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Behaviour Research and Therapy 48 (2010) 974e983

Contents lists available at ScienceDirect

Behaviour Research and Therapy

journal homepage: www.elsevier.com/locate/brat

Specicity of cognitive emotion regulation strategies: A

transdiagnostic examination
Amelia Aldao*, Susan Nolen-Hoeksema 1
Department of Psychology, Yale University, 2 Hillhouse Ave, New Haven, CT 06520, USA

a r t i c l e i n f o

a b s t r a c t

Article history:
Received 8 April 2010
Received in revised form
27 May 2010
Accepted 4 June 2010

Despite growing interest in the role of regulatory processes in clinical disorders, it is not clear whether
certain cognitive emotion regulation strategies play a more central role in psychopathology than others.
Similarly, little is known about whether these strategies have effects transdiagnostically. We examined
the relationship between four cognitive emotion regulation strategies (rumination, thought suppression,
reappraisal, and problem-solving) and symptoms of three psychopathologies (depression, anxiety, and
eating disorders) in an undergraduate sample (N 252). Maladaptive strategies (rumination, suppression), compared to adaptive strategies (reappraisal, problem-solving), were more strongly associated
with psychopathology and loaded more highly on a latent factor of cognitive emotion regulation. In
addition, this latent factor of cognitive emotion regulation was signicantly associated with symptoms of
all three disorders. Overall, these results suggest that the use of maladaptive strategies might play a more
central role in psychopathology than the non-use of adaptive strategies and provide support of a transdiagnostic view of cognitive emotion regulation.
2010 Elsevier Ltd. All rights reserved.

Keywords:
Emotion regulation
Strategies
Transdiagnostic
Eating
Depression
Anxiety

Introduction
Cognitive emotion regulation strategies are cognitive responses
to emotion-eliciting events that consciously or unconsciously
attempt to modify the magnitude and/or type of individuals
emotional experience or the event itself (Campbell-Sills & Barlow,
2007; Harvey, Watkins, Mansell, & Shafran, 2004; Rottenberg &
Gross, 2007; Thompson, 1994; Williams & Bargh, 2007). In recent
years, a substantial amount of work has been devoted to delineating the relationships between dispositions to use certain strategies and a variety of disorders, including depression (Garnefski &
Kraaij, 2006; Nolen-Hoeksema, Wisco, & Lyubomirsky, 2008),
mania (Feldman, Joormann, & Johnson, 2008), generalized anxiety
disorder (Mennin, Holoway, Fresco, Moore, & Heimberg, 2007),
post-traumatic stress disorder (Tull & Roemer, 2003), social anxiety
disorder (Kashdan & Breen, 2008), and eating disorders (NolenHoeksema, Stice, Wade, & Bohon, 2007; Piran & Cormier, 2005).
Overall, several cognitive emotion regulation strategies have
been argued to have negative associations with psychopathology
(i.e., adaptive) whereas others have been associated with the
etiology and maintenance of clinical disorders (i.e., be

* Corresponding author. Tel.: 1 (203) 432 7352.

E-mail addresses: amelia.aldao@yale.edu (A. Aldao), susan.nolen-hoeksema@
yale.edu (S. Nolen-Hoeksema).
1
Tel.: 1 (203) 432 0699.
0005-7967/$ e see front matter 2010 Elsevier Ltd. All rights reserved.
doi:10.1016/j.brat.2010.06.002

maladaptive). Stress and coping theories (Billings & Moos, 1981;

Carver, Scheier, & Weintraub, 1989; Folkman & Lazarus, 1986) and
early cognitive-behavioral approaches to psychopathology (Beck,
1976; Cooper, Russell, Skinner, Frone, & Mudar, 1982; DZurilla,
1988; Marlatt, Baer, Donovan, & Kivlahan, 1988) suggested that
reappraisal and problem-solving should be adaptive across
a variety of contexts. Reappraisal involves generating benign or
positive interpretations of a stressful situation as a way of reducing
distress (Gross, 1998). Cognitive theories put maladaptive appraisal
processes at the core of depression and anxiety (Beck, 1976; Clark,
1988; Salkovskis, 1998). More recently, Grosss (1998) inuential
model of emotion regulation highlights reappraisal as a strategy
that results in positive emotional and physical responses to
emotion-eliciting stimuli. Cognitive-behavioral therapies for
depression and anxiety focus on teaching reappraisal skills (Beck,
Rush, Shaw, & Emery, 1979; Clark & Wells, 1995).
Problem-solving responses are conscious attempts to change
a stressful situation or contain its consequences (Billings & Moos,
1981). Problem-solving measures can include cognitions directed
at solving a problem (e.g., brainstorming solutions, planning
a course of action) or an orientation toward problem-solving as
a way of coping with stressful circumstances. Problem-solving
coping can have benecial effects on emotions by modifying or
eliminating stressors. Low problem-solving orientation or poor
problem-solving skills have been associated with depression
(Billings & Moos, 1981; DZurilla, Chang, Nottingham, & Faccinni,
1988), anxiety (Chang, Downey, & Salata, 2004; Kant, DZurilla, &

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A. Aldao, S. Nolen-Hoeksema / Behaviour Research and Therapy 48 (2010) 974e983

