ORI GI NAL ARTI CLE

Cognitive Control Moderates Relations Between Impulsivity

and Bulimic Symptoms
Michael D. Robinson Elizabeth A. Pearce
Scott G. Engel Stephen A. Wonderlich
Published online: 25 April 2008
Springer Science+Business Media, LLC 2008
Abstract The present study, involving 128 undergraduate
participants, sought to better understand relations between
trait impulsivity, cognitive control, and bulimic symptoms.
Three models were contrasted. One model posited that
impulsivity and cognitive control would be independent,
non-interactive predictors of bulimic symptoms. A second
model posited that cognitive control decits would mediate
relations between impulsivity and bulimic symptoms. A
third model posited that relations between trait impulsivity
and bulimic symptoms might be stronger among individ-
uals lower in cognitive control relative to those higher in
cognitive control. The latter moderation model was sys-
tematically supported across two measures of cognitive
control and two measures of bulimic symptoms. Wider
implications of the ndings are discussed. For example, it
is suggested that treatments facilitating higher levels of
cognitive control can be recommended among patients
high in impulsivity.
Keywords Temperament Impulsivity
Cognitive control Bulimic symptoms
Introduction
Automatic processes are those that rely on habit, whereas
controlled processes are those that allow individuals to
transcend their habits in the service of context-appropriate
behavior (Baneld et al. 2004; Lieberman 2003). The
distinction between automatic and controlled processes has
a long history in cognitive psychology (Luria 1969;
Schneider and Shiffrin 1977), but is somewhat more recent
to social, personality, developmental, and clinical litera-
tures (Chaiken and Trope 1999; Metcalfe and Mischel
1999). From personality and clinical perspectives, auto-
matic processes are likely those that reinforce ones tem-
perament-based habits, whereas controlled processes are
likely those that render one less susceptible to tempera-
ment-based habits (Mischel and Ayduk 2004; Robinson
2007a; Rothbart et al. 2000).
The most extensive body of data along these lines has
been reported in the child development literature. Very
early in life, emotional and behavioral reactions seem
primarily determined by temperament (Kagan and Snid-
man 1991; Rueda et al. 2004). As cortical capacities
develop, however, cognitive control abilities come to play
an increasingly important role in the individuals func-
tioning (Kochanska et al. 2000; Rueda et al. 2004). Of
central interest are robust sources of data suggesting that
temperamental differences in negative affectivity and
impulsivity are less predictive of outcome variables among
children higher in cognitive control (e.g., Eisenberg et al.
2000; Nigg 2006). From such data, one might similarly
expect individual differences in cognitive control to mod-
erate problematic outcomes related to adulthood levels of
neuroticism and impulsivity.
In support of this moderation-related model, Robinson
and colleagues have reported several studies in which
higher levels of cognitive control moderated the tendency
for neurotic individuals to experience higher distress in
everyday life, such that neuroticismdistress relations were
somewhat particular to individuals low in cognitive control
M. D. Robinson (&) E. A. Pearce
Psychology Department, North Dakota State University,
Fargo, ND 58105, USA
e-mail: Michael.D.Robinson@ndsu.edu
S. G. Engel S. A. Wonderlich
Neuropsychiatric Research Institute, Fargo, ND, USA
1 3
Cogn Ther Res (2009) 33:356367
DOI 10.1007/s10608-008-9192-z
(e.g., Robinson et al. 2006a, b). No prior work of this type,
however, has examined the potential moderating role of
cognitive control in understanding impulsivity-linked out-
comes and this was the specic focus of the present study.
For purposes of extending this moderation-related model,
we also focused on a novel dependent measure related to
bulimic symptoms such as binging and purging.
Impulsivity as a Risk Factor for Bulimic Symptoms
Trait impulsivity is a robust predictor of bulimic symptoms
(de Zwaan et al. 1994; Keel and Mitchell 1997; though
such relations are dependent on the type of impulsivity
assessed: Fischer et al. 2003a). Moreover, higher levels of
impulsivity have been linked to a wider variety of purging
methods (e.g., vomiting, laxatives, diuretics: Stein et al.
2004), as well as to an increased tendency toward other
impulsive behaviors such as suicide attempts (Stein et al.
2004) and self-harming behavior (Casillas and Clark 2002).
Thus, there are multiple sources of data linking trait
impulsivity to bulimic symptoms, with further suggestions
that the presence of impulsive traits inuences the form and
severity of such symptoms (Claes et al. 2006; Lyke and
Spinella 2004).
Less clear is why impulsivity is predictive of bulimic
behaviors and we contrast three models to better under-
stand this relationship. The rst model may be termed a
main effect model. According to this model, impulsive
individuals have stronger appetitive urges, and are more
likely to act on them, in the pursuit of desired commodities
like food, sex, drugs, and other potential reinforcers
(Fowles 2001; Gray 1987; Patterson and Newman 1993).
Within this model, it is not clear that cognitive control
would play either mediating or moderating roles in
understanding the correlates of impulsivity. Rather, from
the perspective of this model, both impulsivity and cog-
nitive control are likely to be independent, rather than
interactive, main effects (Pickering et al. 1999). Translated
to the present context, then, the main effect model predicts
a main effect for impulsivity that should be independent of
a potential main effect for cognitive control.
A second model may be termed a mediation model in
which the correlates of impulsivity are likely to be medi-
ated by decits in cognitive control. In support of this
model, impulsive children often exhibit lesser abilities in
inhibitory control tasks, though the data in support of this
perspective are complicated and in need of a rened model
(Nigg 2000). In the adult trait literature, individual differ-
ences in impulsive forms of aggression have been linked to
poorer executive function, although here too such data are
not as consistent as one might like (Wilkowski and Rob-
inson in press). Regardless, there are some hints that
impulsivity may systematically relate to low levels of
cognitive control, which in turn might explain some of the
correlates of impulsivity (Mischel and Ayduk 2004).
Translated to the present context, then, the mediation
model predicts some relation between impulsivity and
cognitive control and further predicts that cognitive control
should mediate relations between impulsivity and bulimic
symptoms.
A third model may be termed a moderation model in
which the link of impulsivity to bulimic symptoms is likely
to be moderated by individual differences in cognitive
control. In general terms, this moderation model is con-
sistent with the developmental literature on effortful con-
trol (e.g., Eisenberg et al. 2000) and with observations that
cognitive control moderates rather than mediates the neu-
roticismdistress relationship (e.g., Robinson 2007a). Such
results presumably occur because temperamental tenden-
cies are a stronger inuence on ones behavior to the extent
that cognitive control is weak (Rothbart et al. 2000).
Translated to the present context, then, the moderation
model predicts that relations between impulsivity and
bulimic symptoms should be stronger among those low in
cognitive control and weaker among those high in cogni-
tive control. To provide further context for these predic-
tions, we next dene cognitive control and its assessment.
