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Cognitive-Behavioral Therapy_ Nature and Relation2016

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Cognitive-Behavioral Therapy
  Cognitive-Behavioral Therapy: Nature and Relationto Non-Cognitive Behavioral Therapy Lorenzo Lorenzo-Luaces John R. KeefeRobert J. DeRubeis University of Pennsylvania Since theintroduction ofBeck ’ scognitivetheory of emotionaldisorders, and their treatment with psychotherapy, cognitive-behavioral approaches have become the most extensivelyresearched psychological treatment for a wide variety of disorders.Despitethis,therelativecontributionofcognitivetobehavioral approaches to treatment are poorly understoodand the mechanistic role of cognitive change in therapy iswidely debated. We critically review this literature, focusingon the mechanistic role of cognitive change across cognitiveandbehavioraltherapiesfordepressiveandanxietydisorders. Keywords:  cognitive-behavioral therapy; cognitive theory;psychotherapy processes; depression; anxiety T HE ORIGIN OF COGNITIVE - BEHAVIORAL THERAPIES (CBTs) as a family of interventions can be traced tothe advent of behavioral treatments for psychopa-thology in the 1950s and, later, the so-called “ cognitive revolution ”  of the 1950 – 1960s (Dobson,2009).Consequently,CBTsblendtechniques thatareemphasized in behavioral therapies (BTs) and cogni-tive therapies (CTs). However, there remains skepti-cism regarding the relative contributions of CTstrategies to BT strategies in promoting symptomchange within the CBTs (Longmore & Worrell,2007).Additionally,criticshaveassertedthatchangesin thinking are not mechanisms of change in CBTs(e.g., Kazdin, 2007), calling into question whetherthereis anykind of contribution of the  “ cognitive ” incognitive-behavioral therapy.Despite debate regarding their active treatmentcomponents as well as working mechanisms, CBTscontinue to be the most widely studied forms of therapy (Hofmann, Asmundson, & Beck, 2013). Auniquely appealing aspect of CBTs is that their theo-ries of therapeutic change comport well with mostmodern conceptualizations of psychopathology. Inthis review, we attempt to reconcile skepticismregarding the relative contribution of CT strategiestoBT,aswellasthemechanismsthataccountfortheirefficacy. First, we provide a very brief historical over-viewoftheoriginsofCBTanddiscussthesupportforthe cognitive vulnerability models to depression andanxiety disorders. We discuss methodological chal-lenges in psychotherapy research that have impededa more thorough understanding of the relative con-tributions of cognitive to behavioral techniques. Wethen focus most of our discussion on research on thecognitivemechanismsofchangeinCT,BT,andCBTsfor depression and anxiety disorders.We use the terms  cognitive therapy  (CT) andcognitive techniques to refer to behaviors therapistsengage in that are targeted towards changing thecontent or process of thoughts, inferences, inter-pretations, cognitive biases, and cognitive schemas. 1  Available online at ScienceDirect  Behavior Therapy 47 (2016) 785 – regarding this article should be addressed toLorenzo Lorenzo-Luaces, University of Pennsylvania, Departmentof Psychology, 3720 Walnut Street D20, Philadelphia PA 19104;e-mail: 0005-7894/© 2016 Association for Behavioral and Cognitive Therapies.Published by Elsevier Ltd. All rights reserved. 1 The terms  “ cognitive therapy ”  (CT) and  “ cognitive-behavioraltherapy ”  (CBT) are often used interchangeably. We believe this issomewhat unfortunate in that it might be informative to reserve theterm CT to a set of interventions within the broader family of CBTsthat are more  “ purely ”  cognitive in nature. However, throughout thearticle, when we refer to findings in studies of CT or CBT, we areadheringtothelabelthestudyauthorsuse.Additionally,weuseCBTs,in plural, to refer to the family of cognitive-behavioral therapies.  These interventions can include Socratic question-ing, examining the evidence for and against beliefs,cognitive restructuring, and adopting alternativecore beliefs. We use the terms  behavior therapy (BT) and behavioral techniques to refer to behav-iors therapists engage in that are targeted towardsa change in observable behavior, including  in vivo exposure, imaginal exposure, and activity sched-uling. We use cognitive-behavioral therapies in theplural (CBTs)torefertothefamilyofinterventionsto which CT and BT belong, and in the singular,CBT,torefertoatreatmentpackagethatcombinescognitive and behavioral techniques. By  cognitivechange , we refer to changes in the content of thoughts, inferences, interpretations, and cognitivebiases. By  behavioral change , we refer to changesin behavior, such as increasing the frequency of selected behaviors (e.g., approaching feared stimuli,engaging with pleasurable activities) or decreasingthe frequency of other behaviors (e.g., safetybehaviors). We include in our paper a discussion of issues related to the conceptualization