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Behavior Therapy 39 (2008) 65–71www.elsevier.com/locate/bt

An Investigation of the Relationship BetweenCognitive Reactivity and Rumination

Michelle L. Moulds, Eva Kandris, Alishia D. Williams, Tamara Lang, Carol Yap, Karolin HoffmeisterThe University of New South Wales, Sydney

Teasdale’s (Teasdale, J.D. (1988). Cognitive vulnerability topersistent depression. Cognition and Emotion, 2, 247–274)differential activation hypothesis refers to the ease withwhich maladaptive cognitive processes are triggered by milddysphoria as cognitive reactivity. Supporting this model isevidence of a differential association between sad mood anddysfunctional cognitions in formerly depressed and never-depressed individuals and the finding that cognitivereactivity predicts depression recurrence in remitted depres-sives. The Leiden Index of Depression Sensitivity–Revised(LEIDS-R; Van der Does, A.J.W., Williams, J.M.G. (2003).Leiden Index of Depression Sensitivity–Revised (LEIDS-R).Retrieved September 4, 2007, from http://www.dousa.nl/publications_depression.htm#LEIDS) is a recently devel-oped self-report measure that provides clinicians andresearchers with a time-efficient means by which to assesscognitive reactivity. This study investigated the relationshipbetween cognitive reactivity (indexed by the LEIDS-R) anddepressive rumination in a nonclinical sample (N=324). Aspredicted, partial correlations between the LEIDS-R (sub-scale and Total scores) and the Ruminative Response Scale(RRS; Nolen-Hoeksema, S., and Morrow, J. (1991). Aprospective study of depression and posttraumatic stresssymptoms after a natural disaster: The 1989 Loma Prietaearthquake. Journal of Personality and Social Psychology,61, 115–121) were significant after controlling for currentdepressive symptoms. A subsample of participants (n=130)

This research was supported by a grant from the AustralianResearch Council awarded to the first author. We thank Dr. WillemVan der Does for kindly providing the Leiden Index of DepressionSensitivity and for his helpful correspondence regarding thismeasure.

Address correspondence to Michelle L. Moulds, School ofPsychology, The University of New South Wales, NSW 2052Australia; e-mail: m.moulds@unsw.edu.au.0005-7894/07/0065–0071$1.00/0© 2007 Association for Behavioral and Cognitive Therapies. Published byElsevier Ltd. All rights reserved.

was administered a structured interview to determinecurrent and past depression diagnostic status. Recovereddepressed individuals scored more highly on the LEIDS-RTotal and LEIDS-R Rumination subscale; however, thegroups did not differ on the remaining subscales. Regressionanalyses indicated that (across all participants) LEIDS-RTotal made a unique contribution to the prediction ofdepression over and above trait level of depressive rumina-tion. Overall, the LEIDS-R is a time-efficient self-reportindex of cognitive reactivity that demonstrates promise indistinguishing recovered and never-depressed individuals.

BIOLOGICAL, BEHAVIORAL, AND COGNITIVE MODELS

have been advanced to account for the processesand features that underpin vulnerability to the onsetand recurrence of depression. Teasdale’s (1988)differential activation hypothesis offers a cognitiveaccount of depression vulnerability. The centralpremise of this model is that the cognitive processesand content that are activated when an individualexperiences sad mood are the critical determinantsof whether the mood disturbance is transient or,alternatively, whether it persists and develops intoan episode of clinical depression. The degree towhich negative cognitive content and maladaptivepatterns of cognitive processing are triggered bymild dysphoric states is referred to as cognitivereactivity. Teasdale (1988) posits that mild ortransient dysphoria will persist and become clinicaldepression if “a vicious cycle based on thereciprocal relationship between the depressed stateand negative thinking” (Teasdale, 1988, p. 254) hasbeen established.Preliminary support for this model comes from

the finding that, whereas initial depressive episodesare typically precipitated by negative life events, therelationship between environmental stressors and

66 moulds et al .

