an investigation of the relationship between positive affect regulation and depression

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Behaviour Research and Therapy 51 (2013) 46e56

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Behaviour Research and Therapy

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An investigation of the relationship between positive affect regulation anddepression

Aliza Werner-Seidler a,b,*, Rosie Banks b, Barnaby D. Dunn b, Michelle L. Moulds a

aUniversity of New South Wales, Sydney, AustraliabMedical Research Council, Cognition and Brain Sciences Unit, Cambridge, United Kingdom

a r t i c l e i n f o

Article history:Received 1 August 2012Received in revised form25 October 2012Accepted 1 November 2012

Keywords:DepressionAnhedoniaPositive affectEmotion regulation

* Corresponding author. MRC Cognition and Brain ScCambridge CB2 7EF, England, United Kingdom. Tel.: þ

E-mail address: [email protected]

0005-7967/$ e see front matter � 2012 Elsevier Ltd.http://dx.doi.org/10.1016/j.brat.2012.11.001

a b s t r a c t

There is preliminary evidence that dysphoric symptoms are associated with maladaptive regulation ofpositive emotion. We investigated to what extent this pattern is unique to depression symptoms, persistsin recovery, and extends to apprehension of intense emotion experience. In Study 1, in a sample ofundergraduates (N ¼ 112), dysphoria was associated with apprehension about experiencing intenseemotion and dampening of positive emotion. Reductions in the amplification of positive emotionexperience were uniquely associated with anhedonic depressive symptoms. Study 2 compared a recov-ered depressed and never-depressed student sample (N ¼ 123), and found that recovered individualsreported using more maladaptive responses to positive affect. In Study 3 we examined community-recruited depressed, recovered and never-depressed groups (N ¼ 50), and found that depressed indi-viduals reported a greater tendency to dampen positive emotion than their never-depressed counter-parts, but did not significantly differ from recovered depressed individuals. Greater dampening andreduced amplification of positive experience were again uniquely associated with anhedonic depressivesymptoms. Our findings converge on the proposal that current depressive symptoms, rather thana history of depression, are more strongly linked to difficulties with emotion regulation, and suggest thattargeting positive emotion could reduce anhedonia and improve treatment outcomes.

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Emotion regulation refers to the processes used by individuals toinfluencehowtheir emotions are experiencedandexpressed (Gross,1998). There is now a growing recognition that emotion regulationinvolves considerable effort and control, and that some emotionregulation strategies are more helpful than others (Gross, 1999).Depression has been increasingly characterised as a disorder ofdysregulated emotion, and there is evidence that clinicallydepressed groups use less adaptive, more dysfunctional and lessflexible strategies than their non-depressed counterparts (e.g.,Aldao, Nolen-Hoeksema, & Schweizer, 2010; Campbell-Sills, Barlow,Brown, & Hofmann, 2006; Garnefski & Kraaij, 2006; Kashdan &Rottenberg, 2010). Interestingly, disturbances in emotion regula-tion donot appear to be limited to the acute phase of depression (i.e.,when individuals are symptomatic) as there is now preliminaryevidence that individuals who have experienced depression in thepast employmore dysfunctional strategies (e.g., catastrophising andrumination) and less functional strategies (e.g., putting things into

iences Unit, 15 Chaucer Road,44 (0) 1223 273 744..ac.uk (A. Werner-Seidler).

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perspective) than never-depressed controls (Ehring, Fischer,Schnulle, Bosterling, & Tuschen-Caffier, 2008; Ehring, Tuschen-Caffier, Schnülle, Fischer, & Gross, 2010). This suggests thatemotion regulation difficulties may play a key role not only incurrent depression, but also in the euthymic phase when the indi-vidual no longer meets criteria for a major depressive episode, withpossible implications for both acute depression and vulnerability torecurrence.

Research on the role of emotion regulation in depression haspredominantly focused on negative emotional experience, which isunderstandable from a conceptual viewpoint because depression isclassified as a disorder of elevated negative affectivity. However, it issurprising that the other cardinal symptom of depression e anhe-donia (i.e., a diminished ability to respond to positive stimuli)e hasbeen relatively less researched. In the context of depression,understanding the regulation of positive emotion is of clear clinicalimportance. Specifically, current gold-standard pharmacologicaland psychological therapies for depression struggle to successfullytreat anhedonia (Dunn, 2012; Treadway & Zald, 2011). For example,while encouraging individuals to reengage with potentiallyrewarding activities is a central componentof cognitive-behaviouraltherapy and behavioural activation (Martell, Addis, & Jacobson,

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A. Werner-Seidler et al. / Behaviour Research and Therapy 51 (2013) 46e56 47

2001), there is very little understanding of how to help depressedclients gain enjoyment from these events. While studies arebeginning to explore the impact of mindfulness based cognitivetherapy and positive psychology approaches on positive affect (e.g.Geschwind, Peeters, Drukker, van Os, & Wichers, 2011; Sin &Lyubomirsky, 2009), insight into the underlying mechanism ofchange is largely absent. Improving understanding of what mech-anisms underpin anhedonia in depression is likely to lead to novel,targeted interventions thatwill in turn improve treatment outcome.In particular, deficits in positive affect predict a poor depressionprognosis (Morris, Blysma & Rottenberg, 2009; Shankman, Nelson,Harrow, & Faull, 2011; Wood & Joseph, 2010), perhaps becausepositive affect makes individuals more resilient to negative lifeevents (Fredrickson & Levenson,1998; Tugade & Fredrickson, 2004).One possibility that follows is that by building positive emotionexperience vulnerable individuals may be protected from an initialepisode of depression or from subsequent relapse.

A critical issue that needs to be explored is whether depressedindividuals employ self-regulatory cognitive strategies when theyencounter positive material which might underpin their anhedonicexperience. That is, it would be helpful to knowwhether depressedindividuals engage in any conscious mental strategies with theintention of reducing the intensity of positive emotional experi-ence. There is some preliminary evidence that depressive symp-toms are associated with effortful attempts to dampen and reducepositive affect (PA; Feldman, Joormann, & Johnson, 2008; Raes,Daems, Feldman, Johnson, & Van Gucht, 2009). In these studies,undergraduate students were administered the Responses toPositive Affect Questionnaire (RPA; Feldman et al., 2008) whichassesses cognitive responding to positive experience. The RPA hasthree subscales e two which measure attempts to amplify positiveemotional experience (emotion-focus and self-focus) and the thirdof which measures attempts to down-regulate positive emotion(dampening). The self-reported tendency to engage in mentalstrategies that dampen positive emotional experience have beenfound to be associated with dysphoric symptoms (Feldman et al.,2008; Raes et al., 2009). However, no consistent pattern of find-ings has emerged between the subscales measuring attempts toamplify positive emotion and dysphoric symptoms. For example, inthe Feldman et al. (2008) study, there was a small negative corre-lation between depressive symptoms and the self-focus subscale,but no correlation with the emotion-focus subscale. Conversely,Raes et al. (2009) found a small negative correlation betweendepressive symptoms and the emotion-focus subscale, but no linkwith the self-focus subscale. Further, a more recent study foundscores on the dampening subscale (but not the emotion-focus orself-focus subscales) were predictive of dysphoric symptoms atthree month and five month follow-up, even when baselinedysphoria was taken into account (Raes, Smets, Nelis, & Schoofs,2012). From this research it is clear that dampening of PA iscross-sectionally and prospectively linked to dysphoric symptoms.However, there has been no consistent pattern of findings for thetwo amplification subscales on this measure, which is notsurprising given the recent development of the instrument. Furtherinvestigation is needed to better understand dysphoric individuals’cognitive responses to PA.