Maydeu-Olivares, 1997), and eating disorders (Van Boven &

Espelage, 2006). Training in problem-solving skills is a component of cognitive-behavioral therapies for all these disorders (Beck
et al., 1979; Fairburn, Shafran, & Cooper, 1998; Marlatt et al., 1988).
In contrast to these adaptive strategies, suppression of distressing thoughts has long been seen as a maladaptive response to
a variety of stressors and a risk factor for psychopathology (Carver
et al., 1989; Folkman & Lazarus, 1980). Wenzlaff and Wegner (2000)
have produced a large body of research showing that attempts to
voluntarily suppress unwanted thoughts result in an increased
accessibility of the suppressed thought (Wegner & Erber, 1992;
Wegner, Schneider, Carter, & White, 1987). More germane to
emotion regulation, suppression of emotional thoughts has been
shown to produce increases in sympathetic activation (Wegner,
Broome, & Blumberg, 1997; Wegner & Gold, 1995), and self-reported anxiety (Roemer & Borkovec, 1994), anxiety and depression
(Borton, Markowitz, & Dieterich, 2005), and discomfort (Purdon &
Clark, 2001). Wegner et al. have also suggested that chronic
suppression of emotionally evocative thoughts might prevent
habituation to emotional stimuli, and as such result in hypersensitivity to depression and anxiety-related thoughts and symptoms
(Wegner & Zanakos, 1994; Wenzlaff & Wegner, 2000). Indeed,
thought suppression has been associated with increased risk for
depression and anxiety in several studies (Purdon, 1999; Wenzlaff
& Wegner, 2000). Similarly, emotion regulation models of eating
disorders suggest that suppression of concerns leads to binge
eating and then maladaptive compensatory behaviors (e.g.,
Heatherton & Baumeister, 1991; McCarthy, 1990; Polivy & Herman,
2002). In addition, thought suppression has been associated with
the frequency with which individuals with borderline personality
disorders engage in self-harm as an emotion regulation mechanism
(Chapman, Specht, & Cellucci, 2005).
Another maladaptive strategy is rumination, the tendency to
repetitively focus on the experience of negative emotion and its
causes and consequences (Nolen-Hoeksema et al., 2008; Trapnell &
Campbell, 1999; Watkins, 2008). Although individuals report that
they engage in rumination to understand the sources of their
distress (Papageorgiou & Wells, 2003), experimental studies have
shown that rumination increases negative mood-congruent
thinking, interferes with problem-solving and instrumental
behavior, and drives away social support (for a review see
Lyubomirsky & Tkach, 2004). In turn, rumination prospectively
predicts symptoms and diagnoses of anxiety and depression (see
Nolen-Hoeksema et al., 2008). Some people who ruminate may
turn to binge eating to escape their aversive self-awareness
(Heatherton & Baumeister, 1991), leading to symptoms and diagnoses of eating disorders (Nolen-Hoeksema et al., 2007).
Thus, two cognitive emotion regulation strategies that have
been widely theorized to be protective against psychopathology are
reappraisal and problem-solving. Two strategies that have consistently been argued to be associated with development and maintenance of psychopathology are thought suppression and
rumination. However, it is not clear whether strategies vary in the
strength of their association to psychopathology.
In a recent meta analysis (Aldao, Nolen-Hoeksema, & Schweizer,
2010), we examined the relationships between self-reports of these

2
We actually examined two additional emotion regulation strategies in the meta
analysis, namely avoidance and acceptance. Avoidance had a very similar pattern of
relationships to psychopathology as suppression, and indeed there appears to be
considerable conceptual and measurement overlap between the two constructs
(Ottenbreit & Dobson, 2004). Thus, we did not include measures of avoidance in
this study. Acceptance was not signicantly associated with psychopathology across
studies in the meta analysis; measures of this construct were not included in this
study.

975

four cognitive emotion regulation strategies and symptoms of four

types of psychopathology: depression, anxiety, eating disorders,
and substance use.2 When we collapsed all the symptom types
together, we found mixed evidence for specicity in the relationship between emotion regulation strategies and psychopathology:
although we found that all four strategies were signicantly associated with psychopathology, the maladaptive strategies of rumination and suppression were more strongly associated with
symptoms than the adaptive strategies of reappraisal and problemsolving. Delineating which strategies have stronger associations
with psychopathology can help us identify the ones that play
a more central role in the development, maintenance, and remission of various disorders. This has implications for prevention
programs that focus on the development of cognitive emotion
regulation skills (e.g., Brackett & Katulak, 2006) as well as treatments that focus on teaching regulatory skills (Beck, 1976; Fairburn
et al., 1998; Fairholme, Boisseau, Ellard, Ehrenreich, & Barlow, 2010;
Hayes, Strosahl, & Wilson, 1999; Roemer, Orsillo, & SaltersPedneault, 2008). Specically, if we can identify what strategies
are more protective against, or stronger risk factors for, psychopathology, we can ensure that these strategies are targeted in
prevention and intervention programs.
Another important question regarding the relationship between
cognitive regulatory strategies and psychopathology involves
whether these strategies are more strongly related to certain
disorders than to others. Leading theorists have argued that difculties using cognitive emotion regulation strategies, including in
rumination, thought suppression, reappraisal, and problemsolving, may be critical transdiagnostic factors underlying several
forms of psychopathology (Ehring & Watkins, 2008; Fairburn,
Cooper, & Shafran, 2003; Gross & John, 2003; Harvey et al., 2004;
Kring & Sloan, 2010; Mansell, Harvey, Watkins, & Shafran, 2009;
Moses & Barlow, 2006; Purdon, 1999; Rassin, Merckelbach, &
Muris, 2000). Unfortunately, most studies on cognitive emotion
regulation have been disorder-specic, limiting tests of transdiagnostic models. Identifying cognitive emotion regulation strategies that have transdiagnostic effects can inform the development
of interventions targeting these strategies, thereby having
preventative and treatment effects across a range of disorders.
In our meta analysis, we found that the relationships between
emotion regulation strategies were stronger for depression and
anxiety than for eating and substance use disorders. These results
suggest that, not surprisingly, mood and anxiety disorders might be
more closely related to certain problems in cognitive emotion
regulation than disorders in which mood disturbances are not as
central (see Garnefski, Kraaij, & van Etten, 2005) and that eating
disorders are more consistently related to cognitive emotion
regulation strategies than substance use.
Our meta analysis provided important clues as to the relative
strength of different cognitive emotion regulation strategies in
predicting psychopathology, and which types of psychopathology
these strategies were most related to. There are signicant limitations of the meta-analytic approach, however. Given the nature of
a meta-analytic review, we could only examine the relationships
between individual strategies and disorders independently of one
another, and thus could not simultaneously model the relationships
among all strategies and disorders (see Rosenthal & DiMatteo,
2001). This is problematic for several reasons. First, we could not
test whether the any lack of specicity found in the relationship
between strategies and psychopathology could be attributed to
shared variance among the strategies. In other words, we could not
test whether each strategy would still show signicant associations
with psychopathology when examined in models that included
other strategies. Additionally, we could not examine whether the
strategies would intercorrelate and potentially load onto latent

