Recent findings from longitudinal studies of patients withborderline personality disorder (BPD) have challengedcommonly held conceptions regarding the long-term stabil-ity and chronic nature of this illness. Specifically, findingsfrom the Collaborative Longitudinal Personality DisordersStudy (CLPS) and the McLean Study of Adult Development(MSAD) revealed that approximately 85%–90% of patientswith BPD experienced symptom remission within a 10-yearperiod [1,2]. The rate of BPD relapse was quite low over thisextended period as well. However, these studies have alsodocumented sustained levels of impairment in this popula-tion, which resulted in more modest rates of full recovery[1,3,2]. These studies highlight the need to think longitudi-nally about the course of BPD and to consider factors thatmay facilitate or impede individuals moving across differentstages of the illness, including onset, maintenance, remis-sion, recovery, and relapse. For instance, situational changes,such as garnering more stable social support, or remissions
of co-occurring Axis I disorders were shown to predict rapidand full recovery among some patients with BPD [4].
The identification of maintenance mechanisms is criticalfor developing and refining interventions as these are theprocesses that impede individuals from moving from onsetto remission or from remission to recovery, for example.We posit that emotion dysregulation is one mechanism thatmaintains BPD features over time. Although there is noconsensus on the definition of emotion dysregulation, wedefine emotion dysregulation as deficits in the ability tomodulate the experience and expression of emotions and tomaintain goal directed behavior in the presence of intensenegative affect [5]. Thus, we conceptualize emotiondysregulation as distinct from negative affect or variabilityin affect. This conceptual distinction is important becauseemotion dysregulation reflects strategies and processes inthe face of emotion rather than merely symptoms that definepsychopathology. Emotion dysregulation has also beenprospectively linked to increases in internalizing andexternalizing psychopathology over a seven-month windowin adolescents [6], highlighting the role of emotiondysregulation as driving increases in psychopathologyover time.
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Emotion dysregulation is hypothesized by severaltheorists to play a central role in the etiology anddevelopment of BPD [7–10], giving rise to affectiveinstability (defined as marked intensity, reactivity, andvariability of moods; [11]) as well as other symptoms ofthe disorder such as identity disturbance, interpersonaldysfunction, and self-harm. According to these theoreticalmodels, transactions between an individual’s innate biolog-ical disposition toward intense emotional reactivity andinvalidating environmental inputs contribute to deficits in theacquisition of effective skills for regulating these intenseemotional experiences. In turn, deficits in emotion regulationcapacities contribute to even more intense and variableaffects (i.e., affective instability) and dysregulated cogni-tions, behaviors, and interpersonal relations. Given thetheorized role of emotion dysregulation in the developmentalpsychopathology of BPD, deficits in the ability to effectivelycope with and modulate affect may also serve to maintainfeatures of the disorder over time.
From the view of emotion dysregulation as a maintenancemechanism, once BPD emerges, emotion dysregulation maysustain BPD symptoms and associated problematic behav-iors, which is consistent with several studies illustrating alink between dysregulated emotion and behavior [12–14].For instance, in a sample of college students, the relationshipbetween BPD and dysregulated behavior (reassuranceseeking, binge-eating, and alcohol use) was mediated byrumination, anger rumination, catastrophizing, and brood-ing, even after controlling for depression [12]. Additionally,in the natural environment, rumination and intense negativeaffect predicted engaging in dysregulated behavior within 2–3 h [14]. Emerging evidence also suggests that emotiondysregulation is associated with interpersonal dysregulation.For instance, a cross-sectional study demonstrated thatemotion dysregulation fully mediated the associationbetween BPD and interpersonal problems [5]. In a recentprospective study, emotion dysregulation mediated therelationship between BPD symptoms at baseline andaggressive behavior over the course of a year.
A number of studies also support a link between emotiondysregulation and non-suicidal self-injury or suicide behav-iors. Additionally, several studies have found that in-dividuals who engage in non-suicidal self-injury reporthigher levels of emotion dysregulation [16–20]. Across twotreatment trials, within-individual improvements in emotionregulation predicted decreases in non-suicidal self-injuryover the course of 14 weeks [21], further supporting thenotion that emotion dysregulation maintains non-suicidalself-injury.