Individual Differences in Cognitive Control
What is cognitive control? Generally dened, it is an
ability to suppress dominant response tendencies in favor
of sub-dominant ones, and is critically reliant on frontal
lobe functioning (e.g., Baneld et al. 2004; Lieberman
2003). Although the developmental literature that we drew
upon has measured cognitive control in a variety of ways,
there is an emerging consensus that cognitive control is
perhaps most directly assessed in behavioral performance
in cognitive tasks suited to its measurement (Rothbart et al.
2004; Rueda et al. 2004). This was the approach taken
here.
The Stroop task is often seen to be the gold standard
of cognitive control and has been used in thousands of
studies along these lines (for a review, see MacLeod 1991).
The task requires responding to an ink color (e.g., green)
that is incongruent with word meaning (e.g., red). Because
word reading is a relatively automatic process, individuals
have difculties with the task and Stroop effects, dened in
terms of slowed responding on incongruent font/word tri-
als, are quite robust across many different stimulus and task
variations (MacLeod). Although extensions of the Stroop
effect to studies of individual differences are relatively
Cogn Ther Res (2009) 33:356367 357
1 3
sparse, there are suggestions that smaller Stroop effects
reect superior abilities in cognitive control (e.g., Morgan
and Lilienfeld 2000; Troyer et al. 2006).
In addition, we drew from a second literature on cog-
nitive control, which has linked it to post-error adjustments
in reaction time (RT). Measures of this type have long been
linked to cognitive control, including lesser tendencies
toward behavioral errors in the future (Rabbitt 1966;
Robinson 2007b). Moreover, it has been shown that ten-
dencies to pause following errors are systematically linked
to the cognitive control regions of the brain, particularly
the anterior cingulate cortex and the lateral prefrontal
cortex (Baneld et al. 2004; Kerns et al. 2004; Lieberman
2003). Self-regulation, from this perspective, involves re-
thinking ones processing strategy following errors, a
process that takes time (Robinson 2007b; Robinson et al.
2007). Given that this cognitive model has considerable
potential in social and clinical domains (van Veen and
Carter 2002), we assessed cognitive control in this second
manner as well.
Interactive Predictions
We contrasted main effect, mediation, and moderation
models in understanding the respective contributions of
impulsivity and cognitive control to bulimic symptomolo-
gy. Based on prior developmental (e.g., Eisenberg et al.
2000) and personality data (e.g., Robinson 2007a), we
predicted that individual differences in cognitive control
would moderate relations between impulsivity and bulimic
symptoms, such that impulsivity would be a lesser (and
potentially non-signicant) predictor of symptoms among
individuals high in cognitive control. To examine such
predictions, we used standard measures of each construct
and collected data from a relatively large sample of non-
clinical participants.
Method
Participants
One hundred and twenty-eight psychology students from a
large state university (83 women & 45 men, M
age = 19.7 years) volunteered for extra credit. Ninety-
three percent of the sample was Caucasian in race. The
study was approved by the IRB at the University. It is
important to add that we did not specically recruit indi-
viduals on the basis of their levels of impulsivity, cognitive
control, or bulimic symptoms, nor did we exclude any
individual on the basis of such criteria. Thus, our ndings
should be viewed in terms of a dimensional model of
personality and psychopathology.
Cognitive Control Measures
Task
Cognitive control is often examined in the traditional
Stroop task (MacLeod 1991), as we did in our study as
well. Participants were asked to classify the font color of
letter strings as quickly and accurately as possible. Stimuli
consisted of three letter strings (green, red, & xxx) in two
font colorsgreen or red. Participants were told that only
the font color, not the letter string in question, was relevant
to the task. If the font color was green (red), they were
asked to respond with the 1 (9) key at the top of the key-
board. The computer randomly assigned stimuli to trials
and there were 252 trials in all. If the response was accu-
rate, there was a 500 ms blank delay until the appearance
of the next stimulus. If the response was inaccurate, there
was a 2,000 ms visual error message before the 500 ms
blank. The error message was designed to insure that an
error had been registered, thereby also insuring that post-
error adjustments in RT reected awareness of having
made an error (Robinson 2007b).
Scoring Reaction Time
Reaction times were scored in a standard manner (Robin-
son 2007c). Inaccurate responses for the current trial were
dropped (M accuracy = 96.2%). Reaction times were then
log-transformed to reduce positive skew. Finally, log-
transformed times 2.5 SDs faster or slower than the grand
log-latency mean were replaced by these 2.5 SD outlier
values. Such procedures reduce the impact of very fast or
slow times, while still including them (Robinson 2007c).
We report millisecond means for ease of interpreting the
results.
Self-Report Measures
Impulsivity
Impulsivity is important to clinical outcomes, but has
proven to be a somewhat heterogeneous construct
(Whiteside and Lynam 2001; Zuckerman et al. 1988). In
the present study, we assessed impulsivity in terms of
Eysenck and Eysencks (1977) narrow impulsivity fac-
tor, which was found to tap core decits in behavioral
control somewhat independently of impulsive behaviors
characteristic of non-planning or risk-taking. This narrow
impulsivity scale consists of 13 items reective of disin-
hibited behavior (e.g., Are you an impulsive person?) and
uses a 4-point response scale (1 = not at all true of me;
4 = very true of me). No items directly reference eating
behaviors or other behaviors reective of bulimic
358 Cogn Ther Res (2009) 33:356367
1 3
symptoms. Alpha was .71 in the present study (M = 2.45;
SD = .37).
Bulimic Symptoms
We assessed bulimic symptoms with two widely used and
validated measures. The rst measure was the Bulimia
Test-Revised (BULIT-R: Smith and Thelen 1984), which
assesses variations in binge eating, use of compensatory
behaviors, and preoccupation with weight and shape, all of
which are diagnostic criteria for bulimia nervosa (Thelen
et al. 1991). The scale has 36 items (e.g., Would you
presently call yourself a binge eater?; 1 = No, probably
not; 5 = Yes, absolutely). Alpha was .94 in our study
(M = 1.66; SD = .57).
We also assessed bulimic symptoms using the Bulimia
subscale of the Eating Disorders Inventory-2 (Garner
1991). Scale scores involving this measure have been
shown to be strong predictors of clinically signicant ten-
dencies toward bulimic nervosa (Pike et al. 2000). The
Bulimia subscale of the general inventory has seven items
(e.g., I have the thought of trying to vomit in order to lose
weight; 1 = never; 6 = always). Alpha was .84 in our
study (M = 1.86; SD = .75).
Procedures
The second author ran all experimental sessions, which
involved groups of less than seven. Following informed
consent and instructions, participants were assigned to
individual rooms, each equipped with its own computer.
Participants rst completed the Stroop task, programmed
with E-Prime software. Second, they completed the buli-
mic symptom measures followed by the impulsivity mea-
sure, programmed for computer administration with
MediaLab software. The order of measures was consistent
with prior recommendations in the literature, which have
suggested that, for reasons of precluding potential order
effects, implicit measures should be assessed rst, behav-
ioral measures should be assessed second, and trait mea-
sures should be administered last (Robinson and Neighbors
2006).