The aim of this cross-sectional series of studies was to furtherinvestigate positive emotion regulation in depression, extendingprevious work in a number of ways. First, drawing from researchestablishing that apprehension towards the experience of negativeemotion is associated with depression (Liverant, Brown, Barlow, &Roemer, 2008), we wanted to examine whether the same wouldhold for positive emotion. That is, we wanted to test whetherapprehension towards experiencing intense emotion in general,and more specifically, positive emotion, would be linked to

dysphoria. A fear of positive emotion could be one importantunderlying factor driving anhedonia and therefore become a targetfor intervention in therapy (for example, using cognitive restruc-turing techniques).

Second, existing studies (e.g., Raes et al., 2012) have relied onmeasures of dysphoric symptoms (e.g. Beck Depression Inventory-II (BDI-II); Beck, Steer, & Brown, 1996), which are not specificmeasures of depression severity. In particular, individuals withanxiety presentations also score highly on the BDI-II. It is importantto establish to what extent positive emotion regulation deficits aredriven by anxiety symptoms, depression symptoms, or a combina-tion of the two, both to aid differential diagnosis and to helpdevelop effective and targeted clinical interventions. One way toestablish specificity within continuous designs is to examine howcandidate processes relate to symptoms common across diagnosesversus those relatively specific to a diagnosis. For example, thetripartite framework (Clark & Watson, 1991; Clark, Watson, &Mineka, 1994) suggests that common to both anxiety and depres-sion is ‘general distress’, consisting of non-specific ‘negative affect’symptoms (e.g., depressedmood, anxious mood, insomnia). Uniqueto anxiety are physiological hyper-arousal and somatic tensionsymptoms (e.g., dizziness, shortness of breath), whereas unique todepression are ‘positive affect’ symptoms of anhedonia and apathy(e.g., loss of interest, feeling nothing is enjoyable). The Mood andAnxiety Symptom Questionnaire (MASQ; Watson & Clark, 1991;Watson et al., 1995) has been developed as a self-report measureof these three symptom clusters. Previous work suggests thatevidence of depression versus anxiety specificity can be gleanedusing this measure. For example, reductions in positive judgementbiases are unique to anhedonia symptoms (Dunn, Stefanovitch,Buchan, Lawrence, & Dalgleish, 2009), whereas hyper-awarenessof the body is largely driven by anxious arousal symptoms (Dunnet al., 2010).

Such an approach has yet to be taken to examine positiveemotion regulation in depression. It may be the case that thesedifferent symptom clusters drive positive emotion regulation indifferent ways. Consequently, global measures of dysphoriaseverity may not be sensitive enough to detect subtle relationshipsin the data. For example, mixed findings regarding the relationshipbetween the amplifying scales of the RPA across different studies(Feldman et al., 2008; Raes et al., 2009) could reflect variation in thespecific symptom clusters that the sample predominantly pre-sented with. In particular, it is likely that reduced positive ampli-fication would be most strongly linked to the anhedonic symptomsof depression, and previous studies may have differed in howanhedonic their samples were. It also seems likely that dampeningof positive emotion would be most strongly associated withanhedonic symptoms, but this possibility has yet to be tested.

A third critical issue to clarify is whether positive emotionregulation disturbances are limited to the acute phase of depressionor also persist in recovery. Existing research suggests that deficits inthe regulation of negative emotion persist in the euthymic phase ofthe disorder (Ehring et al., 2008; Werner-Seidler & Moulds, 2012).This might also be the case for the regulation of positive emotionalstates, although this has not yet been tested. If problems in regu-lating positive emotion during recovery from depression emerge,longitudinal studies would need to establish whether these diffi-culties pose a risk for recurrence (and therefore might be a sensibletarget for relapse prevention approaches). To explore this issue it isfirst necessary to take a diagnostic approach and compare partici-pants who are in remission to never-depressed individuals toascertain whether deficits exist in their regulation of positiveemotion.

To address these goals we conducted three cross-sectionalstudies. The first was a correlational study in which we recruited

Table 1Descriptive information for Study 1.

Mean SD Min Max

MASQ-S e general distress 46.36 16.12 23 93MASQ-S e anxious arousal 25.89 10.05 17 70MASQ-S e anhedonic depression 60.99 13.37 28 94ACS e positive affect 41.03 10.24 18 67ACS e total 141.41 32.48 64 212RPA e dampening 15.62 5.14 8 30RPA e emotion-focus 15.13 3.25 6 20RPA e self-focus 10.05 2.81 4 16

Note. MASQ-S ¼ Mood and Anxiety Symptom Questionnaire e Short Form;ACS ¼ Affective Control Scale; RPA ¼ Responses to Positive Affect Scale.

A. Werner-Seidler et al. / Behaviour Research and Therapy 51 (2013) 46e5648

a non-selected student sample and examined the relationshipsbetween the MASQ, apprehension about emotion experience, andattempts to regulate (dampen or amplify) positive emotion. Inthe second study we examined these variables in a recovereddepressed versus never-depressed student sample, making itpossible to explore if apprehension, amplification and dampeningis found in recovery. In the third study we recruited depressed,recovered depressed and never-depressed individuals from thegeneral community and compared the extent to which they re-ported using specific strategies to regulate positive emotion.Studies 2 and 3 enabled us to test whether the continuous associ-ations found between positive emotion regulation strategies anddysphoric symptoms in Study 1, hold in a more constrainedbetween-groups diagnostic design.

Study 1

Study 1 examined the relationship between scores on theMASQ-S measure and the strategies used to regulate positiveemotion in a sample of undergraduate students. We hypothesisedthat all three MASQ-S factors (i.e., general distress, anhedonicdepression and anxious arousal) would be associated with appre-hension towards experiencing intense emotion and in particular,positive affect. Second, we expected that attempts to dampen theintensity of positive emotion would be related to these symptomdimensions. However, based on the inconsistency of previousfindings we had no clear predications about how the two amplifi-cation factors (self-focus and emotion-focus) would relate tosymptom dimensions. Third, we expected that whenwe controlledfor general distress and anxious arousal, a unique relationshipbetween anhedonia and variables of interest (i.e., apprehensionabout experiencing intense emotion and attempts to down-regulate positive emotion) would emerge. We did not expect anyunique relationships for general distress or anxious arousal.

Method

Participants

One-hundred and twelve undergraduate students from TheUniversity of New South Wales participated in this study in returnfor course credit.

Materials and measures

Mood and Anxiety Symptom Questionnairee Short Form (MASQ-S;Watson & Clark, 1991). The MASQ-S is a 62-item self-report ques-tionnaire that assesses symptoms of anxiety and depressive disor-ders. TheMASQ-S is divided into three dimensions: general distress(common to anxiety and depression; maximum score ¼ 110),anxious arousal (specific to anxiety; maximum score ¼ 85)and anhedonic depression (specific to depression; maximumscore ¼ 115). Individuals are instructed to indicate the extent towhich they have experienced symptoms over the previous week ona 5-point Likert scale ranging from “not at all” to “extremely”. TheMASQ-S has satisfactory psychometric properties (Watson et al.,1995).