Although the link between emotion dysregulation anddysregulated behaviors has been examined generally as wellas for individuals with BPD, the role of emotion dysregula-tion in maintaining other BPD features, such as affectiveinstability and identity problems, has not yet been examined.Additionally, most studies have relied on cross-sectionalreports [8,12,13] or short prospective studies [14,22]. Hence,
within-individual changes, or increases in emotion dysregu-lation over time, as a maintenance factor for BPD featureshave yet to be determined. Finally, it is not clear whetheremotion dysregulation has a unique association with themaintenance of BPD features or if this relationship could beaccounted for by other variables that are linked to BPD andemotion dysregulation, such as interpersonal conflict[23,15,24].
The overall goal of this study was to examine emotiondysregulation (i.e., difficulties with emotion regulation) as amaintenance factor for BPD features over the course of oneyear. Specifically, we expected that the trajectory of emotiondysregulation over one year would predict BPD featureseven after controlling for BPD symptom severity and otheremotion constructs at baseline, specifically angry ruminationand depression. Additionally, we expected the relationshipbetween within-individual changes in emotion dysregulationand BPD features to hold even after controlling for within-individual changes in interpersonal conflict over the courseof the year. Our specific questions for the current study areas follows:
1. What are the patterns of growth (within-individualchanges) in difficulties in emotion regulation over thecourse of one year?
2. Does BPD symptom severity predict growth over thecourse of one year in emotion dysregulation even aftercontrolling for depression, angry rumination anddemographic characteristics?
3. Do within-person changes in emotion dysregulationaccount for the maintenance of BPD features over thecourse of one year? That is, does growth in emotiondysregulation over one year mediate the relationbetween BPD symptom severity at baseline and BPDfeatures (i.e., affective instability, identity problems,negative relationships, and self harm) one year later?Further, is mediation specific to emotion dysregula-tion, or can within-person changes in another coreproblem associated with BPD (specifically, interper-sonal conflict) also mediate these associations?
2. Method
2.1. Sample description
The study sample (N = 150) was comprised of in-dividuals from both psychiatric clinics and the communityrepresenting the full range of BPD features. Patients (n = 75)were solicited from general adult outpatient psychiatricclinics and were active in treatment at the time ofparticipation in this study. The community sample (n = 75)was recruited by telephone through the use of a random digitdialing (RDD) method coordinated by the University Centerfor Social and Urban Research at the University ofPittsburgh. RDD was utilized to yield a probability samplerepresentative of demographic characteristics reflected in theU.S. census for the Pittsburgh metropolitan area with
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oversampling of African Americans to ensure accurate racialminority representation. Participants with psychotic disor-ders, organic mental disorders, mental retardation, and majormedical illnesses that influence the central nervous systemwere excluded. At screening, participants were between theages of 21 and 60.
To capture the full range of BPD features, potentialparticipants were screened using the McLean ScreeningInstrument for Borderline Personality Disorder (MSI-BPD;[25]), a self-report questionnaire that has demonstrated goodsensitivity (0.81) and specificity (.85) for BPD diagnosis[25]. We recruited participants into three strata based on thenumber of criteria endorsed: 0–2, 3–4, or 5 or more. Themajority of participants endorsed 0–2 BPD criteria (66.7%,n = 100), 16% endorsed 3–4 criteria, and 17.3% (n = 26)endorsed 5 or more criteria. Not surprisingly, the patientsample endorsed higher levels of BPD features (53.3% ofpatients vs. 13.3% of community participants endorsed 3 ormore criteria; χ2
(1) = 38.23, p b .001). Thus, we controlledfor referral group status (0 = community participant, 1 =psychiatric patient participant) in analyses.
