was included in the meta-analysis. The results
of these sensitivity analyses can be seen in Table 2. As seen, the pooled effect sizes in the
sensitivity analyses were essentially the same as the effect sizes reported in the main analyses.

Meta-regression
The relationships between the effect size for binge/purge symptoms and the three pur-
ported maintaining mechanisms were examined through meta-regressions. Results from
the meta-regression analyses can be seen in Table 3. As shown, significant and positive
relationships for all diagnoses were observed for the binge/purge symptom effect sizes and
the shape concern, weight concern, and dietary restraint effect sizes. When the dietary
restraint effect sizes were set as the dependent variable, significant and positive relationships
were also observed between dietary restraint and the shape and weight concern effect sizes
(see Table 3).
 COGNITIVE BEHAVIOUR THERAPY  119

Table 3. Results from the meta-regression analyses.

Sample diagnosis Outcome variable Predictor Slope SE p
Any
Binge/purge
Shape concerns .60 .21 .005
Weight concerns .55 .18 .003
Dietary restraint .70 .18 <.001
Restraint
Shape concerns .57 .15 <.001
Weight concerns .53 .13 <.001
Bulimia nervosa
Binge/purge
Shape concerns .58 .35 .100
Weight concerns .60 .25 .019
Dietary restraint 1.03 .20 <.001
Restraint
Shape concerns .77 .23 <.001
Weight concerns .72 .15 <.001
Binge eating disorder
Binge
Shape concerns .55 .21 .008
Weight concerns .43 .18 .015
Dietary restraint .45 .23 .050
Restraint
Shape concerns .71 .27 .010
Weight concerns .54 .27 .047
Note: ES = effect size; Bold indicates statistical significance (p < .05).

Meta-regressions were then repeated separately for BN and BED-only samples. As shown,
the significant relationships between the effect sizes for binge/purge symptoms and the effect
sizes for the purported maintaining mechanisms were also observed for both BN and BED-
samples specifically. The effect sizes for dietary restraint were also significantly predicted
by the effect sizes for weight and shape concerns in both BN and BED-samples (Table 3).

Discussion
Although modifying dietary restraint and shape and weight over-concern are hypothesized
to be the mechanisms through which the original (Fairburn et al., 1993) and enhanced CBT
(Fairburn, 2008) for eating disorders achieves its effects, little evidence exists in support of
this cognitive model of change. Lorenzo-Luaces et al. (2014) suggested that four specific
questions need to be addressed in order to support the validity and specificity of cognitive
models of therapeutic change: (1) differential efficacy of CBT on symptoms; (2) differen-
tial efficacy of CBT on the proposed mechanisms; (3) the relationship between changes
in these maintaining mechanisms and changes in symptoms; and (4) cognitive specificity.
The present meta-analysis aimed to provide an answer to the second question, by testing
whether these forms of CBT for eating disorders are effective in reducing dietary restraint
and shape and weight concerns.
Findings showed that CBT was efficacious in reducing dietary restraint, and shape and
weight concerns in individuals with eating disorders. When comparing CBT to no treatment
(i.e. wait-list or placebo), statistically significant and moderate effect sizes were observed
in favor of CBT for dietary restraint (g = .36) and shape (g = .53) and weight (g = .63) con-
cerns. The effect sizes observed for these maintaining mechanisms were relatively similar
to the effect size observed for binge/purge symptoms (g = .63), suggesting that CBT also
120  J. LINARDON

has a potent effect in modifying these cognitive mechanisms. Further, the fact that these
effects were largely consistent across specific diagnoses provides strong support for the
transdiagnostic theory. In particular, this theory proposes that all eating disorders are main-
tained by a common set of mechanisms, and CBT should therefore be effective in targeting
these mechanisms across all eating disorders (Fairburn et al., 2003). Importantly, however,
whether these effects are sustained in the long-term is unclear, as too few studies that
compared CBT to control conditions on these outcomes conducted follow-up assessments.
The differential efficacy of CBT was also observed, such that CBT delivered in both clini-
cian-led and guided self-help formats was more efficacious in reducing dietary restraint and
shape and weight concerns than non-CBT psychological interventions. Importantly, these
effects were sustained at follow-up periods. The superiority of CBT over other non-CBT
psychological interventions suggests that these versions of CBT have a specific and unique
effect on modifying the mechanisms that are purported to maintain the core behavioral
symptoms of eating disorders. If, as proposed by the cognitive model (Fairburn, 2008;
Fairburn et al., 2003), reducing dietary restraint and extreme concerns about weight and
shape are indeed causal mechanisms of change, then these findings show that these forms
of CBT are better equipped to modify these mechanisms than other psychological inter-
ventions. This finding is not unexpected, as CBT use several strategies designed to directly
target these mechanisms, such as the prescription of regular eating, weekly weighing, body
shape exposure, and cognitive restructuring (Fairburn, 2008). This is in contrast to other
psychological treatments, which either place little emphasis on addressing these mechanisms
(non-specific supportive therapy), or attempt to address them indirectly by targeting other
maintaining factors (e.g. interpersonal therapy).
Meta-regression analyses were also conducted to test whether there were relationships
between changes in the proposed mechanisms and changes in the core behavioral symp-
toms. Significant and positive relationships were observed between the effect sizes for the
three maintaining mechanisms and the effect sizes for binge/purge symptoms, indicating
that greater change in these mechanisms was associated with greater change in binge eat-
ing and/or purging. Critically, however, the nature of the data precludes any inference of
temporal precedence, so it is currently unclear whether changes in these mechanisms are a
cause or consequence of behavioral symptom improvement. Indeed, changes in behavioral
symptoms may actually precede changes in cognitive mechanisms during CBT (MacDonald,
McFarlane, Dionne, David, & Olmsted, 2017), so this study cannot rule out the possibility of
reverse causality. Answering this question, and providing further support for the cognitive
model, will require RCTs to repeatedly assess these mechanisms and symptoms throughout
the course of CBT, so that the trajectory of their change can be tracked, and formal tests of
mediation can be performed (Linardon et al., 2016b). The meta-regressions conducted in
the present study do, however, provide the necessary but not sufficient statistical evidence to
suggest that there is a relationship between changes in the proposed mechanisms of action
and behavioral symptom improvement.
Findings from the present meta-analysis must be interpreted in light of its limitations.
First, the number of trials was relatively small for several subgroup analyses. Finding no
difference while the number of studies is small cannot be considered as conclusive evi-
dence that there are no true differences between the selected subgroup of studies. Second,
it was not possible from the included trials to validate treatment integrity or adherence.
This could mean that (a) certain CBT procedures were not delivered correctly in some
 COGNITIVE BEHAVIOUR THERAPY  121