and measure-mentofcognitivevs.behavioralinterventionsaswellas cognitive vs. behavioral mechanisms of changeand conclude with a summary and with recommen-dations for future research. Cognitive Therapy: Nature and Relation toBehavioral Therapy Behavioral therapies emerged in the 1950s – 1960s(O ’ Donohue & Noll, 1995). The behavioralmodels emphasized maladaptive learning and self-sustaining behaviors as key to the maintenance of psychopathology. This made behavioral changethe obvious target of treatment, an approach thatwas in stark contrast to the previously dominantpsychoanalytic models. Under psychoanalysis,pathological behavior was seen to reflect dysfunc-tion in underlying psychic structures. Behavioralchange was thus seen as surface-level  “ symptomreduction ”  that did not address underlying prob-lems. BTs proved very effective, particularly in thetreatment of phobias and more circumscribedstates of anxiety. Principles of associative learningwere used to account for the efficacy of theseinterventions. To the behaviorists, learning hada specific meaning: an overt change in behavior(e.g., approaching a previously avoided stimulus)in the absence of symptoms (e.g., without display-ing the fear reaction). This definition avoided “ mentalistic ”  terms. Although early behavioralmodels featured theoretical accounts focused onassociative learning, nonassociative learning, in-cluding habituation, was also seen as important.Newer behavioral models also focus on inhibitorylearning (Craske et al., 2008).CT emerged in the context of the so-called cogni-tive revolution (Beck, 1991; O ’ Donohue, Ferguson,& Naugle, 2003) from the writings of  Ellis (1962), who described a form of therapy known as rational-emotive therapy, and Beck (1963). The cognitivemodelsofEllisandBeckfocusedoninferentialerrorsleading to maladaptive views of one ’ s self, world,and the future. According to Beck, cognitive biasesandmaladaptivecognitivecontentaretheproductof the activation of cognitive schemas that typicallydevelopearlyinlife.UnlikeBTs,whichwereinitiallysuccessful in specific phobias and circumscribedanxieties, CTs were focused on depressotypic pre-sentations and more generalized anxiety. Early inhiswriting,Beckrecognizedthathiscognitivetheoryof psychopathology, which gave a central role tocognition in the etiology of disorder, contrastedwith behavioral theories of psychopathology. In hishighly cited article,  “ Cognitive Therapy: Natureand Relation to Behavioral Therapy, ”  Beck (1970)describedimportantdifferencesbetweenthe theories that underlie BT and CT while recognizing areas of overlap in the performance of the  therapies.  Similar-ities include that both therapies deal with issues inthepresent,aresymptom-focused,andrequireactivetherapist contribution.Beck (1970) recognized differences betweenbehavioral and cognitive approaches. He appliedtheprinciplesofhisthennascentcognitivetheorytoaccount for the mechanisms of action of systematicdesensitization, a BT. He concluded that the cog-nitive model  “ provides a greater range of conceptsfor explaining psychopathology as well as themode of action of therapy. ”  That is, Beck made adistinction between the nature of the therapeuticinterventions (i.e., cognitive vs. behavioral) andtheir working mechanisms in providing a cognitiveaccount of the effects of a behavioral intervention.Beck ’ s paper would become one of the early reflec-tions on the relative contributions of cognitive tobehavioral strategies and the relevant mechanismsof change. Although Beck has provided two up-dates to his cognitive model (Beck, 1996; Beck &Haigh, 2014), its basic tenets remain largely intact:that the distinction between different forms of psy-chopathology can be traced to differences in thelocus of the cognitive pathology and that cognitivechange,regardlessofhowthischangeisachieved,isintegral to symptom change. Cognitive Vulnerability to Depressionand Anxiety Basic research supports the notion that cognitivevulnerabilities confer risk to the onset and main-tenance of psychopathology (see Mathews &MacLeod, 2005). Attentional biases to threatening 786  lorenzo-luaces et al.  stimuli, along with overestimation of threat, havebeen implicated in the etiology of anxiety disor-ders (Bar-Haim, Lamy, Pergamin, Bakermans-Kranenburg, & Van Ijzendoorn, 2007). Biasesassociated with depression include difficulties dis-engagingfromnegativematerial,sustainedorsym-metrical attention to negative, relative to positive,stimuli(Kircanski&Gotlib,2015),negative biasesin the appraisal of life events (Mehu & Scherer,2015), symmetric memory for negative vs. neutralor positive information (Kircanski & Gotlib,2015), and negative schemas about the self thatfoster maladaptive and negative thinking (Beck &Haigh, 2014).Overall, existing research is supportive of cog-nitive vulnerability models of affective disorders.For example, cross-cultural research consistentlysuggests that, on average, healthy individuals havea bias towards