The mean age of the sample was 45 years (SD = 10.43)and 97 participants (64.7%) were female. Eighty-sixparticipants (57.3%) identified as Caucasian, 57 (38.0%) asAfrican American, 6 (4.0%) as more than one race, and 1(0.7%) as Asian. Four participants (2.7%) identified theirethnicity as Hispanic. In terms of marital status, 68participants (45.3%) were single and never married, 47(31.4%) were married or in a long-term committedrelationship, 33 (22.0%) were separated or divorced, and 2(1.3%) were widowed. A large majority of the sampleobtained education beyond high school (n = 109; 80.4%with at least some vocational or college training), but themajority of the sample was unemployed (n = 84; 56.0%).
2.2. Procedure
All participants were interviewed by trained research staffwith a minimum of a master’s degree in social work orclinical psychology and at least five years of assessment/clinical experience. All interviewers were blind to theparticipant’s cell assignment (i.e., community or patientstatus and MSI-BPD score). Relevant for this study, duringthe baseline assessment, interviewers administered theStructured Interview for DSM-IV Personality (SIDP-IV;[26]), and the Hamilton Rating Scale for Depression (HAM-D; [27]). Participants completed self-report questionnaires atbaseline and 3 month intervals for one year. All studyprocedures were approved by the University of PittsburghInstitutional Review Board, and participants participatedwith informed, voluntary, written consent.
2.3. Measures
2.3.1. BPD symptoms and featuresThe SIDP-IV rates each DSM-IV criterion on a four-point
strongly present). BPD symptom severity scores werecalculated by summing the 9 BPD criteria ratings from thebaseline assessment. To calculate interrater reliability, 15cases were randomly selected and rated by four judges. Theinternal consistency was deemed adequate (ICC = .80).
At the 12-month follow-up visit, participants completedthe Personality Assessment Inventory — Borderline Fea-tures Scale (PAI-BOR; [28]), which contains 24 items ratedon a four-point scale (0 = false to 3 = very true). The PAI-BOR contains four subscales that tap core features of BPD:affective instability, identity problems, negative relation-ships, and self harm. The self harm subscale taps impulsivityand impulsive behaviors more broadly and is not limited toself harm behaviors. Each subscale contains 6 items (e.g.,“My attitude about myself changes a lot” and “My relation-ships have been stormy”). Elevations on these subscales havebeen identified as markers for a diagnosis of BPD in clinicalsamples [28]. In the current sample, the internal consisten-cies of the four subscales ranged from .77 to .84 for negativerelationships and identity problems, respectively.
2.3.2. Emotion dysregulationParticipants completed the Difficulties in Emotion
Regulation Scale (DERS; [29]) at baseline and at allfollow-up appointments (3, 6, 9, and 12 months). TheDERS is a 36-item self-report measure that assessesdifficulties relating to nonacceptance of emotional re-sponses, difficulties engaging in goal-directed behavior dueto emotional responses, impulse control difficulties due toemotional responses, lack of emotional awareness, and lackof emotional clarity in the past 3 months (e.g., “I experiencemy emotions as overwhelming and out of control” and“When I’m upset, it takes me a long time to feel better”).Each item is rated on a five-point scale (1 = never to 4 =most of the time). Items were summed to create a measureof emotion dysregulation. The mean at baseline was 86.83(SD = 27.12). Across the follow-up assessments, the meanranged from 80.69 (SD = 24.73) at the 12-month follow-upto 83.60 (SD = 27.07) at the 6-month follow-up assessment.In the current sample, the internal consistency for the DERSat each study time point was .96.
2.3.3. Interpersonal conflictParticipants completed the Revised Conflict Tactics Scale
(CTS2; [30]), at all study time points. The CTS2 contained40 items that assessed the frequency of aggression andvictimization involving anyone (not just romantic partners)in the past five years (at baseline) and the past 3 months (atfollow-up visits). The types of experiences measuredincluded psychological aggression perpetration and victim-ization as well as physical assault perpetration andvictimization (e.g., “Did anyone insult or swear at you?”and “Did you throw something at anyone that could havehurt?”). All items are rated on a 7-point scale (0 = 0 times to6 = 21 or more times). Interpersonal conflict was measuredby summing the frequency ratings. The mean at baseline was
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27.98 (SD = 24.45). The mean at follow-ups ranged from5.53 (SD = 8.72) at the 12-month follow-up to 6.74 (SD =11.36) at the 9-month follow-up. In the current sample, themean internal consistency for the CTS2 was .88, rangingfrom .84 to .92 for the 3-month follow-up and baselineassessment, respectively.