Affective Control Scale (ACS; Williams, Chambless, & Ahrens,1997). The ACS is a 42-item self-report measure designed toassess an individual’s apprehension and fear about experiencingintense emotion. The scale is comprised of four subscales: Anger(e.g., “I am concerned that I will say things I’ll regret when I’m angry”),Positive Emotion (e.g., “When I get really excited about something, Iworry that my enthusiasm will get out of hand”), Depressed Mood(e.g., “When I get the blues I worry that they will pull me down too

far”), and Anxiety (e.g., “I am afraid that I will babble or talk funnywhen I am nervous”). Given the targeted nature of our investigation,we examined the PA subscale alone, as well as the total score fromall subscales. Participants are instructed to indicate the extent towhich they agree or disagree with the listed items on a 7-pointLikert scale ranging from “very strongly disagree” to “verystrongly agree”. The ACS has been shown to have good psycho-metric properties (Williams et al., 1997).

Responses to Positive Affect Questionnaire (RPA; Feldman et al.,2008). The RPA is a 17-item self-report measure that assesses theextent to which an individual responds to positive affect in a waythat will either intensify or diminish positive emotional experience.The RPA has three subscales, with both the emotion-focus (e.g.,“Think about how happy you feel”) and self-focus (e.g., “Think I amachieving everything”) subscales evaluating responses which inten-sify positive emotion, while the dampening subscale measures anindividual’s propensity to use mental strategies which reduce theintensity and duration of their positive affective state (e.g., “Remindyourself that these feelings won’t last”). Participants’ rate how likelythey are to respond to positive affect in a particular way on a fourpoint scale ranging from “almost never respond in this way” to“almost always respond in this way”. Although this measure wasdeveloped relatively recently, there is support for its psychometricproperties including acceptable structural validity supporting thethree-factor subscale, with acceptable internal consistency (a¼ .79,a ¼ .71, a ¼ .69 for the dampening, self-focus and emotion-focussubscales respectively; Feldman et al., 2008).

Procedure

The data from this study was collected as a part of a larger study,with all questionnaires completed at the commencement of theexperimental session. Participants were tested in groups of ten inreturn for course credit and after providing written informedconsent theywere instructed to complete the questionnaire batteryincluding the ACS, MASQ-S and RPA in counterbalanced order. Atthe end of the study they were thanked for their time and fullydebriefed. This study was approved by the University of New SouthWales Human Research Ethics Advisory Panel.

Results

Sample characteristics

The mean of age of participants was 19.14 (SD ¼ 2.17), and thesample was comprised of 69 females (i.e., 62%). Descriptive infor-mation is presented in Table 1. There was a broad range of moodand anxiety symptoms, and these symptom levels were compa-rable to those reported in previous studies (e.g., Dunn et al., 2010),indicating that range restriction is unlikely to confound ouranalyses.


Mood/anxiety symptoms and apprehension

To investigate the relationship between symptoms and appre-hension about the experience of intense emotion, a series of zero-order correlations was conducted for each of the three symptomdimension measures, as well as partial correlations controlling forthe other two symptom factors (coefficients are reported inTable 2). General distress symptoms correlated with an overall fearof experiencing intense emotion, r ¼ .61, p < . 001, as well as withthe subscale measuring apprehension about experiencing positiveaffect, r ¼ .35, p < .001. When anxious arousal and anhedonia weretaken into account, there was still a unique relationship betweengeneral distress and fear of experiencing intense emotion, r ¼ .25,p < .01, but not positive affect specifically, r ¼ .15, p ¼ .12. Anxiousarousal correlated significantly with both fear of experiencingintense emotion in general, r ¼ .51, p < .001, as well as positiveaffect specifically, r ¼ .29, p < .01. When the effects of generaldistress and anhedonia were partialled out, there was no longer anassociation between anxious arousal and positive emotion appre-hension, r¼ .07, p¼ .45, although therewas a trend for more overallintense emotion with increasing arousal, r ¼ .18, p ¼ .06. For theanhedonic symptom measure of depression, symptoms correlatedwith both fear of experiencing intense emotion, r ¼ .51, p < .001,and positive affect specifically, r ¼ .25, p< .01. When controlling forgeneral distress and anxious arousal, the association betweenanhedonic depression and overall apprehension of intense emotionremained significant, r ¼ .27, p < .01, but anhedonia was no longersignificantly related to positive affect apprehension, r ¼ .07, p¼ .44.These results suggest that anxious arousal symptoms are limited intheir associationwith positive affect variables but that both generaldistress and anhedonic depression symptoms are associated withapprehension about experiencing both intense emotion and posi-tive affect.

Mood/anxiety symptoms and responses to PA

To examine the relationship between anxiety/depressionsymptoms and the use of strategies to regulate positive emotion,a series of zero-order correlations were conducted (coefficientsreported in Table 2). There were significant correlations betweenattempts to dampen positive emotion and all three symptomdimensions (i.e., general distress, r ¼ .49, p < .001; anxious arousal,r ¼ .45, p < .001; anhedonia, r ¼ .38, p < .001). As expected, thegeneral distress and anxious arousal factors were not associatedwith the two subscales that measured attempts to intensify positiveemotion (smallest p ¼ .35). Interestingly, anhedonia was inverselyrelated to both the emotion-focus, r ¼ �.19, p < .05, and self-focus,

Table 2Correlational table for Study 1.

MASQ-SGD

MASQ-SAA

MASQ-SAD

Depression/Anxiety Symptoms (MASQ)General Distress e

Anxious Arousal .71*** e

Anhedonic Depression .57*** .33** e

Affective Control (ACS)Positive Affect .35*** (.15) .29** (.07) .25** (.07Total .61*** (.25**) .51*** (.18) .51*** (.2Positive Rumination (RPA)Dampening .49*** (.16) .45*** (.19) .38*** (.1Emotion-Focus .09 (.25**) .03 (�.10) �.19* (�Self-Focus �.01 (.15) �.03 (�.07) �.20* (�

Note: Zero-order correlations and (partial correlations controlling for other two MASQ-SGD¼ General Distress, AA¼ Anxious Arousal, AD¼ Anhedonic Depression); ACS¼ Affecti(subscales: Damp ¼ Dampening, E-F ¼ Emotion-Focused, S-F ¼ Self-Focused). *** ¼ sign

r¼�.20, p< .05, subscales, which contrasts to inconsistent findingsin previous studies about the relationship between these amplifi-cation factors and global dysphoria measures (e.g., Feldman et al.,2008; Raes et al., 2009). That is, the higher the level of anhedonicsymptoms, the less likely participants reported they were to usestrategies to intensify their experience of positive emotion.

We conducted a series of partial correlations to examinewhether there was a unique association between responses topositive affect (as measured by the subscales of the RRA) anddistinct symptom dimensions. Our primary analysis was intendedto evaluate whether there was a unique relationship betweenanhedonic symptoms and attempts to regulate PA. When we par-tialled out the effects of general distress and anxious arousal, therewas a trend between anhedonic symptoms and dampening, r ¼ .18,p ¼ .07, such that a greater symptom level was associated withattempts to down-regulate positive emotion. We also found aninverse and significant association between anhedonic symptomsand both the emotion-focus, r ¼ �.32, p < .01, and self-focus,r ¼ �.25, p < .01, subscales, suggesting that greater anhedonicsymptoms share a unique association with reduced attempts tointensify positive emotion.