included trials, or (b) there were spill-over effects, meaning that therapist in some tri-
als may have also implemented certain CBT procedures in the psychological compari-
son group. Consequently, this study cannot conclusively demonstrate that the observed
improvements in these maintaining mechanisms were a direct result of the specific CBT
strategies designed to target them. It would be worthwhile for future dismantling trials
to be conducted, which allows one to examine what impact a treatment has when a core
therapeutic strategy is removed from one condition but not the other. For example, if one
were to find that removing the regular eating strategy (designed entirely to disrupt dietary
restraint) or the weekly weighing procedure (designed to disrupt extreme weight concerns;
Fairburn, 2008) from one condition leads to poorer outcomes than a treatment condition
containing these strategies, then this would provide greater and more conclusive evidence
supporting the validity of this cognitive model and on the importance of these particular
strategies. Third, only RCTs were included in the present review, so these results may not be
generalized to individuals who are treated in routine clinical care because of the exclusion
criteria (e.g. multiple comorbidities) employed in these trials. It is therefore important for
future research to examine whether CBT delivered in “real world” settings can effectively
target these maintaining mechanisms. Finally, for practical reasons, only published RCTs
were included in the present meta-analysis. Unpublished trials may have therefore been
missed. Although there were little indications of publication bias in the present review, the
fact that unpublished studies are more likely to report null results (Rosenthal, 1991) suggests
that the present effect sizes may be slightly inflated.
To conclude, the specific forms of CBT developed by Fairburn and colleagues (Fairburn,
2008; Fairburn et al., 1993) are efficacious in reducing the purported eating disorder main-
taining mechanisms. The current meta-analysis is the first to demonstrate that CBT has a
more potent effect in reducing dietary restraint and shape and weight concerns than non-
CBT psychological interventions. The present findings provide only one piece of evidence
in support of the validity and specificity of the cognitive model of change (Lorenzo-Luaces
et al., 2014). More research is needed to provide convincing support for the underlying
cognitive model of eating disorders, particularly from trials that examine what impact
changes in these mechanisms have on client symptoms.

Notes
1. 
A previous meta-analysis on the efficacy of any type of CBT protocol for eating disorders
analysed CBTs effect “global cognitive symptoms” (Linardon et al., 2017a). In this review,
cognitive symptoms were operationalized as any measure, subscale, or construct that assessed
a cognitive-related symptom, including attitudes toward eating, weight and shape, body
dissatisfaction, thin ideal internalization, and body-related concerns. All of these distinct
symptoms were combined into one overall “cognitive symptom” construct. Thus, the effects
of CBT on the specific maintaining mechanisms as postulated by the cognitive model have
not been examined.
2. 
No trials on CBT for AN-restricting type met full inclusion criteria. For example, previous
trials in this population either did not use a treatment manual based off the Fairburn’s
cognitive model (McIntosh et al., 2005; Touyz et al., 2013), or, rather than reporting data for
the three maintaining mechanisms, reported global scores on measures of eating disorder
psychopathology (Byrne et al., 2017; Zipfel et al., 2014).
3. 
A few trials reported both the EDE restraint subscale and the Three Factor Eating Questionnaire
cognitive restraint subscale. In these instances, only the EDE restraint subscale was analyzed.
122  J. LINARDON

4. 
One trial delivered both an inactive and active comparison group.

Disclosure statement
There are no conflict of interests to report.

ORCID
Jake Linardon http://orcid.org/0000-0003-4475-7139

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