2.3.4. Emotion/mood covariatesIn order to examine the specific relation between BPD
features and difficulties regulating emotions, we controlledfor potential confounds of this relationship at baseline.Specifically, we wanted to differentiate between constructsreflecting general negative affectivity (operationalized asdepression and anger rumination) at baseline and difficultiesregulating emotions as a process over time. Depression atbaseline was assessed via clinician ratings on the HAM-D,which contained 20 items rated on a 5 point scale (0 = notpresent to 4 = very severe), including items related todepressed mood and suicide. To calculate interrater reliabil-ity, 5 cases were randomly selected and rated by five judges.The internal consistency was .93.
Anger rumination was measured at baseline by the AngerRumination Scale (ARS; [31]). The scale contains 19 items(e.g., “I re-enact the anger episode in my mind after it hashappened;” “Whenever I experience anger, I keep thinkingabout it for a while”) scored on a four-point scale (1 =almost never to 4 = almost always) and the mean of itemresponses was calculated. In the current sample, the internalconsistency was .95.
2.4. Data analytic plan
We first examined descriptive statistics and intercorrela-tions between all study variables (Table 1). Next, we fit a
Table 1Descriptive statistics and correlations between study variables.
series of unconditional latent growth curve models (LGCMs)to determine the form of growth across the year-longassessment window (i.e., 5 assessment points) in emotiondysregulation and interpersonal conflict as well as examininggrowth in the dual processes simultaneously. Next, weexamined a conditional dual LGCM in which predictors ofthese trajectories were examined. These conditional modelsalso included BPD features (i.e., affective instability, identitydisturbances, negative relationships, and self harm) at theone year follow-up in order to test whether within-individualchanges in emotion regulation difficulties predicted BPDfeatures at the one-year follow-up even after controlling forwithin-individual change in interpersonal conflict. We testedthe indirect effects of BPD symptom severity at baseline tothe 12-month follow-up assessment via within-individualchanges (i.e., latent intercept and slope factors) of emotionregulation difficulties and interpersonal conflict over thecourse of one year. The tests of indirect effects allowed us toexamine whether emotion regulation difficulties weredistinctive as maintenance mechanisms of BPD featuresover the course of one year.
To handle non-normal distributions of study variables weused a robust maximum likelihood estimator [32]. Missingdata on dependent variables were handled through the use ofthe expectation maximization (EM) algorithm. We used thepercentile bootstrap to test for indirect effects as this methodis recommended for testing mediation with small samples,n b 500 [33]. All models were estimated with Mplus 7.0[34]. Model fit was evaluated using the χ2 goodness of fittest, comparative fit index (CFI), Tucker–Lewis index (TLI),and root-mean-square error of approximation (RMSEA). ForCFI and TLI, we used the conventional cutoff ≥ .90 foracceptable fit, and ≥ .95 for good fit. RMSEA values
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between .05 and .08 represent acceptable fit, whilevalues b .05 indicate good fit [35].
Finally, we tested interactions between demographiccharacteristics (i.e., gender, age, race, and group [communityor clinic]) and BPD symptoms predicting within-individualchanges in emotion dysregulation and interpersonal conflictover the course of one year. Additionally, we testedinteractions between these demographic characteristics andBPD symptoms predicting BPD features at the 12-monthfollow-up visit. None of the interactions significantlypredicted any of these outcomes, indicating that thesecharacteristics do not moderate any of our findings.
For emotion dysregulation and interpersonal conflict, wefirst fit linear models, quadratic model, and growth modelswith free time scores to determine the form of growth overthe year-long assessment window. Since these models werenot nested, we compared fit by examining the match betweenthe model estimated growth and the observed means ofscores at each assessment point as well as examiningmodification indices (c.f. [36]). To disentangle the overalllevel of emotion dysregulation from baseline measures, theintercept was fixed to the 6-month follow-up visit. The 3-month follow-up score was freed, indicating that the rate ofchange was not constant over all time points. Thus, theresulting mean of the slope factors for these scores can beinterpreted as the rate of change for a time score change ofone (rather than as the mean of the slope growth factor). Noother changes to the unconditional models resulted in achange in the interpretation of the within-individual factorscores (Table 2).