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A. Aldao, S. Nolen-Hoeksema / Behaviour Research and Therapy 48 (2010) 974e983

factor of cognitive emotion regulation characterized by frequent

use of maladaptive strategies and infrequent use of adaptive
strategies.
Second, the nature of univariate effect sizes did not allow us to
examine whether the relationships between regulatory strategies
and specic disorders were reecting transdiagnostic processes or
the shared variance resulting from symptom overlap among
disorders. In particular, we could not test whether the relationship
between eating disorders and regulatory strategies would be
maintained when accounting for the roles of depression or anxiety.
That is, eating disorders might be related to regulatory strategies
because of their associations with distress (e.g., Macht, Haput, &
Ellgring, 2005; Polivy & Herman, 2002). Similarly, we could not
address the high comorbidity seen in depression and anxiety
(Watson, 2009). In this respect, a better understanding of the
phenomenology of processes uniquely associated with each of
these disorders requires the isolation of the shared variance
between them. Although the interpretation of the residual variance
that results when a covariate has been included in a multivariate
model is not without problems (see Miller & Chapman, 2001), it is
still a parsimonious and straightforward way to identify which
variables are more strongly associated with anxiety and which with
depression (e.g., Aldao, Mennin, Linardatos, & Fresco, 2010;
Joormann & Stoeber, 1999; Mennin, Heimberg, Turk, & Fresco,
2005).
In the present investigation, we sought to address these limitations by examining the relationships among reappraisal,
problem-solving, thought suppression, and rumination, and their
relationships to symptoms of depression, anxiety, and eating
disorders in one large sample of young adults.3 Consistent with our
previous results (Aldao, Nolen-Hoeksema, et al., 2010), we tested
the hypothesis that all the cognitive emotion regulation strategies
would show high intercorrelations and therefore fall on a latent
factor of cognitive emotion regulation. Additionally, in line with the
results of our meta analysis, we predicted that the maladaptive
strategies would show stronger associations with the latent factor
as well as with psychopathology. Lastly, we examined whether
each of the three symptom types would continue to be associated
with cognitive emotion regulation when interrelationships among
symptom types was taken into account.

Methods
Participants
Participants were 252 undergraduate students at a private
university in the northeastern United States who completed
a battery of self-report questionnaires administered online using
Survey Monkey. All of them received a $5 compensation (in the
form of an Amazon.com gift certicate) and they were also entered
into a lottery to win an iPod Touch (awarded to 1 in 30 participants). They provided online consent according to the guidelines
specied by our Human Subjects Committee. The mean age of the
sample was 18.44 (SD .66) and a little over half the sample
(55.6%) identied as female. In terms of ethnic background, 5.6%
identied as African American, 22.2% as Asian/Asian American,

3
We did not include analyses of substance-related symptoms in the analyses
here because our measures only assessed use (rather than abuse) and in this underage sample the rate of heavy drinking was low. In addition, our meta analysis of
previous studies (Aldao, Nolen-Hoeksema, et al., 2010) showed that substance
abuse was more weakly associated with emotion regulation than any of the other
psychopathologies.

55.2% as Caucasian, 7.9% as Hispanic, .8% as Native American, and

8.3% as mixed or other.

Materials
Participants completed the following measures
Emotion regulation measures. The Problem-Solving subscale of the
COPE (Carver et al., 1989) is a 16-item measure of the tendency to
take a problem-solving approach to stressful situations. It has four
subscales: Active Coping, Planning, Suppression of Competing
Activities, and Restraint Coping. Items are scored on a 4-point scale
with higher scores indicating greater use of problem-solving to
cope. The four subscales have good internal consistency in the
literature (Carver et al., 1989; as .62e.80) and in this study (as
.75e.91). We initially conducted analyses using the four separate
scales; the results across the scales were very similar to the results
using the total scale comprised of the average score across the four
scales. Thus, for parsimony, we report here the analyses using the
total problem-solving score (a .90).
The Emotion Regulation Questionnaire (ERQ; Gross & John, 2003)
is a 10-item measure that assesses individual differences in the
dispositional use of two emotion regulation strategies: cognitive
reappraisal and expressive suppression. Items are scored on a 7point scale with higher scores indicating more use of a strategy. The
internal consistency for the Reappraisal subscale in this sample was
good (a .82).
We chose not to use the expressive suppression subscale and
instead to use a measure of thought suppression (see below)
because Gross and John (2003) have argued that expressive
suppression is a form of response modulation that involves
inhibiting ongoing emotion-expressive behavior.that primarily
modies the behavioral aspect of the emotion response tendencies. and will not be helpful in reducing the experience of negative
emotion, which is not directly targeted by suppression. (Gross &
John, 2003, p. 349). Indeed, in a line of experimental work, Gross
and colleagues have shown that expressive suppression does not
modify the subjective experience of emotion (Gross, 1998, Gross &
John, 2003; Gross & Levenson, 1993; Richards & Gross, 2000) and
that its effects consist of cardiac rebounds (i.e., increased sympathetic activation; Gross, 1998; Gross & John, 2003; Gross &
Levenson, 1993) and cognitive difculties (i.e., memory problems;
Richards & Gross, 2000).4
The Ruminative Response Scale (RRS; Treynor, Gonzalez, & NolenHoeksema, 2003) is a 22-item measure that assesses an individuals
tendency to engage in repetitive, ruminative behavior in response
to distress. Items are score on a 4-point scale, with higher scores
indicating more use of rumination. Treynor et al. (2003) have
removed those items with a strong content overlap with depression
and factor analyzed the remaining items to produce two subscales.