depression progressively diminishes with recurrentepisodes (Kendler, Thornton, and Gardner, 2000).Cognitive theorists have proposed that cognitivereactivity can account for the onset of depression inthe absence of a precipitating event. That is,maladaptive cognitive processing becomes increas-ingly likely to be activated as more depressiveepisodes are experienced, and thus, over time,serves to trigger depressive relapse in the absenceof external stressors (Segal, Williams, & Teasdale,2002; Segal, Williams, Teasdale, & Gemar, 1996).More direct support for the differential activation

hypothesis has been provided by studies thatdemonstrate that although recovered depressedpatients and never-depressed controls do not differon self-report of dysfunctional cognitions (e.g., “If Ifail at my work, then I am a failure as a person”) inneutral mood, following a sad mood induction,recovered depressed patients report elevated levelsof such cognitions compared to controls (Miranda& Persons, 1988). This finding supports a differ-ential association between sad mood and dysfunc-tional cognitions for formerly depressed and never-depressed groups; however, its correlational natureprecludes interpretations about the causal role ofthis mood-cognition relationship in the mainte-nance of depression. An important validation ofTeasdale’s (1988) model was the observation thatthe degree of activation of dysfunctional beliefsfollowing a mood induction predicted depressiverelapse by formerly depressed patients at 30-monthfollow-up (Segal, Gemar, & Williams, 1999).The index of cognitive reactivity employed by

Segal et al. (1999) involved participants completingthe Dysfunctional Attitudes Scale (DAS; Weissman& Beck, 1978) prior to and following a sad moodinduction procedure. In this mood induction,participants listened to a piece of sad music whilerecalling a negative autobiographical memory. Thismethodology is recognized as the gold standardprocedure for indexing cognitive reactivity and hasbeen used in numerous studies. Nonetheless, theprocedure is time-consuming, and moreover, itinvolves either repeated administration of theDAS in one testing session or administration ofparallel forms of the DAS. The latter option isproblematic, given that the degree to which the twoforms are comparable has been questioned (Van derDoes, 2002a).In order to address these challenges, Van der

Does (2002a) developed the Leiden Index ofDepression Sensitivity (LEIDS) as an alternativeself-report and time-efficient tool with whichclinicians and researchers can measure cognitivereactivity, independent of the standard moodinduction procedure described above. Examples of

LEIDS items include: “When in a sad mood, Ibecome more bothered by perfectionism”and“-When I feel sad, I feel less able to cope witheveryday tasks and interests.” The original LEIDSwas a 52-item self-report measure. Initial investiga-tion of its psychometric properties indicated thatthe LEIDS was best described by four factorscomprised of 26 items (Negative Self-Evaluation,Acceptance/Coping, Indifference, and Risk Aver-sion) and that these factors possessed goodpsychometric properties (Van der Does, 2002a).Importantly, analyses confirmed that, as intended,the 26-item LEIDS predicted cognitive change (asmeasured by the DAS) in response to the standardmood induction procedure (see also Van der Does,2002b). By comparison, baseline depression andcognitive dysfunction did not predict cognitivechange. Van der Does therefore concluded that theLEIDS “is a promising measure of cognitivereactivity” (2002a, p.105). A more recent form ofthis measure, the LEIDS-R (Van der Does &Williams, 2003) contains 34 items on six subscales(Hopelessness/Suicidality, Acceptance/Coping,Aggression, Control/Perfectionism, Risk Aversion,and Rumination). This version of the LEIDS-R hasnow been used in a number of studies (e.g., Merenset al., 2005; Williams, Van der Does, Barnhofer,Crane, & Segal, in press), and Van der Doesrecommends use of this version (personal commu-nication, May 20, 2005).Despite the advantages of employing a validated

self-report instrument to index cognitive reactivity,to date the LEIDS-R has not been used widely.Moreover, it has not been extensively applied tocompare formerly and never-depressed individuals.In part one of the initial validation study, partici-pants were asked to indicate whether they hadexperienced a period of sad mood and/or anhedo-nia, and to clarify whether it lasted 2 or moreweeks. This question provided a probable index ofdepression history. Under this classification, theformerly depressed and never-depressed groupsdiffered as expected on all of the LEIDS subscales(Van der Does, 2002a). In the second part of thisstudy a structured clinical interview was adminis-tered to establish the presence of a history ofdepression. Eight of the 48 participants in this partof the study reported a previous depressive episode(Van der Does, 2002a). Accordingly, Van der Doeshighlighted the need for future research to employthe LEIDS to examine cognitive reactivity in thesetwo groups. To our knowledge, only two additionalstudies in the published literature (Merens et al.,2005; Van der Does, 2005) have comparedrecovered and never-depressed participants on theLEIDS. Van der Does (2005) reported higher LEIDS