In order to test the specificity of emotion dysregulation asa maintenance factor, we also modeled the growth ofinterpersonal conflict. For interpersonal conflict, it wasnecessary for model convergence to exclude the baselineassessment from the model. This may be due to the baseline
Table 2Overall model fit and growth factors for the unconditional growth models.
All intercept and slope values are unstandardized. For emotion dysregulation, themean is the rate of change for a time score change of one. RMSEA = Root Mean SLewis Index.
⁎ p ≤ .05.⁎⁎ p ≤ .01.⁎⁎⁎ p ≤ .001.
assessment representing interpersonal conflict over the pastfive years compared to the much shorter past three-monthintervals of the remaining interpersonal conflict assessments.Again, the intercept was fixed to the 6-month follow-up. Alinear growth process was retained as the final model(Table 2).
All unconditional LGCMs fit the data well (Table 2).Emotion dysregulation decreased slightly over the course ofone year. However, the overall rate of change in interper-sonal conflict was not significant, illustrating that, onaverage, these scores remained relatively constant over thecourse of one year. All random effects (variance compo-nents) for the intercept factors were significant, highlightingthe individual variability in emotion regulation difficultiesand interpersonal conflict in the overall level (intercept).Variances for both slope factors were also significant,indicating individual variability in trajectories (slope) overtime for these scales.
For the dual process LGCM, the emotion dysregulationand interpersonal conflict LGCMs were simultaneouslyexamined. The within time-point residuals across the twoprocesses were allowed to freely co-vary (emotion dysre-gulation with interpersonal conflict at 6 month follow-up;emotion dysregulation with interpersonal conflict at9 month follow-up; etc.). The final model fit the data verywell (Table 2). The intercepts across the two processes weremoderately correlated (r = .45, p b .001), suggesting thatindividuals with emotion dysregulation also have problemswith interpersonal conflict. The slopes were not significant-ly related with each other or with intercept factors,suggesting that within-individual changes in one processwere not related to changes in the other and that overalllevel of one process did not influence the rate of change inthe other process.
3.2. Questions 2 and 3: conditioned latent growthcurve models
We examined Questions 2 and 3 simultaneously; that is,all covariates, predictors, and outcomes were simultaneously
I Intercept (6 months) Slope (Across one year)
Mean Variance Mean Variance
0 84.05⁎⁎⁎ 612.22⁎⁎⁎ −1.94⁎⁎⁎ 20.21⁎⁎
0 6.12⁎⁎⁎ 53.86⁎⁎⁎ −.33 4.59 ⁎
01. 84.07⁎⁎⁎ 612.98⁎⁎⁎ −1.94⁎⁎⁎ 19.38⁎⁎
2. 6.12⁎⁎⁎ 52.62⁎⁎⁎ −.34 4.27⁎
3-month time score was freely estimated so the interpretation for the slopequare Error of Approximation; CFI = Comparative Fit Index; TLI = Tucker
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entered into the dual LGCM of emotion dysregulation andinterpersonal conflict (c.f. Fig. 1). By including thecovariates, predictors, and outcomes simultaneously, wetested for the indirect effects (maintenance effects) ofbaseline BPD symptom severity on BPD features one yearlater via the emotion dysregulation and interpersonal conflictlatent growth curve intercept and slope factors (within-individual changes). These models were adjusted for age,gender, race, group, depression, and angry rumination.
We examined the unique effects of age, race, gender,group, depression, angry rumination and BPD features atbaseline on our latent growth factors of emotion dysregula-tion and interpersonal conflict (Table 3A). Age was related tothe interpersonal conflict intercept factor (β = −.16,p b .05), indicating that younger individuals reported moreoverall difficulties with interpersonal conflict at three-monthfollow-up. No other predictors were related to the interceptor slope factors of interpersonal conflict.