Results
Scoring Stroop Interference
The Stroop effect is dened in terms of relatively slow
responses when the stimulus and its color are discrepant
(e.g., the word red in a green font). The benets of a
stimuluscolor match (e.g., the word red in a red font) are
inconsistent across studies, though there is sometimes such
a benet relative to a baseline condition (MacLeod 1991).
To remove ambiguities as to the source of Stroop inter-
ference scores, we contrasted the incongruent condition
(i.e., all trials involving a stimulus-color mismatch) versus
the baseline condition (i.e., all trials involving the stimulus
xxx). As predicted, a contrast of such conditions revealed a
robust Stroop effect across participants, F (1, 127) =
38.76, P\.01, such that responses were faster in the
baseline condition (M = 582 ms) relative to the incon-
gruent condition (M = 603 ms). The size of this normative
Stroop effect was thus 21 ms (SD = 35 ms).
To compute a Stroop interference score for each indi-
vidual, we sought to control for speed of responding on
baseline trials. Toward this end, we performed a simple
regression in which baseline (log) RT was entered as a
predictor of incongruent (log) RT. The results of this
regression were used to remove variance common to the
baseline and incongruent Stroop conditions. That is,
residual Stroop interference scores were necessarily cor-
related with RT performance in the incongruent condition,
but necessarily uncorrelated with RT performance in the
baseline condition. Thus, high residual scores reect
greater difculties with the incongruent condition of the
Stroop task than could be expected based on performance
in the baseline condition of the task.
Scoring Error Regulation
Models of cognitive control emphasize the importance of
adjusting ones behavior following errors (Baneld et al.
2004; Holroyd and Coles 2002). To score post-error
adjustments in the present study, we contrasted (log) RTs
following correct responses versus following errors on the
previous (i.e., n - 1) trial. It was expected that participants
would be slower following errors (M = 881 ms) than fol-
lowing correct responses (M = 577 ms) and this normative
effect was quite robust across participants, F (1, 127) =
793.19, P\.01. This normative pattern establishes robust
tendencies toward error regulation in the task.
To compute an error-regulation score for each individ-
ual, we subtracted post-correct (log) RT from post-error
(log) RT, with higher scores indicating greater behavioral
compensation for errors (M = 304 ms; SD = 208 ms).
This (error minus correct) difference score was correlated
with average speed in the task, r = .57, P\.01. In the
cognitive literature, such correlations are common, but
potentially related to individual differences in speed rather
than to individual differences in cognitive control (i.e.,
those who are slower in speed tend to have larger differ-
ence scores: Faust et al. 1999). We therefore computed a
residual error-regulation measure by statistically removing
the variance common to average speed and the error
minus correct difference score. The residual measure is
Cogn Ther Res (2009) 33:356367 359
1 3
necessarily uncorrelated with average speed in the task.
High residual scores reect a greater post-error adjustment
in RT or, in other words, greater levels of cognitive control
according to this neurocognitive model (Rabbitt 1966;
Robinson 2007b).
Correlations Among Variables and the Mediation
Model
We introduced main effect, mediation, and moderation
models in the introduction. According to the mediation
model, impulsivity should predict bulimic symptoms pri-
marily because impulsive individuals are decient in cog-
nitive control. As a rst test of this model, we examined
correlations among the variables and report them in
Table 1. As shown in the table, impulsivity did not predict
either of the cognitive control variables, whether pertaining
to Stroop interference scores or to post-error adjustments in
RT. Because signicant correlations between an indepen-
dent variable (here, impulsivity) and a potential mediator
(here, cognitive control) are a necessary precondition for
statistical mediation (Baron and Kenny 1986), there is no
need for further analyses here. Rather, the mediation model
was not supported.
As shown in Table 1, impulsivity predicted bulimic
symptoms, but such relations were not large. On the basis
of these ndings, it appears that narrow impulsivity is a risk
factor for bulimic symptoms, but not one invariably asso-
ciated with such symptoms. Also shown in the table, the
cognitive control variables did not predict bulimic symp-
toms in a zero-order manner. Further, the two cognitive
control measures were correlated in a manner to suggest a
relation between them, but there was only a trend along
such lines, P\.10. Such ndings will be interpreted more
extensively in the General Discussion. For now, we suggest
that the relative independence of the two cognitive control
measures offers an opportunity for conceptual replication
in relation to the moderation model, which in fact was the
one that we thought would be most likely supported by our
data.
Main Effect and Moderation Models
The main effect model posits that impulsivity will predict
bulimic symptoms regardless of levels of cognitive control.
The moderation model hypothesizes that impulsivity and
cognitive control will interact to predict bulimic symptoms.
To contrast these two models, we performed multiple
regressions. In these regressions, the two residual measures
of cognitive control were z-scored, as were individual
differences in impulsivity. We then computed interaction
terms to reect potential interactive relations between
impulsivity and the two cognitive control variables (Aiken
and West 1991). We performed four multiple regressions.
In one, impulsivity, Stroop interference scores, and their
interaction were entered as simultaneous predictors of
BULIT-R symptoms. In a second multiple regression, the
same predictor variables were entered as predictors of EDI-
2 bulimia symptoms. Two further multiple regressions
involved potential interactions of impulsivity and error
regulation scores in relation to the same dependent
measures.
The Stroop Effect and BULIT-R Symptoms
A rst multiple regression focused on whether the magni-
tude of the Stroop effect would interact with Impulsivity to
predict BULIT-R symptoms. In this regression, there was a
main effect for Impulsivity, t = 3.56, P\.01, b = .30, no
main effect for Stroop Interference, t = .17, P[.85,
b = .01, and a signicant Impulsivity 9 Stroop Interfer-
ence interaction, t = 2.31, P\.05, b = .20, F (3, 127) =
6.05, P\.01, R
2
= .13, for the full model. Estimated
means for the interaction were calculated by estimating
BULIT-R symptom scores for those low (-1 SD) and high
(?1 SD) in each of the predictor variables. As shown in the
top panel of Fig. 1, the highest BULIT-R symptoms were
observed among those high in impulsivity and high in
Stroop interference.
Follow-up simple slopes analyses were performed for
individuals low (-1 SD) versus high (?1 SD) in their
Stroop Interference scores (Aiken and West 1991). As
suggested by the gure, Impulsivity was a predictor of
BULIT-R symptoms among those exhibiting high levels of
Stroop interference, t = 4.07, P\.01, b = .53, but not
among those exhibiting low levels of Stroop interference,
t = .49, P[.60, b = .06. This moderation-related result
indicates that higher levels of cognitive control (here, in the
form of lower Stroop interference scores) dissociated
relations between trait impulsivity and bulimic symptoms.