4
We calculated correlations between ERQ Suppression and the regulatory
strategies. It did not correlate with ERQ Reappraisal (r .01, p .91), which is in line
with the CFA conducted by Gross and John (2003) in their initial validation of the
ERQ and with subsequent investigations examining both subscales (e.g., Fresco
et al., 2007; Magar, Phillips, & Hosie, 2008). In addition, it did not correlate with
Problem-Solving Total (r .06, p .32), RS Brooding (r .09, p .17), or RS
Pondering (r 06, p .35). However, it did correlate mildly with WBSI (r .13,
p < .05). This pattern of correlations suggests that ERQ suppression does not
correlate with strategies aimed at modifying internal experience, with the exception of thought suppression, which might share a common inhibitory process. In
addition ERQ Suppression did not correlate with MASQ Anxious Arousal (r .06,
p .38) or EDE total (r .01, p .89) and it correlated positively with MASQ
Anhedonic Depression (r .21, p < .01), thus suggesting a limited role in psychopathology symptoms in this normative sample, consistent with the arguments of
Gross and John (2003) that expressive suppression will not have a strong relationship with the subjective experience of emotion.

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The Pondering subscale reects attempts to analyze problems

leading to depression (e.g., analyze recent events to try to understand why you are depressed; write down what you are thinking
about and analyze it). The Brooding subscale reects the moody
rumination at the core of Nolen-Hoeksemas (1991) rumination
theory (e.g., think, What am I doing to deserve this? think about
a recent situation, wishing it had gone better.). The authors
reported adequate reliability (a .77 and a .72 for Brooding and
Pondering, respectively). In our sample the reliability was good
(a .81 and a .83 for Brooding and Pondering, respectively).
The White Bear Suppression Inventory (WBSI; Wegner & Zanakos,
1994) is a 15-item measure designed to assess whether individuals
have a tendency to suppress thoughts and experience thought
intrusion. Items are scored on a 5-point scale, with higher scores
indicating more thought suppression. The internal reliability for
this measure in previous studies has been good (as ranging from
.87 to .89; Wegner & Zanakos, 1994). In the current sample, reliability was also good (a .94). We utilized this measure (instead of
the ERQ Suppression) because of its focus on the regulation of
internal experience.
Psychopathology symptom measures. The Mood and Anxiety
Symptom Questionnaire e Short Form (MASQ-SF; Watson & Clark,
1991) is a 62-item measure that assesses symptoms that
commonly occur in anxiety and mood disorders. Items are rated on
a 5-point scale, with higher scores indicating higher levels of
anxiety and depression. The short form version of the questionnaire
consist of four subscales: General Distress: Anxious Symptoms
(GDA) subscale, which consists of 11 items that reect non-specic
symptoms of anxiety (e.g., was unable to relax), General Distress:
Depressive Symptoms (GDD) subscale, which consists of 12 items
that reect non-specic depression symptoms (e.g., felt sluggish
or tired), Anxious Arousal (AA) subscale, which consists of 17 items
that assess anxiety-specic symptoms (e.g., startled easily), and
Anhedonic Depression (AD) subscale, which consists of 22 items
that assess symptoms specic to depression (e.g., felt withdrawn
from other people). In the present investigation, we only utilized
the AA and AD subscales, since they have lower overlap and are
therefore likely to produce stronger empirical differentiation
between the highly overlapping constructs of anxiety and depression (in this sample, for AA and AD, r .29, p < .01, whereas for GDA
and GDA, r .70, p < .01;). Watson et al. (1995) reported high levels
of internal consistency in multiple samples. In our sample, the as
for AA and AD were .91 and .93, respectively.
The Eating Disorders Examination-Questionnaire (Fairburn &
Beglin, 1995) is adapted from the Eating Disorder Examination
(EDE; Fairburn & Cooper, 1993) and it assesses a broad range of
symptoms of eating disorders. It contains probe items (i.e., yes/no
format) and items on a 7-point scale assessing behavioral features
of eating disorders, with higher scores indicating more psychopathology. The dimensional scores are utilized to calculate the EDE-Q
subscales: Restraint, Shape Concern, Weight Concern, and Eating
Concern. These subscales have shown good internal reliability (as
ranging for the subscales ranging from .78 to .93; Luce & Crowther,
1999). We utilized the total score of the EDE-Q (e.g., Roefs & Jansen,
2002) in order to capture overall eating pathology. This score had
very good reliability in our sample (a 95).
Results
Univariate associations
We rst examined the univariate relationships among the
measures of cognitive emotion regulation strategies and symptoms
of psychopathology (see Table 1). The results suggest that: 1) not all