optimistic thinking that is notfound in individuals who are depressed and who,instead,haveabiastowardsmorenegativethinking(Mezulis, Abramson, Hyde, & Hankin, 2004).Similarly, in a meta-analytic review of 172 studiesexamining biases towards threatening stimuli,Bar-Haim et al. (2007) found that anxious partic-ipants are biased to attend to threatening stimuli,relative to nonanxious participants ( d   = 0.45). Thecausal role of these cognitive vulnerabilities, par-ticularly in depression, has been questioned partlybecause most of the early research on this matterwas correlational in nature (see Ingram et al.,2006). Findings from prospective studies, however,also support cognitive models. For example, dailyfluctuations in negative automatic thoughts havebeen found to predict subsequent negative mood,evencontrollingforpriorlevelsofautomaticthoughts(Wenze, Gunthert, & Forand, 2007; Wenze et al.,2010). Negative dysfunctional attitudes also pre-dict depressed mood following a stressor (Hankin,Abramson, Miller, & Haeffel, 2004). In onestudy, participants who were classified as being athigh cognitive risk were almost 7 times more likelyto report a major depressive episode at 2.5 yearsfollow-up, relative to those at low risk (Alloyet al.,2006).Although prospective studies provide a strongerlevel of evidence for causality than correlationalstudies, findings from these studies are still subjectto third variable confounds, making experimentaldesigns preferable. Relatively few experimentsmanipulating cognitions and assessing the effectsof the manipulation on mood have been conducted.The results of these experiments, however, areconsistent with models of cognitive vulnerability(see Mathews & MacLeod, 2005). For example, ina series of experiments, Mathews and Mackintosh(2000) reported that inducing bias in the interpre-tation of ambiguous information as threateningleads to increases in state anxiety. In another study,MacLeod et al. (2002) manipulated attention toemotionally negative information. After a stressortask, participants who had had their attentionmanipulated towards negatively valenced stimulishowed greater anxiety and depression than par-ticipants in the control group.If cognitive biases increase the risk for depressionand anxiety states, it follows that strategies thataddress these biases should result in a reduction of risk. This hypothesis has support in basic researchon emotion regulation. Webb, Miles, and Sheeran(2012) conducted a meta-analysis of 306 compar-isons of emotion regulation strategies. Strategiesthat focused on cognitive change were estimated tobethe mostconsistently effective waysofregulatingemotions ( d   = 0.36). Strategies aimed at helpingindividuals adopt more rational perspectives, as isencouraged in CT, were associated with the largesteffect ( d   = 0.45). Providing even more support forcognitive theories, studies that examine the bio-logical vulnerabilities to negative emotional statessuggest that, at the phenomenological level, biolog-ical vulnerabilities render individuals more likely toexperience negative emotional states by interferingwith their abilities to engage in cognitive reapprais-al strategies (Firk, Siep, & Markus, 2013; Lemogneet al., 2011).More research is needed that characterizes moreprecisely the nature of the cognitive biases impli-cated in depression and anxiety, especially researchthat is experimental. The relationship betweenaffective disorders and cognition is bidirectional,which must also be accounted for in theories of psychopathology. However, given the amount of evidence and the dearth of competing explanations,it can be safely asserted that the cognitive model isa valid characterization of the  etiology  of affectivedisorders. Thus, one would expect considerablesupport for the hypothesis that change in cognitionmediates symptom change in the context of psy-chotherapy. Instead, the literature contains ques-tionsaboutwhether “ weneedtochallengethoughtsin cognitive behavior therapy? ”  (Longmore &Worrell, 2007) and assertions such as  “ whatevermay be the basis of changes with CT, it does notseem to be the cognitions as srcinally proposed ” (Kazdin, 2007). Why is this so? It  ’ s Complicated Previously, we (Lorenzo-Luaces, German, &DeRubeis, 2015) have argued that disagreementamongcommentators(e.g.,Kazdin,2007;Longmore& Worrell, 2007) regarding the role of cognitive 787 cbt: nature and relation to non-c bt  change in promoting symptom change in psycho-therapy for depression emerges from differentassumptions regarding the inferences that can bedrawn from treatment studies. Below we reviewsome of these issues in psychotherapies for depres-sion and anxiety. experimental designs: additive anddismantling studies When two treatment packages are very different(e.g., psychoanalysis vs. exposure and response-prevention), it is easy and perhaps even appropriateto interpret findings from studies comparing treat-ment packages to reflect the relative efficacy of specific therapy