More associations were revealed between predictors andwithin-individual changes of emotion dysregulation. Mi-nority race was negatively associated with the emotiondysregulation intercept factor (β = −.20, p b .001), indi-cating that Caucasians had higher levels of many emotionregulation difficulties at baseline. Psychiatric group status,depression, and angry rumination were positively associ-ated with the intercept factors of emotion dysregulation(β’s = .21, .28, .40, p’s b .001, respectively), indicatingthat individuals in psychiatric treatment, and those withhigher levels of depression and angry rumination hadhigher overall levels of emotion dysregulation. Out of thecovariates, only depression significantly predicted theslope of emotion dysregulation, (β = −.33, p b .05),
Fig. 1. A path diagram of the conditional latent variable growth model of lack of emdisorder features (BPD features) from baseline to the 12-month follow-up assessrumination were also controlled for in this model. For ease of presentation only thewas modeled as a manifest variable (i.e., four outcome variables). The bold arrowbaseline to the 12 month follow-up assessment via within-individual patternsdysregulation; IC = interpersonal conflict.
indicating that those with higher baseline depressionexperienced faster rates of emotion dysregulation improve-ment over the course of one year. Most importantly, aftercontrolling for all covariates, BPD symptom severity atbaseline was related to emotion dysregulation intercept andslope factors (β = .19, p b .01; β = 26, p b .05, respec-tively), indicating that those with more severe BPDsymptoms at baseline experienced higher levels of emotiondysregulation as well as increases in these difficulties overthe course of one year.
To examine whether within-individual changes inemotion dysregulation maintained BPD features one yearlater, all PAI-BOR subscales (i.e., affective instability,identity disturbances, negative relationships, and self harm)at the 12-month follow-up were regressed simultaneously onthe latent variable growth factors and all covariates(Table 3B). BPD symptom severity at baseline onlypredicted self harm at the one-year follow-up (β = .19,p b .05). Further, emotion dysregulation factors (interceptsand slopes) predicted BPD features at the 12-month follow-up, indicating that within-individual levels and changes inemotion dysregulation are important predictors of thesefeatures. Specifically, the emotion dysregulation interceptand slope factors predicted affective instability (β = .45,p b .001 and β = .34, p b .001, respectively) and identitydisturbance (β = .49, p b .001 and β = .24, p b .001,respectively), indicating that level and growth (increasingdifficulties) in emotion dysregulation predict affectiveinstability and identity problems. Only the slope factorpredicted negative relationships (β = .21, p b .05) and selfharm (β = .27, p b .05), indicating that increasing difficul-ties in emotion regulation over the course of one year, but not
otion dysregulation as a unique maintenance factor of borderline personalityment. Baseline age, race, gender, recruitment group, depression, and angrylatent factors of the growth models are depicted. Additionally, each feature
s indicate expected significant indirect paths from BPD symptom severity atof emotion dysregulation over the course of 12 months. ED = emotion
Table 3Latent growth factors of emotion dysregulation as unique factors predictingBPD features.
Part 3A. Latent growth factors regressed on baseline BPD symptom severityand covariates
Estimates are standardized regression coefficients (β’s). Fit statistics for finalmodel: χ2(84) = 117.02. RMSEA = .05; CFI = .98; TLI = .96.
⁎ p b .05.⁎⁎ p b .01⁎⁎⁎ p b .001.
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higher overall levels, are predictive of interpersonaldifficulties and impulse control problems. In contrast, onlythe intercept factor of interpersonal conflict predictednegative relationships (β = .18, p b .05) and Self harm(β = .22, p b .01), indicating that overall level of interper-sonal conflict, but not changes (increases) in interpersonalconflict, is predictive of interpersonal difficulties andimpulse control problems.