977

strategies were correlated with one another; 2) adaptive strategies

(i.e., reappraisal and problem-solving) showed the expected
negative correlations with psychopathology, and maladaptive
strategies (i.e., brooding, pondering, and suppression) showed the
expected positive correlations; 3) consistent with our previous
meta analysis, the adaptive strategies showed weaker relationships
with psychopathology symptoms than the maladaptive strategies;
4) surprisingly, problem-solving showed no association with eating
symptoms. In order to explore this pattern of results at a multivariate level, we analyzed the relationships between cognitive
emotion regulation strategies and psychopathology using structural equation modeling (SEM; Arbuckle, 2007).
Structural equation modeling
We ran SEM models using Maximum Likelihood estimation.
Although SEM parameters estimated with this method tend to be
robust to deviations from multivariate normality, standard errors
and t indices might still be biased (Bollen, 1989; West, Finch, &
Curran, 1995). Therefore, we ran our models utilizing bootstrapping, a procedure involving the drawing of multiple random
samples by sampling from the original sample with replacement
that results in more stable parameters, particularly with small
samples and samples where multivariate normality may not old
(Byrne, 2010; Nevitt & Hancock, 2001; Preacher & Hayes, 2008). We
obtained 1000 random samples.
We evaluated model t by examining several t indices that are
based on different information, thus producing a comprehensive
evaluation of our models. We examined: 1) chi square, which
should be non-signicant (Hu & Bentler, 1998), but is overly sensitive to sample size, thus resulting in a tendency to reject the null
hypothesis (Ulman, 2007); 2) chi square/df, which adjusts for
sample size and should be lower than 3 or 2 (e.g., Mennin et al.,
2007; Ulman, 2007); 3) Tucker Lewis Index (TLI; Tucker & Lewis,
1973), which should be close to .95 (Hu & Bentler, 1999); 4)
Comparative Fix Index (CFI; Bentler, 1990), which should be close
to .95 (Hu & Bentler, 1999); 5) Root Mean Square Error of Approximation (RMSEA), which should have values close to .06 (Hu &
Bentler, 1999), with values between around .08 representing
reasonable errors of approximation (Browne & Cudeck, 1993); and
6) Hoelters Critical N (Hoelter, 1983), which measures the adequacy
of sample size, and should be higher than 200 (Hoelter, 1983).
Measurement model
We rst tested a structural model with the cognitive emotion
regulation strategies loading onto a single latent factor of cognitive
emotion regulation. We did not correlate the variances between the
two measures coming from a same measure (i.e., RSQ Brooding and
Pondering; Brown, 2006) because this resulted in Heywood cases
(i.e., estimates of negative variance that prevent the model from
running properly; Brown, 2006; Byrne, 2010). Surprisingly,
problem-solving did not load onto the latent factor of cognitive
emotion regulation (p .73) and the overall t of the model was
poor, as evidenced by a large, signicant chi square [c2 (5,
N 252) 40.14, p < .01] and poor t indices (chi square/df 8.03;
TLI .67; CFI .84; RMSEA .17; Hoelters Critical N 95).
Removal of problem-solving in a subsequent model resulted in
a good t, as evidenced by both a non-signicant chi square
(c2 [2, N 252] 5.91, p .05) and appropriate values in the
additional t indices (chi square/df 2.96; TLI .94; CFI .98;
RMSEA .09; Hoelters Critical N 392). As Fig. 1 and Table 2
indicate, brooding, pondering, suppression and reappraisal loaded
signicantly on the latent factor of cognitive emotion regulation.
Three strategies (i.e., brooding, pondering, and suppression) had

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A. Aldao, S. Nolen-Hoeksema / Behaviour Research and Therapy 48 (2010) 974e983

Table 1
Bivariate correlations between measures of emotion regulation and psychopathology.

ERQ Reappraisal
PS total
RSQ Brooding
RSQ Pondering
WBSI
MASQ Anhedonic Depression
MASQ Anxious Arousal
EDE total

Mean (SD)

Range

.27**

.18**
.02

.01
.18**
.54**

.05
.10
.55**
.39**

.32**
.25**
.51**
.24**
.36**

.20**
.17**
.37**
.16*
.33**
.29**

.15*
0
.36**
.29**
.25**
.37**
.27**

4.5
2.62
2.14
2.21
2.84
2.72
1.66
1.34

1e7
1e4
1e4
1e4
1e5
1e3.47
1.10e4.67
0e5.48

(1.05)
(.53)
(.73)
(.79)
(.95)
(.65)
(.59)
(1.19)

Note: ERQ: Emotion Regulation Questionnaire; PS: problem-solving; RSQ: Response Styles Questionnaire; WBSI: White Bear Suppression Inventory; MASQ: Mood and Anxiety
Symptoms Questionnaire; EDE: Eating Disorder Examination. *p < .05; **p < .01.

positive loadings, whereas reappraisal had a negative loading that

was very low in magnitude, yet signicant. Removal of this indicator or creation of a second latent factor with the indicators of
reappraisal and problem-solving both resulted in Heywood cases
and models that could not be run. Thus, we proceeded with the
latent factor that included brooding, pondering, suppression, and
reappraisal. We return to the statistical and conceptual implications
of this issue in the discussion section.

to .37; see Table 3, Fig. 2). In addition, all three symptom measures
had signicant regression weights onto the latent factor of cognitive emotion regulation, suggesting that even when the overlap
between symptoms is taken into account, they are all correlated
with cognitive emotion dysregulation (yet the coefcients were
lager for depression symptoms, followed by anxiety symptoms and
then by eating symptoms).
Discussion

Structural model
We examined a structural model, in which we evaluated the
relationship between the latent factor of cognitive emotion regulation and symptom measures (i.e., MASQ AD, MASQ AA, and EDEQ). Given the high overlap between symptoms of measures of
psychopathology (Watson, 2009), we allowed the MASQ AD, MASQ
AA, and EDE-Q to correlate with each other.
The rst version of the model produced a fair t, with a signicant chi square [X (11, N 252) 41.22, p < .01] and additional t
indices slightly outside of the ranges for good t (chi square/
df 3.75, TLI .85, CFI .92, RMSEA .11, Hoelters Critical
N 151). As a result, we examined the modication indices.
Among the suggestions, one was the addition of a covariance path
between the error variance or ERQ reappraisal and that of the
latent factor of cognitive emotion regulation (M.I. 10.02, parameter
change .08). Since this change would not result in the modication of the conceptual model, we decided to add this path in
a second model.
The second structural model produced good t. The chi square
was still signicant (10, N 252) 19.84, p < .05, but the rest of the
indices were now within the ranges considered to be indicative of
good t (chi square/df 1.98; TLI .95; CFI .97; RMSEA .06,
Holters Critical N 294). In this model, as predicted, the symptom
measures were signicantly correlated with each other (rs from .27

Fig. 1. Measurement model: standardized coefcients.