procedures (e.g., analyzing trans-ference vs. engaging in exposure). However, whenassessingtreatments, suchasCBToreye-movementdesensitization and reprocessing (EMDR), whichcombine multiple active and overlapping elements,in this case exposure and cognitive restructuring(Tolin, 2014), it becomes more difficult to extrap-olate conclusions about therapy procedures fromoutcome data.In lieu of tightly controlled basic research, suchas the research on emotion regulation strategies(Webb et al., 2012), researchers have used compo-nent studies as a way of addressing questions aboutthe differential utility of treatment elements. Thesecomponent studies are often referred to as if theyrepresentasingleclassofstudydesign,butthereareatleasttwodifferenttypesofstudydesigns, additive and  dismantling   designs, that fall under this rubric.As described by Bell, Marcus, and Goodlad (2013),they address different kinds of questions. In additivecomponent studies, in one condition a componentis added to and compared with an already-existing,simpler treatment. Butler, Cullington, Munby,Amies, and Gelder (1984) provide an early exampleof such a study. They examined the value of addinganxiety management to exposure for social anxietyby comparing the combined treatment to exposureonly as well as to exposure plus a nonspecific filler.Their findings suggested that adding anxiety man-agement to exposure improved treatment outcomes.In dismantling designs, at least one component of amulticomponenttreatmentpackageisremovedfromthe treatment and compared to the full treatmentpackage or to the other components. For example,Foa, Steketee, Grayson, Turner, and Latimer (1984)dismantledexposureandresponse-prevention(ERP)and compared its effects with the effects of exposureonly and response prevention only. Their findingssuggestedthatERPwassuperiortoeitherofitssinglecomponents and that, for contamination fears, ex-posure alone may be more effective than response-prevention alone. Bell et al. (2013) conducted ameta-analytic review of components studies andconcluded that it is uncommon, in studies that haveused dismantling designs, for one component of a treatment to outperform another. However, instudies that have used additive designs, adding onetreatment component to another enhances positivetherapeutic outcomes, particularly in the longerterm.Ameta-analysisbyAdamsetal.(2015)addressedthe contribution of CT to BT and did not find anadded benefit of CT to BT and CBT packages.However, this meta-analysis did not differentiatebetween additive and dismantling designs. Al-though, on the face of it the component studies inthe meta-analysis by Adams et al. seem like theyprovide very conclusive answers about the superi-ority or equipotency of CT and BT, componentstudies, as they have been conducted and inter-preted, have been extremely problematic. Summar-ily reviewing some of the limitations of componentstudies, Bell et al. (2013) stated: …  Null results [in component studies] do not directlyaddress the issue of specific versus common factors becausethere is no group that received only common treatmentcomponents. [...] Component designs may also under-estimate the contributions of the component. Rehm (2009)suggested that because much improvement typically occursin the early stages of therapy, whichever component ispresented first will appear to be the most effective. Thus, thedismantled component (which is never introduced) is likelyto appear unnecessary. Component studies are also likely tobe statistically underpowered (Kazdin & Whitley, 2003) todetect the relatively small effect sizes that are likely to occurwith these types of designs. [ … ]. [A] two-group componentstudy with a presumed effect size of .24 (half the treatmentvs. placebo effect size) would require over 250 patientsin each condition to have a power of .80. Even Kazdinand Whitley ’ s (2003) higher estimate of an effect size of .45 for additive design studies would require 78 patientsin each condition. In contrast, the average sample size forthe studies included in the present meta-analysis was 23participants in each condition, which would require a largeeffect size of .84 to have a power of .80. The component methodology evidenced a surgein popularity following a landmark study by Jacobson et al. (1996). Jacobson et al. conjecturedthat the full CBT for depression package could bedivided into three components: (1) behavioralactivation (BA); (2) challenging automatic thoughts(ATs); and (3) modifying core beliefs (CBs). Tocompare the relative efficacy of these procedures,and perceiving limitations in prior work suggestingthat CT for depression was superior to BT (Shaw1977), Jacobson et al. randomized participants tothree conditions lasting a maximum of 20 sessions:(1) 100% BA; (2) a condition that could use allthe elements of BA andcould include ATwork; and(3) a condition that could use all of the elements of  788  lorenzo-luaces et al.
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