Our secondary analyses addressed whether general distressand/or anxious arousal shared a specific association with themeasures of positive affect regulation. When controlling foranxious arousal and anhedonia, general distress was no longerassociated with dampening, r ¼ .16, p ¼ .09 or the self-focussubscale, r ¼ .15, p ¼ .15, but it did correlate with the emotion-focus subscale, r ¼ .25, p < .01. In other words, greater levels ofgeneral distress were linked to a propensity to engage in emotion-focused strategies to amplify positive emotion. For anxious arousal,there was a trend level associationwith dampening, r¼ .19, p¼ .06,but no association between the emotion-focus and self-focussubscales, r ¼ �.07, p ¼ .56.

Taken together, these results suggest that anhedonic symptomsof depression share a unique and specific association with thediminished use of strategies to intensify experiences of positiveemotion, and to a lesser extent, dampening.

Discussion

Supporting our first hypothesis, all three subscales of the MASQwere related to apprehension about intense emotion experience ingeneral, and positive emotion experience specifically. Consistentwith our second prediction, all of the MASQ subscales were posi-tively associated with reported attempts to dampen positive affect,while anxious arousal and general distress were unrelated to theself-focus and emotion-focus strategies that amplify positive affect.

ACSPA

ACStotal

RPAdamp

RPAE-F

RPAS-F

) e

7**) .77*** e

8) .36** .55** e

.32**) �.04 �.09 .02 e

.25**) .03 �.05 �.01 .70** e

factors) presented; MASQ ¼ Mood and Anxiety Symptom Questionnaire (subscales:ve Control Scale (subscales: PA¼ Positive Affect); RPA¼ Responses to Positive Affectificant at .001 level; ** ¼ significant at .01 level; * ¼ significant at .05 level.


Partially supporting our third hypothesis, therewas a trend towardsa significant unique relationship between anhedonia symptomsand dampening. However, a similar trend relationship alsoemerged for anxious arousal, suggesting this association may notbe depression-specific. Interestingly anhedonic symptoms wereuniquely related to reduced use of self-focus and emotion-focusstrategies. This provides a notable contribution to the literaturegiven that previous findings have only inconsistently linkeddepressive symptoms to these subscales (Feldman et al., 2008; Raeset al., 2009, 2012).

These findings broadly replicate the association found betweendysphoric symptoms and dampening reported in other research(e.g. Feldman et al., 2008), and extend these earlier studies byshowing that dysphoria is related to a fear of intense positiveemotion experience. When we examined distinct symptom clus-ters, a more complicated pattern emerged. Attempts to dampenpositive affect were associated with anxious arousal, anhedonicdepression symptoms, and general distress symptoms that arecommon to both anxiety and depression, indicating that this effectis not specific to depression and instead may relate to moregeneral psychopathology. In contrast, we found that the use ofamplifying strategies (emotion-focus and self-focus) wereinversely and uniquely related to depression-specific anhedoniasymptoms.

Given that we examined an unselected sample of undergradu-ates and did not index depression history, we cannot comment as towhether the observed associations between depression andemotion regulation reflect a state marker of acute depressionsymptoms or might be a trait marker that reflecting a history ofdepression. Examining a formerly depressed group is necessary ifthis issue is to be addressed. Notably, recent work from the emotionregulation literature that has shown that deficits in the ability toengage in healthy emotion regulation strategies remain during theeuthymic phase of the disorder (Ehring et al., 2008; Werner-Seidler&Moulds, 2012). If rates of depression recurrence are to be reduced,a more comprehensive understanding of how recovered depressedindividuals regulate mood is needed. This is particularly the casegiven that dominant cognitive models of depression propose thatthe ability to regulate and respond to sad mood is an importantfactor that differs between formerly depressed and never-previously depressed individuals (e.g., Kuyken et al., 2010; Segalet al., 2006; Teasdale, 1988). Whether the same is true forresponding to positive emotional experience needs to be ascer-tained. Therefore, we conducted a second study in order to examinewhether the deficits in positive emotion regulation associated withdepression in Study 1 distinguish individuals with and withouta history of depression.

Study 2

The aim of Study 2 was to compare the relationship betweenapprehension towards and responses to PA in a recovereddepressed and never-depressed sample, using a between-groupsdesign. Informed by evidence that individuals with a history ofdepression have a tendency to use maladaptive emotion regulationstrategies even in remission (Ehring et al., 2008, 2010), we pre-dicted that the positive emotion regulation deficits found in rela-tion to dysphoric symptoms in Study 1 would also be observed ina recovered depressed sample. Derived from our Study 1 hypoth-eses, we predicted that recovered depressed individuals wouldexhibit apprehension towards experiencing intense and positiveemotion, and report greater dampening than non-depressed indi-viduals. We had no clear predictions about how self-reportedattempts to amplify positive emotion (self-focus and emotion-focus on the RPA) would relate to euthymic depression.

Method

Participants

Participants were 151 undergraduate students at The Universityof New South Wales who participated in the study in return forcourse credit. To determine depression status and history, partici-pants were administered the Mood Module of the StructuredClinical Interview for the DSM-IV Axis I Disorders (First, Spitzer,Gibbons, & Williams, 1996). Any participant who endorsed themania screening question was not invited to take part in the study,thereby ruling out individuals with bipolar spectrum disorders.Consistent with prevalence rates of remitted depression in anundergraduate sample, following the initial recruitment phase,there were a greater number of never-depressed participants(Kessler et al., 2005). Therefore, to increase the sample size of therecovered depressed group, suitable individuals were identified byspecifying a history of depression as necessary for study inclusion,which was verified by administration of the SCID-IV. A similarstratified recruitment method for identifying formerly depressedindividuals within a student sample has been used in previousresearch (Ehring et al., 2010).


Beck Depression Inventory e Second Edition (BDI-II; Beck et al.,1996). The BDI-II is a 21-item self-report measure of depressionseverity over the previous two weeks. The BDI-II possesses strongpsychometric properties, including internal consistency of .92. Weused the BDI-II rather than the MASQ-S primarily for practicalreasons as it is substantially shorter than theMASQ-S and exploringthe specificity of any effects to anhedonia was not the principal aimof Study 2. Using the BDI-II also provides the benefit of establishingthe generalisability of our Study 1 results across different self-reportmeasures of depression symptoms and to make comparisons toexisting research that relied on the BDI-II (e.g., Raes et al., 2009).

Structured Clinical Interview for DSM-IV e Mood Module (SCID-IV;First et al., 1996). The SCID-IV is a semi-structured interview that iswidely used in clinical research to diagnose DSM-IV (Diagnostic andStatistical Manual of Mental Disorders, Fourth Edition, AmericanPsychiatric Association, 1994) Axis 1 psychological disorders. Themood module was administered to assess current and previousMajor Depressive Episodes (MDEs). Any participant that met criteriafora currentMDEwasexcluded (n¼4). Participantswere allocated tothe never-depressed group if they reported no symptoms consistentwith a diagnosis of current or past MDE (n¼ 90). For inclusion in therecovered depressed group, participants needed to report symptomsconsistent with at least one previous MDE but not have experiencedthese symptoms in past month (n ¼ 57). The sample recruited re-ported relatively high levels of depressive symptoms based on theBDI-II. While it is common for formerly depressed individuals toexperience subthreshold residual symptoms (Judd et al., 2000) wedecided to exclude highly symptomatic individuals as a way toexamine a more fully-remitted sample in the between-group anal-yses. Accordingly, participants that were experiencing symptoms inthe moderate range on the BDI-II (>19), were excluded (n ¼ 24).There were 123 participants in the final sample (n¼ 82 in the never-depressed group and n ¼ 41 in the recovered sample).