A plethora of cognitive emotion regulation strategies has been

conceptualized and operationalized in recent decades (e.g., Billings
& Moos, 1981; Carver et al., 1989; Folkman & Lazarus, 1986;
Garnefski & Kraaij, 2006; Gross, 1998; Nolen-Hoeksema et al.,
2008; Wenzlaff & Wegner, 2000). These various strategies have
generally been studied for their individual contributions to
psychopathology; however, the studies that have compared several
different strategies in the same sample have found that they tend to
intercorrelate (e.g., Garnefski, Kraaij, & Spinhoven, 2001; Hong,
2007; Wenzlaff & Luxton, 2003), thus suggesting they might have
low specicity.
In this study, we examined the relationships among four
commonly studied cognitive emotion regulation strategies (i.e.,
reappraisal, problem-solving, rumination, and suppression) and
found that three of them (reappraisal, suppression, and rumination,
with its subcomponents of brooding and pondering) loaded on
a single latent factor of cognitive emotion regulation. These results
overall support a model of low specicity of regulatory strategies,
with one exception: adaptive strategies appear to play a smaller
role in cognitive emotion regulation than maladaptive strategies.
Reappraisal loaded on the cognitive emotion regulation latent
factor, yet its loading was negative and extremely low. Its removal
from the model substantially deteriorated it, generating Heywood
cases and preventing it from running. Similarly, alternative models
in which reappraisal and problem-solving loaded onto a different
latent factor of adaptive cognitive emotion regulation also resulted
in Heywood cases and extremely poor t. This suggests that reappraisal might belong in this latent factor of cognitive emotion
regulation, yet its role in the process might be weaker. For example,
most individuals who tend to use maladaptive strategies such as
rumination and thought suppression may try to use reappraisal to
improve their emotional responses to stress, but their maladaptive
tendencies may be stronger than their ability to use reappraisal
successfully.
Although problem-solving was correlated with reappraisal and
the pondering subcomponent of rumination, it did not load onto
the latent cognitive emotion regulation factor in the structural
model. This suggests that problem-solving might be fundamentally
different from other regulatory strategies, as it is an attempt to
change a situation rather than an emotion. The adaptiveness of
problem-solving may also depend even more on the context than

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Table 2
Measurement model coefcients.
Path
Cognitive
Cognitive
Cognitive
Cognitive

emot
emot
emot
emot

reg / ERQ Reappraisal

reg / RSQ Brooding
reg / RSQ Pondering
reg / WBSI total

Parameter
estimate

Standard
error

Standardized
estimate

p-Value

Bootstrap mean
estimate bias

Bootstrap SE
estimate bias

.37
1.41
1.00
1.22

.15
.20
e
.16

.17
.90
.60
.61

<.05
<.01
e
<.01

.001
.009
.001
.003

.003
.002
.002
.002

Note: ERQ: Emotion Regulation Questionnaire; RSQ: Response Styles Questionnaire; WBSI: White Bear Suppression Inventory. There is p-value for RSQ Pondering, since its
loading was xed to 1.

for other strategies. For example, problem-solving may not be an

adaptive strategy when facing an uncontrollable situation in which
there is no problem to solve (e.g., Cheng, Hui, & Lam, 1999; Folkman
& Lazarus, 1986).
Moreover, the bivariate correlations showed that problemsolving was signicantly correlated with depression and anxiety
symptoms but not with eating symptoms (see Table 1). This nding
was at odds with the results from our meta analysis, which suggested a small-to-medium effect size between problem-solving and
eating symptoms. A few explanations come to mind. First, the meta
analysis results were calculated using only two effect sizes (one
from a clinical population and one from a normative population) so
this might have resulted in a spurious nding. Second, problemsolving (and perhaps adaptive strategies at large) might have
a different relationship with psychopathology symptoms.
The notion that adaptive strategies might play a smaller role in
the cognitive emotion regulation process is consistent with the
results from our meta analysis, in which we found that suppression,
rumination, and avoidance were more strongly associated with
psychopathology then problem-solving, reappraisal, and acceptance (Aldao, Nolen-Hoeksema, et al., 2010). Adaptive strategies
might have lower associations with psychopathology symptoms at
the dispositional level because their adaptiveness might be more
context-dependent than the maladaptiveness of maladaptive
strategies. For example, reappraisal might only be adaptive when
the situation can actually be reframed, whereas rumination is
maladaptive most of the time (Nolen-Hoeksema et al., 2008).
Indeed, recent work suggests that when reappraisal is deployed
later in the emotion regulation process, it results maladaptive
outcomes, such as increased sympathetic activation (Sheppes,
Catran, & Meiran, 2009) and diminished self-control (Sheppes &
Meiran, 2008). In this respect, the temporal dynamics of the
deployment of emotion regulation strategies might be critical to
the adaptiveness of strategies (Davidson, 1998; Thompson, 1994). In
addition, recent work suggests that the relationship between
adaptive strategies and symptoms of anxiety and distress might be
moderated by gender (Zlomke & Hahn, 2010). Future work on the