These data also rule out the main effect model as impul-
sivity/symptom relations were particular to those low in
cognitive control. Such effects were conceptually repli-
cated in the other multiple regressions as well.
Table 1 Correlations among variables
Stroop ErrReg EDI BULIT
Imp .08 .04 .17* .27*
Stroop -.16 -.08 -.01
ErrReg .03 .01
EDI - .82*
Note: Imp = narrow impulsivity; Stroop = Stroop interference
scores; ErrReg = error regulation scores; EDI = EDI-2 bulimia
symptoms; BULIT = BULIT-R symptoms
* P\.05
360 Cogn Ther Res (2009) 33:356367
1 3
The Stroop Effect and EDI-2 Bulimic Symptoms
In the prediction of EDI-2 bulimic symptoms, a parallel set
of ndings emerged. There was a main effect for Impul-
sivity, t = 2.45, P\.05, b = .21, no main effect for
Stroop Interference, t = -.56, P[.55, b = -.05, and a
signicant interaction among these predictors, t = 2.22,
P\.05, b = .19, F (3, 127) = 3.97, P\.01, R
2
= .09,
for the full model. Estimated means, graphed in the bottom
panel of Fig. 1, again indicate that impulsivity appeared to
be a predictor of bulimic symptoms exclusively among
individuals low in cognitive control. Simple slopes analy-
ses conrmed this view as Impulsivity predicted EDI-2
symptoms among individuals high in Stroop Interference,
t = 3.29, P\.01, b = .44, but not among those low in
Stroop Interference, t = -.15, P[.85, b = -.02.
Error Regulation and BULIT-R Symptoms
Recall that we also assessed cognitive control in terms of
post-error adjustments in RT, which were not signicantly
correlated with Stroop interference scores. In the prediction
of BULIT-R symptoms, the multiple regression revealed
that there was a main effect for Impulsivity, t = 3.34,
P\.01, b = .28, no main effect for Error-Regulation,
t = -.74, P[.45, b = -.06, and a signicant interaction
among these variables, t = -3.08, P\.01, b = -.26,
F (3, 127) = 7.29, P\.01, R
2
= .15, for the full model.
Estimated means for the interaction are displayed in the top
panel of Fig. 2. As shown there, the highest levels of
bulimic symptoms were observed among individuals high
in impulsivity and low in error regulation. Indeed, Impul-
sivity predicted BULIT-R symptoms among those exhib-
iting low levels of error regulation, t = 4.66, P\.01,
b = .56, but did not predict BULIT-R symptoms among
1.3
1.5
1.7
1.9
2.1
Low Stroop Interference
B
U
L
I
T
-
R

S
y
m
p
t
o
m

S
c
o
r
e
s
Low Impulsivity
High Impulsivity
1.4
1.6
1.8
2
2.2
2.4
E
D
I
-
2

B
u
l
i
m
i
a

S
y
m
p
t
o
m
s
Low Impulsivity
High Impulsivity
High Stroop Interference
Low Stroop Interference High Stroop Interference
Fig. 1 Interactions of trait impulsivity and Stroop interference scores
in predicting bulimia symptoms, BULIT-R scores (Top Panel) and
EDI-2 bulimia symptom scores (Bottom Panel)
1.3
1.5
1.7
1.9
2.1
Low Error Regulation
B
U
L
I
T
-
R

S
y
m
p
t
o
m

S
c
o
r
e
s
Low Impulsivity
High Impulsivity
Low Impulsivity
High Impulsivity
1.4
1.6
1.8
2
2.2
2.4
E
D
I
-
2

B
u
l
i
m
i
a

S
y
m
p
t
o
m
s
High Error Regulation
Low Error Regulation High Error Regulation
Fig. 2 Interactions of trait impulsivity and error regulation scores in
predicting bulimia symptoms, BULIT-R scores (Top Panel) and EDI-
2 bulimia symptom scores (Bottom Panel)
Cogn Ther Res (2009) 33:356367 361
1 3
those exhibiting high levels of error regulation, t = -.01,
P[.95, b = .00. Such interactive ndings converge with
those presented above.
Error Regulation and EDI-2 Bulimic Symptoms
In the prediction of EDI-2 bulimic symptoms, there was a
main effect for Impulsivity, t = 2.16, P\.05, b = .18, no
main effect for Error-Regulation, t = -.57, P[.55,
b = -.05, and a signicant interaction among these pre-
dictors, t = -3.22, P\.01, b = -.28, F (3, 127) = 5.33,
P\.01, R
2
= .11, for the full model. Estimated means for
the interaction are reported in the bottom panel of Fig. 2.
Simple slopes analyses replicated those reported above in
that impulsivity was a predictor of bulimic symptoms
among those low in Error-Regulation, t = 3.95, P\.01,
b = .48, but not among those high in Error-Regulation,
t = -.89, P[.35, b = -.11. Again, then, it appears that
narrow impulsivity is a risk factor for bulimic symptoms
particularly (and indeed exclusively) among those low in
cognitive control.
Potential Sex Differences
Women are more vulnerable to eating disorders in general
terms (American Psychiatric Association 2000). In the
present study, however, sex (1 = male; 2 = female) was a
very modest predictor of bulimic symptoms, r = .19,
P\.05 for EDI-2 bulimia symptoms and r = .14, P[.10
for BULIT-R symptoms. It is also important to note that
sex was not correlated with impulsivity, r = -.12,
P[.15, nor with the cognitive control measures,
|rs| \.10, ps [.40. Thus, these zero-order correlations
suggest that potential sex differences are likely to be
somewhat unimportant in relation to our ndings.
Yet, it is possible that the interactive results reported
above could vary by sex of participant. To examine this
possibility, we re-ran the multiple regressions reported
above with sex as an additional factor. Of particular
interest is whether Participant Sex moderated the Impul-
sivity 9 Cognitive Control interactions reported above,
which would result in a three-way interaction. There were
no three-way interactions of this type, |ts| \.90, ps [.35,
|bs| \.10. Thus, the present interactive ndings are equally
characteristic of women and men.
Simple Slopes by Trait Impulsivity
In all gures, estimated means suggest that higher levels of
cognitive control were associated with fewer bulimic
symptoms among individuals high in trait impulsivity, as
hypothesized. That is, impulsive individuals appear to
benet from higher levels of cognitive control in the form
of reduced symptoms. On the other hand, the estimated
means also suggest that higher levels of cognitive control
are associated with higher symptomology among individ-
uals low in trait impulsivity.
To statistically assess such trends, we performed simple
slopes analyses in which the predictive effects of cognitive
control were examined separately for those low (-1 SD)
versus high (?1 SD) in trait impulsivity. The results of
these analyses were less robust than those reported above.