Previously Used Measures e The ACS and RPA were used exactlyas described in Study 1.

Procedure

The data from were collected as a part of two separate, largerexperimental studies. The clinical interview and questionnaires


were completed prior to all experimental manipulations. Afterproviding written informed consent, participants were tested indi-viduallyandadministered themoodmodule of the SCID-IV to screenfor current andpast depression. Participantswere then instructed tocomplete the questionnaire battery that included the ACS, RPA andBDI-II. When they had finished, participants completed the relevantexperiment and at its conclusion, were thanked for their time andfully debriefed. This study was approved by the University of NewSouth Wales Human Research Ethics Advisory Panel.

Results


Descriptive information is presented in Table 3. There were nodifferences between the recovered depressed and never-depressedgroup according to gender, age, ethnicity or depressive symptoms(all ps > .05).

Group analyses

A series of analyses of variance (ANOVAs) were conducted tocompare the groups on the ACS and the RPA. The formerlydepressed group scored more highly than did never-depressedindividuals on the ACS for general apprehension about experi-encing intense emotion, F (1,121)¼ 12.40, p< .01, h2¼ .93, althoughthere was no statistically significant group difference for the posi-tive affect subscale specifically, F (1, 121) ¼ .97, p ¼ .33, h2 ¼ .01. Thegroups did not differ on the RPA subscales that measure attempts toamplify positive emotion, specifically the emotion-focus, F (1,121) ¼ 1.05, p ¼ .31, h2 ¼ .01, or self-focus, F (1, 121) ¼ 3.05, p ¼ .08,h2 ¼ .03, subscales. However, recovered depressed individuals re-ported greater attempts to dampen PA compared with never-depressed control participants, F (1, 121) ¼ 4.74, p < .05, h2 ¼ .04.

To examine whether these group differences were driven bysubthreshold residual depressive symptoms, we repeated theanalysis controlling for symptom levels as measured by BDI-IIscores. Although we had excluded highly symptomatic individ-uals from the previous between-groups analyses, controlling forremaining symptoms enables a more rigorous test of whether theobserved group differences truly reflect euthymic depression, orwhether they are influenced by the presence of any residualsymptoms. An identical pattern of findings emerged, except thatthere was now only a trend towards a between-group difference fordampening, F (1, 120) ¼ 3.77, p ¼ .055, h2 ¼ .03.

Continuous analyses

Given that we recruited participants according to depressivehistory for this study, it is important to establish that the data meet


Recovered depressedn ¼ 41

Never-depressedn ¼ 82

Gender (% female) 85% 76%Age 20.68 (4.87) 19.24 (3.33)Ethnicity (% Caucasian) 59% 56%BDI-II 8.21 (5.64) 7.32 (4.54)ACS e positive affect 41.73 (1.58) 39.88 (1.09)ACS e total 153.98 (4.30) 135.45 (3.04)RPA e dampening 15.51 (.80) 13.38 (.57)RPA e emotion-focus 14.34 (.47) 14.93 (.33)RPA e self-focus 9.27 (.39) 10.10 (.27)

Note: Mean (and standard deviation) values presented. BDI-II ¼ Beck DepressionInventory-II; ACS ¼ Affective Control Scale; RPA ¼ Responses to Positive Affect.

assumptions of correlation analyses before proceeding further.Therefore, we checked that scores for the combined sample formeda single continuous distribution and were not significantly skewedin terms of depressive symptoms. Skew and kurtosis were withinacceptable ranges for the BDI-II (�3 to þ3; Streiner & Norman,1995) meaning the data were sufficiently normally distributed. Asthis was a continuous analysis, we conducted this analysis using theentire sample of individuals recruited into Study 2 (i.e. includingthose with elevated BDI-II scores; total N ¼ 147). Replicating theanalytic approach of Study 1, a series of zero-order correlations wasconducted to investigate the relationship between depressionseverity (BDI-II scores) and the ACS and RPA (see Table 4).

Consistent with Study 1 and previous findings symptoms ofdepression were correlated with overall fear of intense emotion onthe ACS, r ¼ .54, p < .01, and with the positive emotion subscale ofACS, r¼ .27, p< .01. BDI-II scores were also related to dampening ofpositive emotion, r ¼ .50, p < .001, and were inversely associatedwith the emotion-focus subscale, r ¼ �.17, p < .05, but not the self-focus subscale, r ¼ .08, p ¼ .32.

Discussion

The primary goal of Study 2 was to examine whether havinga history of depression is related to apprehension about experi-encing intense and positive emotion, as well as the regulation of PA.Individuals who had recovered from depression were moreapprehensive about experiencing intense emotion, but not specif-ically positive feelings, than their never-depressed counterparts,and also reported a greater propensity to dampen positiveemotional experience. There were no group differences on the twoamplifying strategies (self-focus and emotion-focus), although thedifference approached significance on the self-focus subscale.Overall, these results indicate that aspects of positive regulationalterations extend into the euthymic phase of depression, and mayreflect a trait like (as well as state like) propensity.

Consistent with Study 1 and attesting to the generalisability ofthese findings, in continuous analyses depressive symptoms werestrongly correlated with apprehension about experiencing intenseemotions and, specifically, positive emotion. Further, depressionseverity was associated with attempts to dampen PA, and reducedattempts to amplify PA (as measured on the emotion-focus but notthe self-focus subscale). This finding replicates previous work thathas used the BDI-II to measure positive emotion regulation strat-egies in which researchers found that symptoms were inverselyrelated to the emotion-focus but not the self-focus subscale (Raeset al., 2009). Notably, this finding contrasts to the negative associ-ation found in Study 1 between self-focus and anhedonic symp-toms, highlighting the benefit of fractionating depression into

Table 4Correlational table for Study 2.

BDI-II ACSPA

ACStotal

RPAdamp

RPAE-F

RPAS-F

BDI-II 1Affective Control (ACS)Positive Affect .27** 1Total .54** .77** 1Positive Rumination (RPA)Dampening .50*** .43** .55** 1Emotion-Focus �.17* �.03 �.16 .00 1Self-Focus �.08 �.16* �.15 .07 .66** 1

Note: BDI-II ¼ Beck Depression Inventory-II; ACS ¼ Affective Control Scale(subscales: PA ¼ Positive Affect); RPA ¼ Responses to Positive Affect (subscales:Damp ¼ Dampening, E-F ¼ Emotion-Focused, S-F ¼ Self-Focused). *** ¼ significantat the .001 level; ** ¼ significant at .01 level; * ¼ significant at .05 level.