Lastly, to test whether within-individual changes inemotion regulation difficulties uniquely maintained BPDfeatures over the course of one year, we examined theindirect effects of BPD features at the 12 month-follow-upregressed on BPD features at baseline via the intercepts andslopes of emotion dysregulation and interpersonal conflicteven after controlling for demographic features, depression,
and angry rumination at baseline. There was a significantindirect effect through the emotion dysregulation interceptfactor for affective instability (β = .08, p b .05; 95% CI [.02,.15]) and identity disturbance (β = .09, p b .05; 95% CI[.01, .16]), indicating that higher overall level of emotiondysregulation accounted for the stability of these BPDfeatures over the course of one year. There were nosignificant indirect effects of interpersonal conflict, suggest-ing that within-individual changes in interpersonal conflictdo not significantly maintain BPD features over the course ofone year after controlling for emotion dysregulation.
4. Discussion
The current study examined within-individual changesin emotion dysregulation as a maintenance factor of BPDfeatures over the course of one year in a sample enrichedwith BPD symptoms. Results demonstrated that, onaverage, emotion dysregulation decreased slightly overthe course of the year. However, after controlling fordemographic characteristics, depression, and angry rumi-nation, BPD symptom severity at baseline predicted higheroverall levels and increases in emotion dysregulation overtime. Further, increases in emotion dysregulation over theyear predicted greater BPD features (i.e., affective insta-bility, identity problems, negative relationships, and selfharm) at 12-month follow-up, even after controlling forconcurrent changes in interpersonal conflict. Our analysesdemonstrated the overall level of emotion dysregulationdifficulties fully mediated the association between BPDsymptom severity at baseline and both affective instabilityand identity disturbance at 12-month follow-up, suggestingthat emotion dysregulation accounted for the stability ofthese features over the course of one year. Our resultsextend previous work that has found rumination and otheraspects of emotion dysregulation to be related to hallmarkbehavioral problems in this population [20,12,14]. Thesefindings also expand on our conceptualization of emotiondysregulation as an underlying factor of the disorder to amaintenance mechanism.
Although the rate of change in emotion dysregulationpredicted all four categories of BPD features at follow-up (i.e.,affective instability, identity disturbance, negative relation-ships, and self harm), the overall level of emotion dysregula-tion only predicted affective instability and identifydisturbance. Thus, as compared to overall levels of emotiondysregulation, it appears that the chronicity and exacerbationof emotion regulation difficulties over time are predictive of abroader range of BPD features. In addition, rate of change ininterpersonal conflict did not predict BPD features at follow-up. These findings demonstrate that within-individual changesin emotion dysregulation over the course of one yearspecifically predict BPD features. However, it was not therate of change, but the overall level of emotion dysregulationthat emerged as a maintaining mechanism for BPD features,
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and specifically for affective instability and identity distur-bance. It is possible that difficulties regulating emotions, suchas deficits in strategies for identifying and modulating affectsand for controlling impulses when experiencing intenseemotions, perpetuate chaotic and variable experiences withregard to mood and sense of self, thereby serving to maintainaffective instability and identity problems over time.
Although increases in emotion dysregulation predictedmore negative relations and self harm at follow-up, emotiondysregulation did not mediate associations between BPDsymptom severity at baseline and these difficulties, suggest-ing that other processes might maintain problems withinterpersonal relations and impulsive behavior. Interestingly,BPD symptom severity at baseline directly predicted higherself harm at 12-month follow-up, even after controlling forall other predictors. In addition, overall level of interpersonalconflict over the year predicted both negative relationshipsand self harm at follow-up, which is consistent with studiesdemonstrating associations between externalized aggression,self-injurious behavior, and suicide attempts [37]. It ispossible that these difficulties may reflect greater impulsiv-ity, which may be expressed in aggression directed at self orothers [38]. These findings suggest that more severelyimpaired individuals who experience more chaotic interper-sonal relationships are at greater risk for impulsive behaviorand continued interpersonal problems a year later, even aftercontrolling for the influence of emotion dysregulation, whichserves to further exacerbate these problems.