67cogn i t i ve react i v i ty and ruminat ion

scores for recovered depressed compared to never-depressed participants. In addition, cognitive reac-tivity as indexed by the LEIDS was positivelycorrelated with self-reported thought suppressionand an experimental index of suppression, leadingto the conclusion that suppression may be linked tothe “apparent inactive state of depressive cogni-tions during remission” (p. 1). More broadly, therelationship between cognitive reactivity and othercognitive features of depression, such as depressiverumination, have not been explored.The response styles theory of depression (Just &

Alloy, 1997; Nolen-Hoeksema, 1991) contendsthat the duration and course of depression aredetermined by how one responds to depressivesymptoms. That is, individuals who respond to lowmood and associated symptoms by engaging inrumination about their causes and consequencesare more likely to remain depressed for longer.Prospective studies have confirmed the role ofrumination in the onset (Nolen-Hoeksema, Mor-row, & Fredrickson, 1993) and maintenance ofdepression (Nolen-Hoeksema, 2000). In addition,experimental manipulations of rumination in dys-phoric and clinically depressed samples havedemonstrated a number of deleterious outcomes,including poor problem solving (Lyubomirsky &Nolen-Hoeksema, 1995; Watkins & Moulds,2005), overgeneral autobiographical memory(Watkins & Teasdale, 2004; Watkins, Teasdale, &Williams, 2000), and negative cognition (Lavender& Watkins, 2004). These convergent findingssupport the role of rumination in the maintenanceof depression-related deficits.Rumination and cognitive reactivity both repre-

sent ways in which individuals respond to lowmood. Moreover, both rumination (Nolen-Hoek-sema, 2000) and cognitive reactivity (Segal et al.,1999) are established vulnerability factors forrecurrence of depression. Surprisingly, however,their relationship has not been explored. Van derDoes (2002a, 2005) has called for research toexamine the relationship between the LEIDS andthe well-established gold standard measure ofrumination, the Ruminative Response Style sub-scale of the Response Style Questionnaire (Nolen-Hoeksema & Morrow, 1991).On the basis that depressive rumination and

cognitive reactivity are both dysfunctional cognitiveprocesses activated in response to low mood, wehypothesized that cognitive reactivity (indexed bythe LEIDS-R) and depressive rumination (measuredby the RRS) would be correlated in our nonclinicalsample after controlling for current depressionsymptoms. Specifically, it was predicted thatdepressive rumination would be positively corre-

lated with Hopelessness/Suicidality, Aggression,Control/Perfectionism, Risk Aversion and Rumina-tion, but negatively associated with Acceptance/Coping (Van der Does, 2002a). Second, in order toexamine the capacity of the LEIDS to indexcognitive reactivity, and so to discriminate betweenrecovered and never-depressed individuals, weadministered a structured interview to a subset ofparticipants to index depression status (i.e., cur-rently depressed, previously depressed, never-depressed). In line with the focus of the differentialactivation hypothesis, our predictions were made interms of recovered depressed and never-depressedparticipants. Specifically, we predicted that recov-ered depressed participants would report higherlevels of cognitive reactivity (i.e., higher scoresacross all subscales of the LEIDS-R) and ruminationthan their never-depressed counterparts and thatthese variables would be positively correlated aftercurrent depression symptoms were partialled out.