contextual adaptiveness of strategies would benet from the use of

experience sampling designs (e.g., Ebner-Priemer et al., 2007;
Feldman-Barrett & Barett, 2001), the manipulation of several
contextual factors within one experimental session, and the use of
functional analyses as a framework (e.g., Ferster, 1973; Kohlenberg
& Tsai, 1991; Linehan, 1993).
Another possibility is that, once individuals start using maladaptive strategies frequently, these quickly become their default way
of managing affective states. As a result, they start using the
adaptive strategies more haphazardly, which would result in more
noise and therefore weaker correlations with psychopathology
symptoms. This notion is consistent with models of emotion
regulation that stress exibility in the use of strategies as a sign of
adaptive regulation (e.g., Bonanno, Papa, ONeill, Westphal, &
Coifman, 2004; Coiffman & Bonanno, 2010; Cole, Martin, &
Dennis, 2004; Gratz & Roemer, 2004). Future work on this respect
should focus on quantifying the ability to exibly switch strategies
as the contingencies in the environment change.
The latent cognitive emotion regulation factor did include both
the brooding and pondering subcomponents of rumination. Many
studies have conrmed that the brooding subcomponent is associated with a variety of psychopathological symptoms (see reviews by
Aldao, Nolen-Hoeksema, et al., 2010; Nolen-Hoeksema et al., 2008).
The relationships between the pondering subcomponent and
psychopathology have been more mixed (see review by NolenHoeksema et al., 2008). The items on this subcomponent seem to
reect attempts to understand and solve ones problems (e.g.,
analyze recent events to try to understand why you are depressed;
write down what you are thinking about and analyze it). In this
study, the pondering subcomponent was positively correlated with
problem-solving, but it was also positively correlated with brooding,
suppression, and all the symptom types (for similar patterns in other
studies, see review by Nolen-Hoeksema et al., 2008). Thus, although
people may engage in pondering to try to understand and solve their
problems, pondering is associated with a pattern of maladaptive
emotion regulation strategies and psychopathology symptoms.
Some individuals may try to engage in pondering about their

Table 3
Structural model coefcients.
Path
Regression paths
Cognitive emot reg / ERQ Reappraisal
Cognitive emot reg / RSQ Brooding
Cognitive emot reg / RSQ Pondering
Cognitive emot reg / WBSI total
EDE total / cognitive emot reg
MASQ Anx Arousal / cognitive Emot Reg
MASQ Anhedonic Dep / cognitive emot reg
Correlations
EDE total 4 MASQ Anhedonic Dep.
EDE total 4 MASQ Anx Arousal
MASQ Anhedonic Dep 4 MASQ Anx Arousal

Parameter
estimate

Standard
error

Standardized
estimate

p-Value

Bootstrap mean
estimate bias

Bootstrap SE
estimate bias

1.19.
1.43
1.00
1.28
.06
.19
.32

.27
.17
e
.17
.02
.05
.05

.53
.90
.59
.62
.15
.24
.44

<.01
<.01
e
<.01
<.01
<.01
<.01

.002
.001
.001
.000
.000
.000
.002

.004
.001
.002
.002
.002
.002
.002

.37
.27
.29

<.01
<.01
<.01

.002
.001
.001

.002
.002
.002

Note: ERQ: Emotion Regulation Questionnaire; RSQ: Response Styles Questionnaire; WBSI: White Bear Suppression Inventory; EDE: Eating Disorder Examination; MASQ:
Mood and Anxiety Symptom Questionnaire. There is no p-value for RSQ Pondering, since its loading was xed to 1.

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Fig. 2. Structural model: standardized coefcients.

problems but fall into rumination and/or suppression. Interventions

for such people may need to help them recognize when they are
moving from pondering into rumination or suppression and then
prevent this, perhaps through concreteness training (i.e., having
individuals focus on the concrete details of a situation rather than on
abstract evaluations of the situation). Watkins (2008) has shown
that concreteness training can allow individuals to think about
important self-relevant situations without falling into rumination.
The latent factor of cognitive emotion regulation, composed of
rumination (brooding and pondering), suppression, and reappraisal
was signicantly related to all three types of psychopathology:
depressive symptoms, anxiety symptoms, and eating disorders
symptoms. An initial examination of the standardized coefcients
suggests that depressive symptoms had the largest coefcients,
followed by anxiety symptoms and then by eating symptoms. This
is in line with the results of our meta analysis showing that the
individual cognitive emotion regulation strategies had stronger
relationships to depression and anxiety than to eating disorders
(Aldao, Nolen-Hoeksema, et al., 2010) and with previous ndings
suggesting that internalizing symptoms are more strongly associated with emotion regulation than non-internalizing symptoms
(e.g., Garnefski et al., 2005). Although premature to draw conclusions from this preliminary observation, the consistency between
our previous ndings and the trends in this study lead us to speculate on some explanations for the potential stronger relationships
between cognitive regulatory strategies of depression and anxiety.
The larger coefcients for depression and anxiety might be the
result of more overlap in item content between these measures
than with eating disorder measures. The rumination scale has been
criticized for its item overlap with depression (e.g., I think about
my feelings of sadness). However, we used the version of the
rumination questionnaire (i.e., the brooding and pondering
subscales) from which Treynor et al. (2003) removed items that
most obviously overlapped with distress and found they were still
strongly related to depressive and anxiety symptoms. Similarly, our
meta analysis found that the brooding subscale was as strongly
related to depression and anxiety as was the full rumination scale
(Aldao, Nolen-Hoeksema, et al., 2010).