Currentlydepressedn ¼ 14

Recovereddepressedn ¼ 15

Never-depressedn ¼ 21

Age 49.15 (14.15) 41.71 (17.43) 36.18 (13.97)Gender (% female) 78.0 60.0 43.0Ethnicity (%) 86.0 73.0 62.0MASQ-S e general

distress62.43 (19.43) 37.87 (9.64) 28.67 (4.15)

MASQ-S e anhedonicdepression

77.50 (10.73) 57.73 (16.21) 46.00 (6.05)

MASQ-S e anxiousarousal

29.71 (7.97) 20.73 (2.34) 19.24 (2.28)

BDI-II 19.71 (7.63) 5.80 (1.33) 1.76 (2.32)RPA e dampening 17.36 (1.33) 15.07 (1.29) 13.00 (1.09)RPA e emotion-focus 11.64 (.79) 14.13 (.76) 13.10 (.65)RPA e self-focus 7.93 (.68) 9.07 (.66) 9.10 (.56)

Note: Mean (and standard deviation) values presented except where stated. MASQ-S ¼ Mood and Anxiety Symptom Questionnaire e Short Form; BDI-II ¼ BeckDepression Inventory-II; RPA ¼ Responses to Positive Affect Scale.


theoretically derived separate symptom clusters to provide a morenuanced understanding of emotion regulation in the disorder.

A number of limitations deserve mention. First, our use ofa student samplemeant that participants were generally young andwell-educated.Whether the findings of this study would generaliseto an older, less-educated sample needs to be tested. Second,although we established the generalisability of the findings byusing a different symptommeasure in Study 2, the use of the BDI-IImeant that we were unable to examine the anhedonia symptomdimension specifically, as we did in Study 1. Third, it is unclear towhat extent residual depressive symptoms are driving the differ-ence between recovered and never-depressed individuals ondampening, given that this effect was only trend-level significantwhen partialling out current depression symptoms. To explore thispossibility further it would be helpful to compare currentlydepressed, formerly depressed and never-depressed individuals onmeasures of positive emotion regulation.

To address these issues, a third study was conducted, contrast-ing currently, previously and never-depressed individuals recruitedfrom a community sample and administering both the BDI-II andthe MASQ for continuous analyses. Study 3 focused exclusively onthe positive emotion regulation measure, as the issue regarding theimpact of residual depressive symptoms did not complicate theinterpretation of the apprehension towards emotion intensityfindings in Study 2.

Study 3

The goal of Study 3 was to replicate and extend Studies 1 and 2by examining positive emotion regulation in a community sampleof depressed, recovered depressed and never-depressed individ-uals. We hypothesised that the recovered depressed group wouldreport greater attempts to dampen positive emotion than never-depressed individuals, and that the currently depressed groupwould report greater attempts to dampen PA than both of the othertwo groups. Reflecting our logic in Study 1, based on limitedexisting research we did not have any clear predictions aboutdifferences that may emerge on the emotion-focus and self-focussubscales of the RPA. On the basis of findings from the contin-uous symptom measures in Study 1 we expected that overalldepression severity would be correlated with reported attempts todampen PA, but that there would be no specificity for anxiousarousal and general distress symptom clusters. Further, we pre-dicted that anhedonia would be uniquely related to reductions inthe two amplifying strategies (self-focus and emotion-focus).

Method

Participants

Participants were 50 community volunteers recruited from theMRC Cognition and Brain Sciences Participant Panel in Cambridge,UK. To determine depression status and history, participants wereadministered the Mood Module of the SCID-IV to screen for thepresence of past and current MDE (First et al., 1996).


Structured Clinical Interview for DSM-IV eMood Module (SCID-IV;First et al., 1996). The SCID-IV was used exactly as described inStudy 2. Participants were included in the current MDE group ifthey met criteria for a current MDE (n ¼ 14). For inclusion in therecovered depressed group, participants needed to report symp-toms consistent with at least one previous MDE but not haveexperienced an episode in past month (n ¼ 15). The same exclusion

criteria as was used in Study 2 was imposed to ensure that recov-ered depressed participants experiencing mild depression symp-toms were not included (all participants had a BDI-II score of <19and so no participant in the recovered group were excluded on thisbasis). A group of age comparable controls who had never experi-enced a past or current MDE were also included (n ¼ 21), all ofwhom had a BDI-II score < 9. The final sample consisted of 50participants (29 females; mean age ¼ 41.47; SD ¼ 15.74).

Previously Used Measures e The MASQ-S, BDI-II and RPA wereused exactly as described in Studies 1 and 2.

Procedure

After providing informed consent, participants were testedindividually and administered the mood module of the SCID-IV toscreen for current and past depression. Participants were instructedto complete the questionnaire battery including the MASQ-S, BDI-IIand RPA (along with other measures not reported here). Partici-pants were then thanked for their time and fully debriefed.Participants were given an honorarium of £6 per hour for their timeand a £3 contribution was made towards their travelling expenses.The studywas approved by the University of Cambridge PsychologyResearch Ethics Committee.

Results


Demographic and descriptive information is presented inTable 5. Analyses indicated that groups were comparable in termsof age, gender and ethnicity (all ps > .05). As expected, groupdifferences emerged on both depression measures (i.e., the BDI-IIand MASQ-S). For depressive symptoms (as measured by the BDI-II) there was an overall effect of group, F (2, 47) ¼ 53.05, p < .001,h2 ¼ .40, and post-hoc comparisons indicated that depressedindividuals reported more depressive symptoms than either therecovered or the never-depressed groups (ps < .01). Notably, therecovered depressed group were less symptomatic (i.e., had lowerBDI-II scores) in Study 3 (M ¼ 5.80), than the recovered depressedgroup in Study 2 (M ¼ 8.21).

For the MASQ-S subscales, groups differed on the generaldistress subscale, F (2, 47) ¼ 35.05, p < .001, h2 ¼ .60, the anxiousarousal, F (2, 47) ¼ 23.32, p < .001, h2 ¼ .50 and anhedonicdepression, F (2, 47) ¼ 33.19, p < .001, h2 ¼ .59, scales. Post-hoc


analyses indicated that for both general distress and anhedonicdepression, the depressed group reportedmore symptoms than dideither recovered depressed or never-depressed individuals(ps < .01), and recovered depressed individuals reported signifi-cantly more symptoms than never-depressed individuals (p < .05).For anxious arousal, the currently depressed group reported moresymptoms than both the recovered and never previously depressedgroups (ps < .01), but the recovered and never-depressed groupsdid not differ (p ¼ .34). That is, currently depressed participantsreported experiencing more symptoms of depression than eitherthe recovered and never-depressed groups. Further, the recovereddepressed group reported higher depression symptom levels thannever previously depressed individuals, but as indicated by themeans, these symptomswere in theminimal range. Notably, resultswere consistent across both symptom measures (i.e., BDI-II andMASQ-S).

Group analyses

To examine group differences on the RPA, a series of one-wayANOVAs were conducted. Consistent with hypotheses, a groupdifference emerged on the dampening subscale, F (2, 47) ¼ 3.24,p < .05, h2 ¼ .12. Follow-up analyses indicated that the currentlydepressed group reported greater levels of attempting to dampenPA than never-depressed individuals (p < .05). In contrast to Study2, the recovered depressed group did not differ from never-depressed group, p ¼ .24, and nor did they differ from thecurrently depressed group, p ¼ .23. However, results were in theexpected direction, with the recovered group falling in between thenever-depressed and currently-depressed groups.

Interestingly, groups did not differ on the self-focus subscale, F(2, 47) ¼ 1.04, p ¼ .36, h2 ¼ .04, but there was a trend for groupdifferences on the emotion-focus subscale, F (2, 47) ¼ 2.56, p ¼ .08,h2 ¼ .09. While the presence of a trend precludes follow up anal-yses, an examination of the means suggests that the currentlydepressed group were less likely than never-depressed or recov-ered participants to attempt to intensify positive emotion.