Methodparticipants

Participants were 324 undergraduate students inthe School of Psychology at The University of NewSouth Wales, who participated in the study inexchange for course credit. Participants had a meanage of 20.07 years (SD=4.73), and the total samplewas comprised of 215 females and 109 males. Asubset of 130 participants was administered themood module of the Structured Clinical Interviewfor DSM-IV (SCID; Spitzer, Williams, Gibbon, &First, 1996) in order to establish current moodstatus. The SCID was administered by a master’s-level clinical psychologist (EK) with extensiveexperience in the use of this instrument in clinicalresearch settings.

measures

Leiden Index of Depression Sensitivity–Revised(LEIDS-R; Van der Does & Williams, 2003). TheLEIDS-R is a self-report measure that indexescognitive reactivity in response to low mood.Participants are instructed to think about the lasttime they felt “somewhat sad,” and to indicate thedegree to which a list of statements describe theirtypical cognitions and behaviors in response to sadmood. The LEIDS has good psychometric proper-ties (Van der Does, 2002a), and responses on thismeasure correlate with a mood induction procedureemployed to index cognitive reactivity (e.g., Segal etal., 1999). Internal consistency in the currentsample was strong (.88).

Beck Depression Inventory-II (BDI-II; Beck,Steer, & Brown, 1996). The BDI-II is a self-report

Table 1Mean scores (and standard deviations) on study measures(N=318)

BDI-II 8.74 (6.82)RRS 41.98 (11.24)LEIDS-R Total 46.61 (17.20)LEIDS-R Hopelessness 4.90 (4.23)LEIDS-R Acceptance 3.53 (3.20)LEIDS-R Aggression 8.44 (4.59)LEIDS-R Control 7.77 (3.85)LEIDS-R Risk Aversion 10.60 (4.00)LEIDS-R Rumination 11.48 (4.68)

Note. BDI-II=Beck Depression Inventory-II; RRS=RuminativeResponse Scale; LEIDS-R Total=Leiden Index of DepressionSensitivity Total; LEIDS-R Hopelessness=Hopelessness/Suicid-ality subscale; LEIDS-R Acceptance=Acceptance/Coping sub-scale; LEIDS-R Aggression=Aggression subscale; LEIDS-RControl=Control/Perfectionism subscale; LEIDS-R Risk Aver-sion=Risk Aversion subscale; LEIDS-R Rumination=Ruminationsubscale.

68 moulds et al .

measure of depressive symptoms that possessesstrong psychometric properties, including internalconsistency of .92 in a sample of psychiatricoutpatients and .93 in college students (Becket al., 1996).

Ruminative Response Scale of the ResponseStyles Questionnaire (RRS; Nolen-Hoeksema &Morrow, 1993). The RRS is a self-report measurethat indexes the tendency to ruminate in response todepressed mood. The RRS contains symptom-focused and self-focused items. The RRS possessesgood internal consistency and validity (Nolen-Hoeksema & Morrow, 1991).

procedure

After providing written informed consent, partici-pants completed a package of self-report question-naires (described above) in a counterbalancedorder, so as to avoid potential order effects.Participants were then thoroughly debriefed andinformed about the aims of the research. Partici-pants whose responses indicated high levels ofanxiety or depression were provided with informa-tion about relevant clinical services.

ResultsPreliminary screening of the data (prompted by thelarge standard deviations for BDI-II and LEIDS-Rscores) indicated that 6 participants’ scores on thesemeasures were outliers (i.e., more than twostandard deviations above the mean). These parti-cipants were excluded from the analyses. Specifi-cally, 3 never-depressed participants were excludedon the basis of their LEIDS-R score, 1 recovereddepressed participant was excluded owing to anextreme BDI-II score, and 1 never-depressed and 1recovered depressed participant were excludedowing to outlying scores on both measures. Thus,the analyses reported below were carried out withthe data of 318 participants.Mean scores on the questionnaire measures

across the total sample are presented in Table 1.Partial correlations controlling for BDI-II scoreswere conducted to explore the association betweenrumination and cognitive reactivity. As shown inTable 2, significant positive correlations weredetected between the RRS and the LEIDS-R Totaland subscale scores after controlling for currentdepressive symptoms, confirming that the observedrelationships between these measures are indepen-dent of current mood state. The hypothesizedinverse correlation between RRS and Acceptance/Coping was not observed (r=.01, pN .05).In the second part of the study, participants were