However, a general pattern was evident. Consider, in this
connection, the simple slopes particular to the last inter-
action reported, in which impulsivity and error regulation
tendencies interacted to predict EDI-2 symptoms. In this
set of simple slopes analyses, we found that higher levels of
Error-Regulation were associated with lower levels of
bulimic symptoms among those high in Impulsivity, t =
-2.45, P\.05, b = -.35, but were associated with higher
levels of bulimic symptoms among those low in Impul-
sivity, 2.24, P\.05, b = .25. Thus, the predictive value of
cognitive control was drastically different depending on
whether individuals were low or high in impulsivity.
Clearly, such results reinforce the moderation model pre-
sented above, while raising additional questions worthy of
discussion.
Discussion
Summary of Findings
We sought to better understand relations between trait
impulsivity and bulimic symptoms. We contrasted three
models in understanding this relationship. The main effect
model posited that impulsivity would predict bulimic
symptoms irrespective of levels of cognitive control. This
model was undermined by systematic interactions between
impulsivity and cognitive control. The mediation model
posited that relations between impulsivity and bulimic
symptoms would be due to, or in other words mediated by,
links of higher levels of impulsivity to lower levels of
cognitive control. This model was undermined by the fact
that trait impulsivity did not predict cognitive control
performance.
The third moderation model predicted that higher levels
of cognitive control would be associated with weaker
relations between impulsivity and bulimic symptoms. This
moderation model was supported by our ndings. Speci-
cally, relations between impulsivity and bulimic symptoms
were especially strong at low levels of cognitive control.
By contrast, we found that relations between impulsivity
and bulimic symptoms were absent at high levels of cog-
nitive control. Such results support previous data in
developmental (e.g., Eisenberg et al. 2000) and personality
362 Cogn Ther Res (2009) 33:356367
1 3
(e.g., Robinson 2007a) literatures, but do so in a manner
that begins to support the clinical signicance of this
moderation-related framework.
Toward an Understanding of Impulsivity as a Risk
Factor
Results have documented, time and time again, the pre-
dictive value of trait impulsivity in understanding disin-
hibited behaviors of major interest to both personality and
clinical psychologists (Baumeister et al. 1994). However,
the reason for such relations is not entirely clear. The
present data, we suggest, are important to understanding
such systematic relations. On the basis of our data, we do
not believe that decits in cognitive control are the primary
reason that some individuals are more impulsive than
others. Instead, we side with the child development liter-
ature in suggesting that temperamental impulsivity is a risk
factor for disinhibited behavior, but need not result in such
behavior given sufcient cognitive control (Gerardi-Caul-
ton 2000; Kochanska et al. 2000; Rothbart et al. 2000).
If this analysis is sound in general terms, it could also be
the case that other behaviors linked to high levels of
impulsivity, such as criminal behavior (Eysenck and Ey-
senck 1985) or behaviors reective of borderline person-
ality disorder (Linehan 1993), might similarly be
moderated by higher levels of cognitive control. In support
of this point, effective treatments for impulsivity-linked
disorders typically seek to train impulsive individuals to
control their impulsive habits (Moeller and Dougherty
2002; Robins et al. 2004). Further clinical implications will
be discussed below. For now, the point is that relations
between impulsivity and outcome variables can be miti-
gated through the use of cognitive control resources.
Toward an Understanding of Cognitive Control
Two aspects of the cognitive control ndings deserve fur-
ther comment. A rst result was that there was only a trend
toward a relation between Stroop interference scores and
post-error adjustments in RT. Such data are important in
part because there are in fact two major neurocognitive
models of control. One model emphasizes the ability to
override cognitive conicts (such as an incongruent Stroop
trial) prior to making a response (Carter et al. 1998). The
other model emphasizes post-error adjustments designed to
minimize error likelihood in the future (Holroyd and Coles
2002).
At the present time, it is clear that both forms of cog-
nitive control are likely to draw upon similar neural regions
including the anterior cingulate and lateral prefrontal cor-
tex (van Veen and Carter 2002). Yet, the present data also
make it clear that these two assessments of cognitive
control cannot be equated with each other in psychometric
terms. From a correlational perspective, that is, there is not
a strong relation between these two forms of cognitive
control. These data reinforce other suggestions that various
measures of cognitive control appear to tap different,
though often related, individual difference constructs
(Friedman and Miyake 2004). Irrespective of such con-
siderations, though, we were able to provide replication
across both cognitive control measures, thus strengthening
condence in the moderation model that guided our
predictions.
An important feature of our interactive ndings was that
cognitive control had very different associations with
bulimic symptoms at low versus high levels of impulsivity.
These results make sense from a neurocognitive perspec-
tive, in that reliance on automatic versus controlled modes
of processing are not independent, as held by many social
cognitive models (Lieberman 2003), but rather trade off in
their inuence (McClure et al. 2007; Zelazo and Cunn-
ingham 2007). Those who perform processing in a more
controlled manner, as would be true of individuals higher
in cognitive control in the present studies, would be less
inuenced by their temperamental tendencies, whether
functional (i.e., low impulsivity) or dysfunctional (i.e., high
impulsivity).
From this automatic/controlled trade off perspective, a
greater reliance on cognitive control equalizes individuals,
regardless of the benecial or costly nature of their tem-
peramental predispositions. Findings of this type have been
reported in relation to the neuroticism/distress relationship
(for reviews, see Robinson 2007a; Robinson and Compton
2007). Thus, the present ndings add to an important
perspective on individual differences in cognitive control.
Cognitive control is desirable particularly if ones tem-
perament predisposes one to emotional and behavioral
problems. By contrast, if ones temperament is well
adjusted, a more automatic mode of responding may often
be more benecial. Regardless, cognitive control does
appear functional among vulnerable individuals and we
discuss such implications next.
Toward the Clinical Relevance of Individual
Differences in Cognitive Control
We collected data from a non-clinical sample and it is
uncertain whether our moderation model would be sup-
ported among those suffering from clinically signicant
bulimic symptoms. We believe that the answer is yes, but
important qualications must be offered. First, impulsivity
is a predictor of bulimic symptoms (Claes et al. 2006; Lyke
and Spinella 2004), but it is also thought that that there are
subgroups of bulimia nervosa patients, some of who are
compulsive rather than impulsive (Engel et al. 2005). Our
Cogn Ther Res (2009) 33:356367 363
1 3
cognitive control model has specic relevance to under-
standing impulsivity-driven symptoms, but is unlikely to
account for other pathways toward bulimia nervosa.
Second, it may seem puzzling that we found no relation
between impulsivity and cognitive control because prior
studies have implicated cognitive control decits in com-
parisons of patient and control groups in relation to drug
abuse (Bolla et al. 2004), borderline personality disorder
(de Bruijn et al. 2006), and criminal levels of psychopathy
(Davidson et al. 2000). From the present view, such
extremes in behavior are likely to be particular to indi-
viduals high in impulsivity and low in cognitive control,
much as we found that the highest levels of bulimic
symptoms were particular to this interactive combination
of variables. For this reason, those meeting diagnostic
criteria are likely to suffer from dual decits and it is
therefore not surprising that designs contrasting patient and
control groups have led to the conclusion that patient
groups have decient levels of cognitive control. Regard-
less, we are in agreement with prior suggestions that de-
cient levels of cognitive control are likely to exacerbate
impulsivity-linked tendencies. Thus, we also suggest that
treatments designed to facilitate cognitive control are likely
to be particularly useful among patient populations exhib-
iting impulsive symptoms.