An alternate explanation for the larger coefcients between

cognitive emotion regulation measures and depression and anxiety
symptoms is that eating disorder symptoms might themselves
regulatory mechanism utilized when experiencing high levels of
anxiety and depression (Polivy & Herman, 2002). Evidence supporting this notion comes from ndings showing that a history of
negative affect is predictor of future onset or exacerbation of
anorexic and bulimic symptoms (Burton, Stice, Bearman, & Rohde,
2007; Stice, Burton, & Shaw, 2004; Stice, Presnell, & Spangler,
2002). Further, Stice et al. (2002) have found that disordered
eating behaviors in response to negative emotions more strongly
predicted the development of bulimia nervosa in adolescent girls
than did disordered eating behaviors that were in response to
shape and weight concerns. Additionally, Macht et al. (2005) have
found that students reported engaging in eating behaviors to
distract themselves during periods of elevated stress.
Still, the results from this study indicate that eating disorder
symptoms are signicantly related to cognitive emotion regulation
strategies, even after accounting for the relationships between
eating disorder symptoms and depressive and anxiety symptoms.
This suggests that cognitive emotion dysregulation has unique
relationships to eating disorder symptoms, even if this relationship
is smaller in magnitude than the one between cognitive emotion
dysregulation and depressive and anxiety symptoms. At the same
time, it does not completely invalidate the notion that eating
disorders might be developed and/or maintain as strategies to
regulate negative affect. Future studies using longitudinal designs
should clarify the predictive relationships over time between
cognitive emotion regulation strategies, eating disorder symptoms,
and depressive and anxiety symptoms and directly compare the
role of cognitive strategies across these disorders.
An important goal for future research is to identify the mechanisms by which the latent cognitive emotion regulation factor might
lead to more symptoms of depression, anxiety, and eating disorders.
Previous work on rumination, thought suppression, and reappraisal
provide some clues as to the mechanisms by which each of these
contributes to psychopathology (Gross & Thompson, 2007; NolenHoeksema et al., 2008; Purdon, 1999; Watkins, 2008; Wenzlaff &
Wegner, 2000). The conuence of tendencies to both ruminate
and suppress thoughts, and difculties in reappraisal, may have
deleterious effects on the quality of thought and exacerbation of
mood that go beyond the effects of any of these regulatory decits
individually, however. For example, people who ruminate and do
not try to reappraise may experience particularly rapid escalation of
catastrophizing thoughts and distressing emotions; if they are also
prone to suppression, they may turn to food, substances, or selfdestructive behavior to escape from their thoughts and moods. As
a result, people with the conuence of regulatory problems indexed
by our latent cognitive emotion regulation factor may be especially
emotionally reactive to stressors and prone to escapist behaviors
that may be self-destructive.
Limitations
A rst limitation was the use of self-report measures for both
psychopathology and emotion regulation, thus resulting in shared
method variance. In addition, self-reports of psychopathology
symptoms provide an incomplete picture of an individuals
pathology and should therefore be administered as part of a multimethod assessment including diagnostic interviews (e.g.,
Achenbach, Krukowski, Dumenci, & Ivanova, 2005; Meyer et al.,
2001). To this end, structured clinical interviews could be used to
assess psychopathology in future studies in order to: reduce shared
method variance, compensate for the biases resulting from selfreport measures, and provide a more precise delineation of

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A. Aldao, S. Nolen-Hoeksema / Behaviour Research and Therapy 48 (2010) 974e983

individual disorders (in this paper, we focused on general symptoms of depression, anxiety, and eating disorders). Our meta
analysis found stronger relationships between several emotion
regulation measures and psychopathology in clinically diagnosed
samples than in general population samples (Aldao, NolenHoeksema, et al., 2010), underscoring the importance of assessing
psychopathology with a multi-method approach.
Additionally, assessing emotion regulation strategies by selfreport is problematic for several reasons, including the blurry lines
between emotion generation and emotion regulation (Campos,
Frankel, & Camras, 2004; Cole et al., 2004) and reporting biases
(Robinson & Clore, 2002). In this respect, a comprehensive study of
regulatory strategies will require a multi-modal method of
assessment capturing the subjective, physiological, and behavioral
emotional domains utilizing multiple measures of each domain.
Future work examining the relationship between cognitive
emotion regulation strategies and psychopathology as assessed by
structured diagnostic interviews is needed to conrm the results
here.
A second limitation of the present investigation is that we
limited our scope to four cognitive regulatory strategies. We chose
these strategies because they are among the most commonly
studied ones in the eld and therefore the most representative of
current conceptualizations of emotion regulation. However, these
strategies have been largely studied within the context of mood
and anxiety disorders and might not be as relevant to the main
affective processes to be regulated in other disorders (e.g., positive
emotions resulting from the consumption of foods and other
substances; elevated positive affect in mania). Future transdiagnostic work on regulatory strategies should take this issue into
account and seek to identify process that might be germane to
specic disorders. Additionally, in light of our surprising results on
problem-solving, future work should focus on carefully delineating
strategies theoretically and empirically, as there is substantial
heterogeneity in the conceptualization of strategies. Lastly, it will
be important to more systematically examine the relationship
between strategies aimed at the modication of subjective versus
expressive emotional processes.
A third limitation of this study is its cross-sectional design,
which did not allow for modeling of relationships among variables
over time. Lastly, a fourth limitation stems from the nature of the
population we studied, as we utilized an undergraduate sample,
therefore restricting the range of psychopathology and potentially
also that of cognitive emotion regulation strategies. Indeed, the
models presented in this manuscript had good t, but it could have
certainly been higher. It therefore becomes critical to replicate the
structural ndings in a wide range of samples varying in severity of
the symptoms and pervasiveness of the emotion regulation decits.
Conclusion
We found mixed evidence for specicity in the relationship
between multiple cognitive emotion regulation strategies and
psychopathologies. The adaptive strategy of reappraisal showed
a weaker association with a latent factor of cognitive emotion
regulation and with psychopathology symptoms than maladaptive
strategies. Clinically, this might help account for the difculties
teaching clients to incorporate adaptive strategies to their repertoire; the maladaptive strategies of rumination and thought
suppression may often overwhelm clients attempts to reappraise.
This suggests that interventions that directly focus on reducing
rumination and thought suppression, such as teaching mindfulness
meditation practices, may be critical precursors to interventions to
teach clients to use reappraisal more successfully (e.g., Segal,
Williams, & Teasdale, 2002; Watkins et al., 2007).

981

A latent factor of cognitive emotion regulation was signicantly

associated with symptoms of all three disorders, suggesting it has
transdiagnostic effects. These results encourage the development
of prevention and intervention programs focused on cognitive
emotion regulation strategies, because such programs may have
positive effects across a range of disorders.

Acknowledgements
We would like to thank Blair Wisco for her assistance in data
collection and her comments on this manuscript. We would also
like to thank Kirsten Gilbert, Andrea Gold, Yael Levin, Brett
Marroquin, and Vera Vine for their insightful comments on this
manuscript.

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