classified according to their responses on the major

depression component of the SCID. After theremoval of excluded participants (as notedabove), 6 participants (4.8%; 3 male, 3 female)met criteria for a current major depressive episode(MDE; American Psychiatric Association, 1994).Of the remaining participants, 40 (32.3%) reporteda previous episode of major depression, and 78(62.9%) denied any current or past MDE. Thenever-depressed group had a mean age of 19.05years (SD=3.28) and was comprised of 53 femalesand 25 males. Recovered depressed participantshad a mean age of 23.33 years (SD=10.09), andincluded 30 females and 10 males. As a group, theyreported an average of 1.79 (SD=3.14) previousdepressive episodes. On average, their last depres-sive episode ended 36.93 months (SD=44.69) priorto participation in the study. The mean duration ofthe last MDE was 6.10 months (SD=10.67).Independent samples t-tests demonstrated that

the recovered depressed group was older than thenever-depressed group, t(43.27)=−2.61, pb .05,unequal variance estimate. The recovered depressedand never-depressed group did not differ in theircurrent level of depression, as indexed by the BDI-II, t(61.00)=− .37, pN .05, unequal variance esti-mate (see Table 3). Thus, any observed differencescannot be accounted for by between-group differ-ences in current mood. The recovered depressedgroup scored more highly on the LEIDS-R (Total), t(95.64)=−2.13, pb .05, unequal variance estimate.Not surprisingly, the recovered depressed groupreported higher levels of trait rumination on theRRS, t(61.90)=−2.02, pb .05, unequal varianceestimate, and on the Rumination subscale of theLEIDS-R, t(116)=−2.37, pb .05. The two groupsdid not differ significantly on the remaining LEIDS-R subscales: Hopelessness, t(116)=− .75, pN .05;

Table 2Correlations between rumination and cognitive reactivity controlling for depression (BDI-II) (N=318)

RRS LEIDS-R Hopeless Accept Aggress Control Risk Rum

RRS –LEIDS-R .41⁎⁎⁎ –Hopeless .33⁎⁎⁎ .61⁎⁎⁎ –Accept .01 .40⁎⁎⁎ .06 –Aggress .26⁎⁎⁎ .70⁎⁎⁎ .41⁎⁎⁎ .15⁎⁎ –Control .13⁎ .60⁎⁎⁎ .10 .37⁎⁎⁎ .23⁎⁎⁎ –Risk .30⁎⁎⁎ .73⁎⁎⁎ .38⁎⁎⁎ .16⁎⁎ .30⁎⁎⁎ .37⁎⁎⁎ –Rum .51⁎⁎⁎ .77⁎⁎⁎ .40⁎⁎⁎ .03 .51⁎⁎⁎ .31⁎⁎⁎ .58⁎⁎⁎ –

Note. BDI-II=Beck Depression Inventory-II; RRS=Ruminative Response Scale; LEIDS-R Total=Leiden Index of Depression SensitivityTotal; Hopeless=LEIDS-R Hopelessness/Suicidality subscale; Accept=LEIDS-R Acceptance/Coping subscale; Aggress=LEIDS-RAggression subscale; Control=LEIDS-R Control/Perfectionism subscale; Risk=LEIDS-R Risk Aversion subscale; Rum=LEIDS-RRumination subscale.⁎pb .05, ⁎⁎pb .01, ⁎⁎⁎pb .001.

69cogn i t i ve react i v i ty and ruminat ion

Aggression, t(96.15)=− .33, pN .05, unequal var-iance estimate; Control, t(116)=−1.45, pN .05;Risk Aversion, t(115)=−1.75, pN .05. An unex-pected observation was that the recovereddepressed participants scored more highly thantheir never-depressed counterparts on the Accep-tance/Coping subscale, although this difference didnot reach statistical significance, t(116)=−1.48,pN .05.To investigate whether cognitive reactivity, as

indexed by the LEIDS-R Total score, explained anyof the variance in depression beyond depressiverumination (a well-established predictor of depres-sion), we conducted a multiple regression with BDI-II scores as the dependent variable, RRS scoresentered on the first step, and LEIDS-R total scoresentered on the second step. Across the recovered

Table 3Mean participant characteristics for recovered depressed andnever-depressed groups

Neverdepressed (n=78)

Recovereddepressed (n=40)