In short, there are two concrete ways in which the
present analysis may be of use in understanding clinically
signicant symptoms of an impulsive nature. First, the
assessment of cognitive control seems promising in deter-
mining the extent to which vulnerable individuals are likely
to display symptoms of clinical signicance. Second, these
results have treatment implications because if cognitive
control can be systematically targeted and improved, vul-
nerable individuals might learn to systematically control
their temperament-linked tendencies in a manner support-
ing more effective functioning. Cognitive control can be
systematically trained, unlike trait impulsivity, and thus
training of this type is likely to be benecial among trait-
vulnerable individuals (Robinson 2007c).
Limitations and Future Directions
Our sample was very predominantly Caucasian and it thus
is somewhat uncertain whether similar ndings would
occur among other ethnic groups or cultures. Mitigating
this concern somewhat is our focus on very basic neuro-
cognitive processes that are likely to operate in a similar
manner cross-culturally (MacLeod 1991; van Veen and
Carter 2002). From the perspective of the present ndings,
though, this is uncertain. The cross-sectional nature of the
study must also be mentioned. There are data suggesting
that impulsive tendencies precede the development of
bulimic symptoms (e.g., Wonderlich et al. 2004), but there
are also at least a few sources of data to suggest that suc-
cessful treatment for bulimia nervosa can lead to reduced
levels of more general forms of impulsivity (e.g., Kennedy
et al. 1990). Although we regard it likely that impulsivity
and cognitive control would interact to predict bulimic
symptoms in a prospective fashion, longitudinal designs
are necessary to substantiate this point.
We chose to assess trait impulsivity in terms of the
narrow impulsivity scale of Eysenck and Eysenck (1977).
What attracted us to this scale was the focus on core
behavioral issues in impulsivity independent of the non-
planning or risk-taking components of this trait. However,
impulsivity can certainly be assessed in other ways (e.g.,
Zuckerman et al. 1988). Particularly helpful here is the
psychometric analysis of Whiteside and Lynam (2001),
which resulted in the suggestion that there are at least four
components of impulsivity labeled urgency, (lack of) pre-
meditation (here, non-planning), (lack of) perseverance,
and sensation seeking. Although moderately correlated,
these different components of impulsivity are likely to
predict different behavioral outcomes (Whitehead and
Lynam).
Using scales recommended by Whiteside and Lynam
(2001), Fischer and colleagues (2003a, b) found that buli-
mic symptoms were predicted by urgency impulsivity, but
not by non-planning impulsivity, a result that has since
been conceptually replicated (Anestis et al. 2007). How-
ever, the analysis of Whiteside and Lynam did not include
the narrow impulsivity scale assessed here, but rather a
subsequent scale of impulsivity developed by Eysenck and
colleagues (1985). This appears to be an important dis-
tinction because the narrow impulsivity scale of Eysenck
and Eysenck (1977) was shown to be psychometrically
distinct from non-planning tendencies, but this is not true
of the subsequent 1985 scale (Whitehead and Lynam). In
fact, we suggest that the 1977 scale that we used captures at
least certain components of urgency impulsivity, for
example in relation to the item Do you hate standing in a
long line for anything? This item, as others included,
would seem to tap behavioral tendencies motivated by
intolerance of negative emotional states, more or less the
denition of urgency impulsivity.
This said, we acknowledge that it would be of great
value to replicate our interactive pattern in relation to
impulsivity-linked traits, particularly urgency impulsivity,
that have been shown to be more closely associated with
bulimic symptoms (Fischer et al. 2003a, b). We believe
that individual differences in cognitive control would be
effective in this context as well because data have
increasingly highlighted an inverse relation between cog-
nitive control and biases induced by negative emotional
states or stimuli (Mischel and Ayduk 2004; Ochsner and
Gross 2005; Zelazo and Cunningham 2007). However,
364 Cogn Ther Res (2009) 33:356367
1 3
because we did not administer a psychometrically pure
measure of urgency impulsivity in our study, future
research would be necessary to conrm this interactive
prediction.
Conclusions
We sought to examine the potential role that individual
differences in cognitive control might play in understand-
ing relations between impulsivity and bulimic symptoms.
Cognitive control was measured in objective cognitive-
behavioral terms and it was found that higher levels of
cognitive control were associated with non-signicant
relations between trait impulsivity and bulimic symptoms.
This was true across two measures of cognitive control and
two measures of bulimic symptoms. On the basis of this
data, we suggest that impulsivity cannot be equated with
cognitive control, but that cognitive control is likely to play
an important moderating role in understanding impulsivity-
linked outcomes.
Acknowledgment The authors acknowledge support from MH
59674 (Wonderlich & Engel).
References
Aiken, L. S., & West, S. G. (1991). Multiple regression: Testing and
interpreting interactions. Thousand Oaks, CA: Sage
Publications.
American Psychiatric Association. (2000). Diagnostic and statistical
manual of mental disorders (4th ed., text revision). Washington,
DC: Author.
Anestis, M. D., Selby, E. A., & Joiner, T. E. (2007). The role of
urgency in maladaptive behaviors. Behaviour Research and
Therapy, 45, 30183029.
Baneld, J. F., Wyland, C. L., Macrae, C. N., Munte, T. F., &
Heatherton, T. F. (2004). The cognitive neuroscience of self-
regulation. In R. F. Baumeister & K. D. Vohs (Eds.), Handbook
of self-regulation: Research, theory, and applications (pp. 62
83). New York: Guilford Press.
Baron, R. M., & Kenny, D. A. (1986). The moderatormediator
variable distinction in social psychological research: Conceptual,
strategic, and statistical considerations. Journal of Personality
and Social Psychology, 51, 11731182.
Baumeister, R. F., Heatherton, T. F., & Tice, D. M. (1994). Losing
control: How and why people fail at self-regulation. San Diego,
CA: Academic Press.
Bolla, K., Ernst, M., Kiehl, K., Mouratidis, M., Eldreth, D.,
Contoreggi, C., et al. (2004). Prefrontal cortical dysfunction in
abstinent cocaine abusers. Journal of Neuropsychiatry and
Clinical Neurosciences, 16, 456464.
Carter, C. S., Braver, T. S., Barch, D. M., Botvinick, M. M., Noll, D.,
& Cohen, J. D. (1998). Anterior cingulate cortex, error detection,
and the online monitoring of performance. Science, 280, 747
749.
