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. 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