Age 19.05 (3.28) 23.33 (10.09)BDI-II 8.44 (5.29) 8.93 (7.27)RRS 40.32 (9.25) 44.45 (12.47)LEIDS-R Total 42.77 (17.99) 49.18 (13.84)LEIDS-R Hopelessness 4.47 (4.02) 5.05 (3.80)LEIDS-R Acceptance 2.88 (2.85) 3.73 (3.07)LEIDS-R Aggression 8.23 (4.85) 8.53 (3.84)LEIDS-R Control 6.94 (4.66) 8.20 (4.10)LEIDS-R Risk Aversion 9.78 (4.07) 11.15 (3.82)LEIDS-R Rumination 10.46 (5.02) 12.60 (4.44)

Note. Standard deviations appear in parentheses. Means areunadjusted. BDI-II=Beck Depression Inventory-II; RRS=Rumina-tive Response Scale; LEIDS-R Total=Leiden Index of DepressionSensitivity Total; LEIDS-R Hopelessness=Hopelessness/Suicid-ality subscale; LEIDS-R Acceptance=Acceptance/Coping sub-scale; LEIDS-R Aggression=Aggression subscale; LEIDS-RControl=Control/Perfectionism subscale; LEIDS-R Risk Aver-sion=Risk Aversion subscale; LEIDS-R Rumination=Ruminationsubscale.

depressed and never-depressed participants, RRSscores accounted for 33% of the variance in BDI-IIscores (adjusted R2 = .33, β=.57, SE=.03, t=12.18,pb .001). Interestingly, LEIDS-RTotal made a small(but significant) contribution, accounting for 6% ofthe variance in BDI-II (adjusted R2 = .39, β=.31,SE=.02, t=5.69, pb .001). Thus, cognitive reactiv-ity made a unique contribution to the prediction ofdepression, over and above trait level of depressiverumination.

DiscussionOur first goal in this study was to examine theinterrelationship of cognitive reactivity and rumi-nation. As predicted, these cognitive processes werepositively correlated even when current level ofdepression was partialled out—confirming anassociation that is independent of current sympto-matology. Consistent with clinical observation, thisrelationship demonstrates that individuals whorespond to depressed mood by ruminating aboutthe causes, meanings, and implications of theirsymptoms (Nolen-Hoeksema, 1991) are also likelyto engage in an array of additional maladaptivecognitive and behavioral responses, including feel-ing hopeless and suicidal, responding with aggres-sion, and attempting to avoid harm/conflicts.A second goal was to compare cognitive reactiv-

ity, as indexed by the LEIDS-R, in recovered andnever-depressed individuals. As predicted, therecovered depressed participants indicated greatercognitive reactivity generally (i.e., LEIDS-R Total),and scored more highly on the LEIDS-R Rumina-tion subscale and the RRS. However, the twogroups did not differ on the remaining LEIDS-Rsubscales. Thus although the LEIDS-R Totaldifferentiated how formerly depressed and never-depressed individuals respond when they experi-ence sad mood, this effect was accounted for mainlyby the LEIDS-R Rumination subscale. This finding,

70 moulds et al .

combined with the observation that formerly andnever-depressed individuals differed on the basis ofRRS scores, accords with extensive empiricalsupport for the role of depressive rumination inthe persistence of depression (Nolen-Hoeksema,2000) and associated cognitive and behavioraldeficits (e.g., impoverished problem solving, Wat-kins & Moulds, 2005; overgeneral autobiographi-cal memory retrieval, Watkins, Teasdale, &Williams, 2000). At this stage, the degree towhich the Hopelessness, Acceptance, Aggression,Control, and Risk Aversion subscales are able todifferentiate remitted and never-depressed indivi-duals remains unclear. Replication of this investiga-tion is needed for clarification.Importantly, across the sample of recovered and

never-depressed participants, the Total LEIDS-Rscore explained unique variance in depression overand above that accounted for by theRRS. TheRRS isthe gold standard instrument used to measuredepressive rumination that has convincingly pre-dicted depression across multiple longitudinal stu-dies. Our finding therefore underscores the utility ofthe LEIDS-R as a clinical instrument that gaugesresponses to low mood that are predictive ofconcurrent depression. Future studies should investi-gate whether the LEIDS-R has the capacity to predictdepression across time within a longitudinal design.The construct of cognitive reactivity incorporates