Given that we controlled for baseline depression and angerrumination, our results are consistent with findings that theeffects of emotion dysregulation on psychopathology cannotsimply be accounted for by these general forms of negativeaffect [39]. Even though individuals with greater depressionand angry rumination had higher overall levels of emotiondysregulation, depression actually predicted faster rates ofimprovement in emotion dysregulation over the course of theyear, whereas, BPD symptom severity predicted slower ratesof improvement in emotion dysregulation over time.Although speculative, it is possible that those who reportmore negative emotions at baseline tend to bemore motivatedand engaged to make changes in their lives, which maythereby influence their rate of improvement in emotiondysregulation. Alternatively, it could be that these findingsrepresent a ceiling effect, such that an individual with highernegative emotions is restricted in terms of how much worsehe/she can get over time. Additionally, changes in emotiondysregulation had strong and consistent effects across all fourBPD features at 12-month follow-up, even after controllingfor the influence of depression, angry rumination, and BPDsymptom severity at baseline. These findings suggest that it isnot merely the experiencing of intense negative affects, butalso, chronic deficits in the ability to effectively identify,tolerate, and regulate these emotions that are predictive ofincreased BPD features over the course of one year.
Our findings with regard to patterns of change in emotiondysregulation and interpersonal conflict are similar to
previous studies finding stability of BPD features over thecourse of one year [40,41]. The slight decrease in emotiondysregulation over the year, in comparison to the lack ofsignificant change in interpersonal conflict during thisperiod, is consistent with previous studies suggesting thatproblems in social relationships are among the mostintransigent of personality disorder symptoms [42].
4.1. Strengths and limitations
The strengths of this study are the intensive repeatedassessments over the course of one year and the ability toexamine within-individual changes in putative maintainingmechanisms for BPD. This time frame has practicalimplications as a year reflects a typical course of treatmentfor most randomized controlled clinical trials. Although wecannot determine the degree of change in these constructsthat is due to treatment effects, the inclusion of communityparticipants with a range of BPD symptoms in addition topatients receiving psychiatric treatment provides someperspective on naturalistic change in these constructs acrossthese populations. Another strength of this study is therepeated assessment of interpersonal conflict over the courseof the year, which enabled us to demonstrate the specificityof changes in emotion dysregulation for predicting BPDfeatures at follow-up.
This study is not without limitations. First, we were notable to examine changes or maintenance in BPD diagnosis orDSM-IV symptoms, as these clinician-rated interviewmeasures were not re-administered at follow-up appoint-ments. Additionally, the measurement of emotion dysregula-tion, interpersonal conflict, and BPD features at 12-monthfollow-up relied on self-reports, which are susceptible to biasand shared method variance between these measures mayhave inflated associations between constructs. On a relatednote, our measure of emotion dysregulation may not havecomprehensively assessed this complex and multidimen-sional construct. For instance, this measure does not generalrumination tendencies. Although we controlled for angryrumination at baseline, we did not have repeated measures ofthis emotion-related construct and thus could not examinechange in angry rumination over the year as a potentialmaintaining mechanism. Additionally, depression and angryrumination represent only a subset of the broader range ofnegative affect experiences that could be captured with a traitmeasure of negative affect or neuroticism. Future work mayfocus on emotion regulation strategies in vivo and usingmultiple methods of assessment, including objective mea-sures such as observer ratings, psychophysiological assess-ments, neurobiological measures, and intensive repeatedassessments in daily life to examine state versus trait-likeexperiences of negative affect. Given that we have identifiedwithin-individual variability and change in emotion dysre-gulation, future research on the short-term malleability ofthis construct and its effects on short-term changes in BPDfeatures is needed.
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4.2. Clinical implications
These findings suggest that enhancing emotion regulationskills may lead to improvements in treatment, which isconsistent with previous findings of skills targeting emotionregulation resulting in improvements in features associatedwith BPD [21,43,44]. In particular, these results suggest thatattention should be focused on accepting emotions, improv-ing strategies for coping with negative emotion, andenhancing emotional clarity. Although Dialectical BehaviorTherapy [9] focuses on improving emotion regulation skillsexplicitly, other empirically supported treatments for BPDalso target emotion regulation by attending to affectiveprocesses in session, increasing the ability to recognize andlabel emotions, and improving patients’ awareness ofemotional states as precipitants to behavior [45]. It mayprove useful to carefully monitor emotion regulationcapabilities throughout the course of treatment as this maybe an important indicator that other BPD features may alsobe likely to improve over time.
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