Continuous analysis

As in Study 2, we needed to establish that the data pooled acrossgroups in this Study met the assumptions of correlational analyses.Accordingly, prior to continuous analyses we checked that thescores for the combined sample formed a single continuousdistribution and were not significantly skewed. Skew and kurtosiswerewithin acceptable ranges for mood symptoms as measured byeach of the mood variables (i.e., between �3 and 3; Streiner &Norman, 1995) with the exception of skewedness of the BDI-II

Table 6Zero order (and partial) correlations for Study 3.

BDI-II MASQ-SGD

MASQ-SAA

BDI-II 1Depression/Anxiety Symptoms (MASQ)General Distress .85*** 1Anxious Arousal .71*** .61*** 1Anhedonic Depression .75*** .78*** .66***Positive Rumination (RPA)Dampening .45*** .33* (.14) .30* (�.04Emotion-Focus �.25 �.09 (.29*) �.27 (�.1Self-Focus �.18 �.23 (�.14) �.17 (.05

Note: Zero-order correlations and (partial correlations controlling for other twoMASQ-S fSymptom Questionnaire (subscales: GD ¼ General Distress, AA ¼ Anxious Arousal,Damp ¼ Dampening, E-F ¼ Emotion-Focused, S-F ¼ Self-Focused). *** ¼ significant at .0

scores. Accordingly, Spearman’s rho correlations were calculatedfor this measure.

To examine the relationship between anxiety/depressionsymptoms and the use of strategies to regulate positive emotion,a series of zero-order correlations were conducted (coefficientsreported in Table 6). Replicating results from the Study 1, therewere significant associations between attempts to dampen positiveemotion and all three symptom dimensions of the MASQ-S (i.e.,general distress, r ¼ .33, p < .05; anxious arousal, r ¼ .30, p < .05;anhedonic symptoms, r ¼ .52, p < .001), as well as depressivesymptoms as measured on the BDI-II, r ¼ .45, p < .001. As expected,attempts to intensify positive emotion were not associated withgeneral distress or anxious arousal subscales, and this was also thecase for depression symptoms on the BDI-II (ps > .10). Notably, andagain consistent with the findings of Study 1, anhedonic depressionsymptoms were inversely related to both the emotion-focus,r ¼ �.32, p < .05, and self-focus, r ¼ �.31, p < .05, subscales. Thatis, the higher their level of anhedonic symptoms, the less likelyparticipants were to report using strategies to intensify theirexperience of positive emotion.

Taking the same analytic approach as in Study 1, partial corre-lations were conducted to control for the other two symptomdimensions on the MASQ-S as a way to examine whether there wasa unique relationship between anhedonic depression symptomsand attempts to regulate positive emotion. When partial correla-tions were conducted to control for the other two symptomdimensions, the relationship between dampening and generaldistress was no longer significant, nor was there an associationbetween anxious arousal and dampening (ps> .05). However, evenwhen controlling for general distress and anxious arousal symp-toms, there was still a large and significant association betweenanhedonic symptoms and dampening, r ¼ .44, p < .01. As measuredby the emotion-focus subscale, there was a significant uniqueinverse association between anhedonic depression symptoms,r ¼ �.33, p < .05, and a positive relationship between this scale andgeneral distress, r ¼ .29, p < .05, but no association with anxiousarousal, p > .10. For the self-focus subscale that also measuresattempts to intensify positive emotion, there were no associationswith any of the symptom measures (all ps > .10).

Discussion

Study 3 explored positive emotion regulation strategies incurrently depressed, formerly depressed, and never-depressedindividuals. Consistent with findings of Study 2, the groups didnot differ in their attempts to intensify their experience of PA. Inline with hypotheses, depressed individuals reported greaterattempts to dampen PA than never-depressed individuals. Contraryto predictions and the findings of Study 2, the recovered depressed

MASQ-SAD

RPAdamp

RPAE-F

RPAS-F

1

4) .52*** (.44**) 15) �.32* (�.33*) �.15 1) �.31* (�.22) �.17 .61*** 1

actors) presented. BDI-II¼ Beck Depression Inventory-II; MASQ¼Mood and AnxietyAD ¼ Anhedonic Depression); RPA ¼ Responses to Positive Affect (subscales:01 level; ** ¼ significant at .01 level; * ¼ significant at .05 level.


group did not differ statistically from either the depressed or never-depressed group; the means indicated that recovered depressedparticipants scored in themid-range between the two other groupsin their attempts to dampen positive emotion.

It is possible that this failure to detect a statistical differencebetween the recovered depressed and never-depressed groups inStudy 3 may have been a consequence of low levels of power, giventhat the sample size was considerably smaller than in Study 2. Thatsaid, the effect size for the difference in dampening between therecovered depressed and never-depressed group in Study 3 wasnegligible (h ¼ .05), illustrating that increased power is unlikely toyield significant results. Therefore the results of Study 3 suggestthat current symptoms (rather than simply having a depressivehistory) are more closely linked to alterations in the use of positiveemotion regulation strategies.

In the case of disturbed positive emotion regulation strategies inrecovered depressed individuals (e.g., findings of Study 2), thedifference between recovered and never-depressed individuals wasrelatively small in magnitude (i.e., effect size of .04). Our datasuggest that this difference is likely to be driven by residualdepression symptoms rather than reflecting an altered propensityto dampen positive emotion in the euthymic phase of the disorder,as residual symptoms were greater in the recovered-depressedgroup in Study 2 than in Study 3. Moreover, when controlling forresidual symptoms in Study 2, group differences were no longersignificant e providing further support for our interpretation thatdifferences in emotion regulation are linked to symptoms ratherthan to having a depressive history.

In addition to conducting a between-group analysis, a secondaryaim of Study 3 was to examine the generalisability of the correla-tional findings obtained in the first two studies. Replicating theirresults, we showed that depression symptoms measured using theBDI-II and the MASQ-S shared a large and significant correlationwith attempts to dampen positive emotion. Further, dampening ofPAwas related to anhedonia, indicating this is a depression specificprocess. This provides further evidence supporting the relationshipbetween dampening and anhedonia that approached significancein Study 1.

With respect to the subscales that measure attempts to intensifypositive emotion, an inverse association between anhedoniasymptoms and the emotion-focus subscale emerged. That is, greaterlevels of anhedoniawere associatedwith decreased attempts to up-regulate the experience of positive emotion. While the relationshipbetween anhedonia and the self-focus subscale was in the sameexpected direction, it did not reach significance, in contrast to ourfindings in Study 1. These findings underscore the theoretical andclinical value of differentiating symptomdimensions and examiningthe relation between these dimensions and clinically importantvariables (such as attempts to regulate positive emotion) rather thansolely relying on a global measure of depression severity such as theBDI-II.

General discussion

The aim of this series of studies was to investigate the rela-tionship between depression and the use of regulatory tendenciesin response to positive emotion. Our findings extend the existingliterature in this area in some important ways. First, in order toexamine PA more broadly than had been done previously, weassessed apprehension about experiencing intense emotion and PA,in addition to attempts to dampen or amplify positive emotion.Second, we explored whether the relationships observed werespecific to depression symptoms, or are shared by other symptomtypes (ie., anxiety). Third, we extended previous continuous studiesby contrasting individuals with a current, past or no history of

major depressive disorder, making it possible to explore whetherpositive emotion regulation deficits persist in the euthymic phaseof depression.