both depression-related cognitive processes andcontent that are theorized to be activated in responseto sad mood. However, beyond studies that indexcognitive content—i.e., maladaptive cognitions—following induced negative mood, experimentalwork in this area to date has not tested thedifferential activation hypothesis more broadlyand indexed a range of potential dysfunctionalprocesses (cognitive and behavioral) that character-ize depressed individuals’ responses to low mood.By measuring a range of cognitive and behavioralprocesses that an individual may engage in at timesof low mood, the LEIDS-R has the capacity to testthe differential activation hypothesis more broadly.Moreover, as a clinical tool, responses on theLEIDS-R have the capacity to provide invaluableinformation about a range ofmaladaptive responsesthat clients may engage in, including both dysfunc-tional cognitive content and processes. These canthen serve as key targets in therapy. Related to this,future work would benefit from extending investi-gations in this area to more broadly incorporateadditional well-established cognitive processes thatoperate in depression; for example, memory dis-turbances such as overgeneral memory, intrusivememories and biased retrieval of negative material.The possibility that such processes of memory are

activated in response to (and exacerbated by) sadmood, and whether their activation predicts depres-sion relapse, is worthy of examination.A number of limitations warrant acknowledg-

ment. First, we did not employ a treatment-seekingsample. Participants were an unselected sample ofundergraduate students. Nonetheless, participantsin the second phase of the study were administereda structured clinical interview by a qualified clinicalpsychologist. Thus, although the sample was notdrawn from a clinical population per se, it isnoteworthy that their responses on an establishedstructured interview (conducted by an experiencedclinician) were used to ascertain their depressiondiagnostic history. However, future research thatinvolves the recruitment of formerly depressedparticipants (e.g., posttreatment) would supportthe generalizability of our findings to treatment-seeking individuals in the wider community. Sec-ond, we note that the scores obtained on the self-report measures for the never-depressed group wererelatively high for a healthy participant group. Asdepression was the focus of our study, we adminis-tered only the major depression component of theSCID. Thus, we cannot rule out the possibility thatparticipants also satisfied diagnostic criteria foradditional psychological conditions (e.g., anxietydisorders, eating disorders), and thus that the scoresobserved on self-report measures were an artifact ofcomorbidity that was not indexed in the currentdesign. Similarly, we did not assess current oradditional depressive conditions such as dysthymiaand minor or subclinical depression; again, thismay have inflated scores in the never-depressedgroup. Future studies that incorporate a morethorough screening to rule out the influence ofcomorbidity and include extensive backgrounddetails (e.g., history of psychological treatment)will provide an important extension of our findings.Our sample included more female than male

participants, and future studies should employgender-balanced samples. An additional aspect ofour sample that should be kept in mind wheninterpreting the results is the age of participants; thenever-depressed group was significantly youngerthan the recovered depressed group. The possibilitythat some of the never-depressed participants may,in fact, be vulnerable to depression, but had not yetexperienced a depressive episode at the time ofinvolvement in the research, cannot be ruled out.Despite potentially possessing features that confervulnerability to depression, it is plausible thatindividuals in this younger group had not experi-enced a sufficiently aversive life event to precipitatea depressive episode. Thus, in comparing the never-depressed and remitted depressed group, we must

71cogn i t i ve react i v i ty and ruminat ion

limit our interpretations so as not to draw conclu-sions about depression-vulnerable versus non-depression-vulnerable individuals.Related to this point, an outstanding question in

the field is whether cognitive reactivity encompassesa range of maladaptive cognitive processes that aresequelae of experiencing depression, or whether thepresence of these processes confers vulnerability tothe onset of an initial depressive episode. As raisedby Van der Does (2002a), future studies thatinvestigate cognitive processes in high-risk samplesusing prospective designs (e.g., Bryant & Guthrie,2005) are needed in order to disentangle whethercognitive reactivity is a vulnerability factor thatincreases the likelihood of initial depression onset,as well as recurrence. The development of easilyadministered self-report instruments that indexcomplex constructs such as cognitive reactivityincreases the likelihood that clinical researcherswill tackle such research questions in the future.

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RECEIVED: July 2, 2006ACCEPTED: May 1, 2007Available online 26 October 2007