Casillas, A., & Clark, L. A. (2002). Dependency, impulsivity, and
self-harm: Traits hypothesized to underlie the association
between cluster B personality and substance use disorders.
Journal of Personality Disorders, 16, 424436.
Chaiken, S., & Trope, Y. (1999). Dual-process theories in social
psychology. New York: Guilford Press.
Claes, L., Nederkoorn, C., Vandereycken, W., Guerrieri, R., &
Vertommen, H. (2006). Impulsiveness and lack of inhibitory
control in eating disorders. Eating Behaviors, 7, 196203.
Davidson, R. J., Putnam, K. M., & Larson, C. L. (2000). Dysfunction
in the neural circuitry of emotion regulationa possible prelude
to violence. Science, 289, 591594.
de Bruijn, E. R. A., Grootens, K. P., Verkes, R. J., Buchholz, V.,
Hummelen, J. W., & Hulstijn, W. (2006). Neural correlates of
impulse responding in borderline personality disorder: ERP
evidence for reduced action monitoring. Journal of Psychiatric
Research, 40, 428437.
de Zwaan, M., Mitchell, J., Seim, H., Specker, S., Pyle, R., Raymond,
N., et al. (1994). Eating related and general psychopathology in
obese females with binge-eating disorder. International Journal
of Eating Disorders, 15, 4352.
Eisenberg, N., Fabes, R. A., Guthrie, I. K., & Reiser, M. (2000).
Dispositional emotionality and regulation: Their role in predict-
ing quality of social functioning. Journal of Personality and
Social Psychology, 78, 136157.
Engel, S. G., Corneliussen, S. J., Wonderich, S. A., Crosby, R. D., le
Grange, D., Crow, S., et al. (2005). Impulsivity and compulsivity
in bulimia nervosa. International Journal of Eating Disorders,
38, 244251.
Eysenck, S. B. G., & Eysenck, H. J. (1977). The place of
impulsiveness in a dimensional system of personality descrip-
tion. British Journal of Social and Clinical Psychology, 16, 57
68.
Eysenck, H. J., & Eysenck, M. W. (1985). Personality and individual
differences: A natural science approach. New York: Plenum.
Eysenck, S. B., Pearson, P. R., Easting, G., & Allsopp, J. F. (1985).
Age norms for impulsiveness, venturesomeness and empathy in
adults. Personality and Individual Differences, 6, 613619.
Faust, M. E., Balota, D. A., Spieler, D. H., & Ferraro, F. R. (1999).
Individual differences in information processing rate and
amount: Implications for group differences in response latency.
Psychological Bulletin, 125, 777799.
Fischer, S., Smith, G. T., & Anderson, K. G. (2003a). Clarifying the
role of impulsivity in bulimia nervosa. International Journal of
Eating Disorders, 33, 406411.
Fischer, S., Smith, G. T., Anderson, K. G., & Flory, K. (2003b).
Expectancy inuences the operation of personality on behavior.
Psychology of Addictive Behaviors, 17, 108114.
Fowles, D. C. (2001). Biological variables in psychopathology: A
psychobiological perspective. In P. B. Sutker & H. E. Adams
(Eds.), Comprehensive handbook of psychopathology (3rd ed.,
pp. 85104). New York: Plenum.
Friedman, N. P., & Miyake, A. (2004). The relations among inhibition
and interference control functions: A latent-variable analysis.
Journal of Experimental Psychology: General, 133, 101135.
Garner, D. M. (1991). The Eating Disorders Inventory-2 professional
manual. Odessa, FL: Psychological Assessment Resources.
Gerardi-Caulton, G. (2000). Sensitivity to spatial conict and the
development of self-regulation in children 2436 months of age.
Developmental Science, 3, 397404.
Gray, J. A. (1987). The neuropsychology of emotion and personality.
In S. M. Stahl, S. D. Iverson, & E. C. Goodman (Eds.), Cognitive
neurochemistry (pp. 171190). New York: Oxford University
Press.
Holroyd, C. B., & Coles, M. G. H. (2002). The neural basis of human
error processing: Reinforcement learning, dopamine, and the
error-related negativity. Psychological Review, 109, 679709.
Cogn Ther Res (2009) 33:356367 365
1 3
Kagan, J., & Snidman, N. (1991). Temperamental factors in human
development. American Psychologist, 46, 856862.
Keel, P. K., & Mitchell, J. E. (1997). Outcome in bulimia nervosa.
American Journal of Psychiatry, 154, 313321.
Kennedy, S. H., McVey, G., & Katz, R. (1990). Personality disorders
in anorexia nervosa and bulimia nervosa. Journal of Psychiatric
Research, 24, 259269.
Kerns, J. G., Cohen, J. D., MacDonald, A. W., III, Cho, R. Y.,
Stenger, V. A., & Carter, C. S. (2004). Anterior cingulate conict
monitoring and adjustments in control. Science, 303, 10231026.
Kochanska, G., Murray, K. T., & Harlan, E. T. (2000). Effortful
control in early childhood: Continuity and change, antecedents,
and implications for social development. Developmental Psy-
chology, 36, 220232.
Lieberman, M. D. (2003). Reexive and reective judgment
processes: A social cognitive neuroscience approach. In J. P.
Forgas, K. D. Williams, & W. von Hippel (Eds.), Social
judgments: Implicit and explicit processes (pp. 4467). New
York: Cambridge University Press.
Linehan, M. M. (1993). Cognitive-behavioral treatment of borderline
personality disorder. New York: Guilford Press.
Luria, A. R. (1969). The higher cortical functions in man and their
disturbance in local lesions of the brain (2nd ed.). Oxford,
England: Moscow University.
Lyke, J. A., & Spinella, M. (2004). Associations among aspects of
impulsivity and eating factors in a nonclinical sample. Interna-
tional Journal of Eating Disorders, 36, 229233.
MacLeod, C. M. (1991). Half a century of research on the Stroop
effect: An integrative review. Psychological Bulletin, 109, 163
203.
McClure, S. M., Botvinick, M. M., Yeung, N., Greene, J. D., &
Cohen, J. D. (2007). Conict monitoring in cognitionemotion
competition. In J. J. Gross (Ed.), Handbook of emotion
regulation (pp. 204226). New York: Guilford Press.
Metcalfe, J., & Mischel, W. (1999). A hot/cool-system analysis of
delay of gratication: Dynamics of willpower. Psychological
Review, 106, 319.
Mischel, W., & Ayduk, O. (2004). Willpower in a cognitive-affective
processing system: The dynamics of delay of gratication. In R.
F. Baumeister & K. D. Vohs (Eds.), Handbook of self-
regulation: Research, theory, and applications (pp. 99129).
New York: Guilford Press.
Moeller, F. G., & Dougherty, D. M. (2002). Impulsivity and substance
abuse: What is the connection? Addictive Disorders and Their
Treatment, 1, 310.