In Study 1, we replicated the previous demonstration thatsymptoms of dysphoria are related to dampening of PA, andextended this to demonstrate that this was also the case withrespect to apprehension about experiencing intense emotion andPA. The fact that we found this effect using a different measure ofdepressive symptoms than has been used previously (e.g., Feldmanet al., 2008) attests to the robust nature of this association. Inter-estingly, we also found a specific association between anhedonicsymptoms and reduced attempts to amplify positive emotionalexperience e something that has not been reported previouslyowing to the use of depression symptom measures that do notdifferentiate symptom dimensions (e.g., Raes et al., 2012).

In Study 2, having a history of depression was related to bothdampening and apprehension about experiencing intense emotion.However, when the effects of depressive symptoms were removed,recovered and never-depressed individuals did not significantlydiffer in their self-reported attempts to dampen positive emotion(although this difference approached significance). Guided by thisindication that an individual’s responses to PA might be moreclosely tied to symptoms than to the fact that they have a history ofdepression, in Study 3 we took a more focused approach andexamined responses to PA in a community-recruited clinicalsample. We found that depressed individuals had a greatertendency to dampen positive emotion than their never-depressedcounterparts. A recovered depressed group fell in the middle ofthese two groups, but did not significantly differ from either.Accordingly, the propensity to dampen positive emotion appears tobe more problematic in acute depression than it is in remitteddepression. When such a difference does emerge, it tends to bemoremarked in thosewith residual dysphoric symptoms. Althoughresearch on this issue is in its infancy, based on our findings, wepropose that focusing on adaptive emotion regulation strategiesmay be most helpful for acutely depressed individuals and recov-ered depressed individuals that have marked residual (and partic-ularly anhedonic) symptoms.

In summary, across three studies symptoms of depression wereassociated with apprehension towards and attempts to dampenexperiences of PA. Further, individuals who were currentlydepressed responded differently to PA compared to healthy indi-viduals; specifically, depressed individuals reported attempting todampen this experience. This extends previous findings that reliedon continuous measures of depression severity (e.g. Feldman et al.,2008), by confirming that clinically depressed groups also showalterations in how they try to regulate positive emotion.

It is noteworthy that there was some evidence of these effectsbeing relatively specific to the anhedonic symptoms of depression.In particular, the positive relationships between anhedonicdepression and dampening that approached significance in Study 1and reached significance in Study 3, even when controlling forgeneral distress and arousal symptoms. Moreover, anhedonicsymptoms were uniquely related to less emotion-focus in bothStudies 1 and 3. In light of this evidence linking anhedonia to thedown-regulation of PA, the next step will be to identify the direc-tional nature of this association. That is, whether the reducedcapacity to experience pleasure leads individuals to try to dampenpositive emotion, or whether efforts to dampen positive emotionlead to attenuated experience of positive affect is unknown. Onceexperimental work is conducted to identify the directional linkbetween these variables, focused clinical inventions can be devel-oped to target the factor that is driving the effect.

It is concerning that depressed individuals (especially thosewhoexperience anhedonic depressive symptoms) endorse maladaptive


attitudes towards experiencing positive emotion, andwhen they doexperience these emotions, report engaging strategies in order todown-regulate their experience of it. Clearly, this has potential tolimit the benefits that patients can derive from existing treatmentcomponents that focus on PA; e.g., pleasant activity scheduling.While gold-standard evidence-based treatments for depressionsuch as cognitive behavioural therapy focus on alleviating andreducing negative emotional experience (Beck, Rush, Shaw, &Emery, 1979), the findings of this and other studies (e.g., Feldmanet al., 2008; Raes et al., 2012) present an emerging case for PA tobe more strongly targeted in treatment. That is, if individuals whoexperience depressive disorders employ strategies to down-regulate positive emotion, treatments designed to increase posi-tive emotion would be of little value without first addressingthoughts and behaviours that are held by patients in regard toexperiencing PA. Interestingly, there has been a recent call fortherapeutic approaches to teach patients how to engage withpositive material (Dunn, 2012; Wood & Tarrier, 2010). If depressionis to be better treated in the future, ways to modify maladaptiveattitudes towards PA, and methods to teach patients how toadaptively regulate PA will need to be developed. Of relevance arepromising findings from a recent trial that evaluated the efficacy ofmindfulness-based cognitive therapy in preventing relapse whichdemonstrated that mindfulness training was not only associatedwith reduced residual depression symptoms, but led to increasedexperience of positive emotion and enhanced responding to plea-surable activity (Geschwind et al., 2011). One possibility is thatmindfulness might bolster positive affect by encouraging a non-judgemental attitude towards emotional experience (and hencereduce the use of dampening in response to positive affect). Thisproposal awaits empirical test in future research.

A number of limitations with the present studies deservemention. First, as is the case when using cross-sectional designs, noinferences can bemadewith respect to causality.While the findingsreported by Raes et al. (2012) demonstrate that attempts to dampenPA are predictive of depressive symptoms, whether this is also thecase in a clinical sample and for apprehension towards experiencingpositive affect will need to be tested using longitudinal and exper-imental designs. Forexample, individuals couldbe encouraged to tryto dampen positive emotion in the laboratory and the impact thatthis has on subjective and physiological responses to a positivemood induction could be evaluated. Second, the administration ofonly the moodmodule of the SCIDmeans that important diagnosticinformation such as the presence of comorbid conditions or medi-cation status is not known and whether such characteristics wouldinfluence the data therefore cannot be ascertained. In particular,another way to establish specificity of the effects to depressionwould be to contrast pure depressed groups to pure anxious groups,defined on the basis of structured clinical interviews. In practice,however, very few pure presentations of anxiety and depression arefound in the clinic, and so the dimensional approach used here toexplore specificity arguably has greater clinical validity. Moreover,previous attempts to examine specificity using a pure groups designhas met with mixed success (see Dunn et al., 2009, 2010 for furtherdiscussion of this issue). Third, the sole reliance on self-report dataacross the three studies means the findings may be subject todemand effects. However, it is unclear howwe could have assessedcognitive variables such as appraisals and attitudes without usingself-report methods.

To conclude, our study has contributed to the growing recog-nition of the role of PA in depression and underscores the need forcontinued examination of the role of positive emotion regulation indepression. We have presented three studies in which weemployed undergraduate, clinical and community samples andhave shown that being clinically depressed or having marked

(particularly anhedonic) symptoms is related to apprehensionabout, and attempts to dampen, PA. These positive emotion regu-lation difficulties only persist in individuals with a history of pastdepression if they present with marked residual symptoms.Whether these maladaptive processes can be successfully targetedin treatment will need to be addressed by future research.

Acknowledgements

This study was supported by an Australian Postgraduate Awardto Aliza Werner-Seidler, and also received some support from anAustralian Research Council Discovery Grant (DP0984791) awardedto Michelle Moulds. Michelle Moulds is supported by an AustralianResearch Fellowship from the Australian ARC Council. BarnabyDunn’s involvement was supported by the UK Medical ResearchCouncil (U1055.02.002.00001.01). The idea for this study camefrom a working visit of Barnaby Dunn to Sydney, Australia, fundedby the Royal Society International Outgoing Short Visit scheme. Thefirst two studies were conducted in Sydney by AW-S under thesupervision of MM, the third study was conducted in Cambridge byRB under the supervision of BD.

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an investigation of the relationship between positive affect regulation and depression

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