Morgan, A. B., & Lilienfeld, S. O. (2000). A meta-analytic review of
the relation between antisocial behavior and neuropsychological
measures of executive function. Clinical Psychology Review, 20,
113156.
Nigg, J. T. (2000). On inhibition/disinhibition in developmental
psychopathology: Views from cognitive and personality psy-
chology and a working inhibition taxonomy. Psychological
Bulletin, 126, 220246.
Nigg, J. T. (2006). Temperament and developmental psychopathol-
ogy. Journal of Child Psychology and Psychiatry, 47, 395422.
Ochsner, K. N., & Gross, J. J. (2005). The cognitive control of
emotion. Trends in Cognitive Sciences, 9, 242249.
Patterson, C. M., & Newman, J. P. (1993). Reectivity and learning
from aversive events: Toward a psychological mechanism for
the syndromes of disinhibition. Psychological Review, 100, 716
736.
Pickering, A. D., Corr, P. J., & Gray, J. A. (1999). Interactions and
reinforcement sensitivity theory: A theoretical analysis of
Rusting and Larsen (1997). Personality and Individual Differ-
ences, 26, 357365.
Pike, K. M., Wolk, S. L., Gluck, M., & Walsh, B. T. (2000). Eating
disorder measures. In American Psychiatric Association (Eds.),
Handbook of psychiatric measures (pp. 647671). Washington,
DC: American Psychiatric Association.
Rabbitt, P. M. (1966). Errors and error correction in choice-response
tasks. Journal of Experimental Psychology, 71, 264272.
Robins, C. J., Schmidt, H., III, & Linehan, M. M. (2004). Dialectical
behavior therapy: Synthesizing radical acceptance with skillful
means. In S. C. Hayes, V. M. Follette, & M. M. Linehan (Eds.),
Mindfulness and acceptance: Expanding the cognitive-behav-
ioral tradition (pp. 3044). New York: Guilford Press.
Robinson, M. D. (2007a). Personality, affective processing, and self-
regulation: Toward process-based views of extraversion, neu-
roticism, and agreeableness. Social and Personality Psychology
Compass, 1, 223235.
Robinson, M. D. (2007b). Gassing, braking, and self-regulating: Error
self-regulation, well-being, and goal-related processes. Journal
of Experimental Social Psychology, 43, 116.
Robinson, M. D. (2007c). Lives lived in milliseconds: Using
cognitive methods in personality research. In R. W. Robbins,
R. C. Fraley, & R. Krueger (Eds.), Handbook of research
methods in personality psychology (pp. 345359). New York:
Guilford Press.
Robinson, M. D., & Compton, R. J. (2007). The happy mind in action:
The cognitive basis of subjective well-being. In M. Eid & R. J.
Larsen (Eds.), The science of subjective well-being (pp. 220
238). New York: Guilford Press.
Robinson, M. D., Goetz, M. C., Wilkowski, B. M., & Hoffman, S. J.
(2006a). Driven to tears or to joy: Response dominance and trait-
based predictions. Personality and Social Psychology Bulletin,
32, 629640.
Robinson, M. D., & Neighbors, C. (2006). Catching the mind in
action: Implicit methods in personality research and assessment.
In M. Eid & E. Diener (Eds.), Handbook of multimethod
measurement in psychology (pp. 115125). Washington, DC:
American Psychological Association.
Robinson, M. D., Ode, S., Wilkowski, B. M., & Amodio, D. M.
(2007). Neurotic contentment: A self-regulation view of neurot-
icism-linked distress. Emotion, 7, 579591.
Robinson, M. D., Wilkowski, B. M., Kirkeby, B. S., & Meier, B. P.
(2006b). Stuck in a rut: Perseverative response tendencies and
the neuroticismdistress relationship. Journal of Experimental
Psychology: General, 135, 7891.
Rothbart, M. K., Ahadi, S. A., & Evans, D. E. (2000). Temperament
and personality: Origins and outcomes. Journal of Personality
and Social Psychology, 78, 122135.
Rothbart, M. K., Ellis, L. K., & Posner, M. I. (2004). Temperament
and self-regulation. In R. F. Baumeister & K. D. Vohs (Eds.),
Handbook of self-regulation: Research, theory, and applications
(pp. 359370). New York: Guilford Press.
Rueda, M. R., Posner, M. I., & Rothbart, M. K. (2004). Attentional
control and self-regulation. In R. F. Baumeister & K. D. Vohs
(Eds.), Handbook of self-regulation: Research, theory, and
applications (pp. 283300). New York: Guilford Press.
Schneider, W., & Shiffrin, R. M. (1977). Controlled and automatic
human information processing: I. Detection, search, and atten-
tion. Psychological Review, 84, 166.
Smith, M. C., & Thelen, M. H. (1984). Development and validation of
a test for bulimia. Journal of Consulting and Clinical Psychol-
ogy, 52, 863872.
Stein, D., Lilenfeld, L. R. R., Wildman, P. C., & Marcus, M. D.
(2004). Attempted suicide and self-injury in patients diagnosed
with eating disorders. Comprehensive Psychiatry, 45, 447451.
Thelen, M. H., Farmer, J., Wonderlich, S., & Smith, M. (1991). A
revision of the Bulimia Test: The BULIT-R. Psychological
366 Cogn Ther Res (2009) 33:356367
1 3
Assessment: A Journal of the Consulting and Clinical Psychol-
ogy, 3, 119124.
Troyer, A. K., Leach, L., & Strauss, E. (2006). Aging and response
inhibition: Normative data for the Victoria Stroop test. Aging,
Neuropsychology, and Cognition, 13, 2035.
van Veen, V., & Carter, C. S. (2002). The timing of action-monitoring
processes in the anterior cingulate cortex. Journal of Cognitive
Neuroscience, 14, 593602.
Whiteside, S. P., & Lynam, D. R. (2001). The Five Factor Model and
impulsivity: Using a structural model of personality to under-
stand impulsivity. Personality and Individual Differences, 30,
669689.
Wilkowski, B. M., & Robinson, M. D. (2008). The cognitive basis of
trait anger and reactive aggression: An integrative analysis.
Personality and Social Psychology Review, 12, 321.
Wonderlich, S. A., Connolly, K. M., & Stice, E. (2004). Impulsivity
as a risk factor for eating disorder behavior: Assessment
implications with adolescents. International Journal of Eating
Disorders, 36, 172182.
Zelazo, P. D., & Cunningham, W. A. (2007). Executive function:
Mechanisms underlying emotion regulation. In J. J. Gross (Ed.),
Handbook of emotion regulation (pp. 135158). New York:
Guilford Press.
Zuckerman, M., Kuhlman, D. M., & Camac, C. (1988). What lies
beyond E and N?: Factor analyses of scales believed to measure
basic dimensions of personality. Journal of Personality and
Social Psychology, 54, 96107.
Cogn Ther Res (2009) 33:356367 367
1 3