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Cognitive Behavioral Theory Versus Rational Emotive Behavioral Theory Paper

Cognitive Behavioral Theory Versus Rational Emotive Behavioral Theory PaperCognitive Behavioral Theory Versus Rational Emotive Behavioral Theory PaperBriefly describe how cognitive behavioral therapy (CBT) and rational emotive behavioral therapy (REBT) are similar.Explain at least three differences between CBT and REBT. Include how these differences might impact your practice as a mental health counselor.Explain which version of cognitive behavioral therapy you might use with clients and why. Support your approach with evidence-based literatureSince the introduction of Beck’s cognitive theory of emotional disorders, and their treatment with psychotherapy, cognitive- behavioral approaches have become the most extensively researched psychological treatment for a wide variety of disorders. Despite this, the relative contribution of cognitive to behavioral approaches to treatment are poorly understood and the mechanistic role of cognitive change in therapy is widely debated. We critically review this literature, focusing on the mechanistic role of cognitive change across cognitive and behavioral therapies for depressive and anxiety disorders.Cognitive Behavioral Theory Versus Rational Emotive Behavioral Theory PaperKeywords: cognitive-behavioral therapy; cognitive theory; psychotherapy processes; depression; anxietyTHE ORIGIN OF COGNITIVE-BEHAVIORAL THERAPIES (CBTs) as a family of interventions can be traced to the advent of behavioral treatments for psychopa- thology in the 1950s and, later, the so-called “cognitive revolution” of the 1950–1960s (Dobson, 2009). Consequently, CBTs blend techniques that are emphasized in behavioral therapies (BTs) and cogni- tive therapies (CTs). However, there remains skepti- cism regarding the relative contributions of CT strategies to BT strategies in promoting symptom change within the CBTs (Longmore & Worrell, 2007). Additionally, critics have asserted that changes in thinking are not mechanisms of change in CBTs (e.g., Kazdin, 2007), calling into question whetherCorrespondence regarding this article should be addressed to Lorenzo Lorenzo-Luaces, University of Pennsylvania, Department of Psychology, 3720 Walnut Street D20, Philadelphia PA 19104; e-mail:© 2016 Association for Behavioral and Cognitive Therapies. Published by Elsevier Ltd. All rights reserved.there is any kind of contribution of the “cognitive” in cognitive-behavioral therapy. Despite debate regarding their active treatmentcomponents as well as working mechanisms, CBTs continue to be the most widely studied forms of therapy (Hofmann, Asmundson, & Beck, 2013). A uniquely appealing aspect of CBTs is that their theo- ries of therapeutic change comport well with most modern conceptualizations of psychopathology. In this review, we attempt to reconcile skepticism regarding the relative contribution of CT strategies to BT, as well as the mechanisms that account for their efficacy. First, we provide a very brief historical over- view of the origins of CBT and discuss the support for the cognitive vulnerability models to depression and anxiety disorders. We discuss methodological chal- lenges in psychotherapy research that have impeded a more thorough understanding of the relative con- tributions of cognitive to behavioral techniques. We then focus most of our discussion on research on the cognitive mechanisms of change in CT, BT, and CBTs for depression and anxiety disorders. We use the terms cognitive therapy (CT) andcognitive techniques to refer to behaviors therapists engage in that are targeted towards changing the content or process of thoughts, inferences, inter- pretations, cognitive biases, and cognitive schemas.1The terms “cognitive therapy” (CT) and “cognitive-behavioral therapy” (CBT) are often used interchangeably. We believe this is somewhat unfortunate in that it might be informative to reserve the term CT to a set of interventions within the broader family of CBTs that are more “purely” cognitive in nature. However, throughout the article, when we refer to findings in studies of CT or CBT, we are adhering to the label the study authors use. Additionally, we use CBTs, in plural, to refer to the family of cognitive-behavioral therapies.Cognitive Behavioral Theory Versus Rational Emotive Behavioral Theory Paper A PLAGIARISM-FREE PAPER HERE786 l o re n zo – l ua c e s et a l .These interventions can include Socratic question- ing, examining the evidence for and against beliefs, cognitive restructuring, and adopting alternative core beliefs. We use the terms behavior therapy (BT) and behavioral techniques to refer to behav- iors therapists engage in that are targeted towards a change in observable behavior, including in vivo exposure, imaginal exposure, and activity sched- uling. We use cognitive-behavioral therapies in the plural (CBTs) to refer to the family of interventions to which CT and BT belong, and in the singular, CBT, to refer to a treatment package that combines cognitive and behavioral techniques. By cognitive change, we refer to changes in the content of thoughts, inferences, interpretations, and cognitive biases. By behavioral change, we refer to changes in behavior, such as increasing the frequency of selected behaviors (e.g., approaching feared stimuli, engaging with pleasurable activities) or decreasing the frequency of other behaviors (e.g., safety behaviors). We include in our paper a discussion of issues related to the conceptualization and measure- ment of cognitive vs. behavioral interventions as well as cognitive vs. behavioral mechanisms of change and conclude with a summary and with recommen- dations for future research.Cognitive Behavioral Theory Versus Rational Emotive Behavioral Theory PaperCognitive Therapy: Nature and Relation to Behavioral TherapyBehavioral therapies emerged in the 1950s–1960s (O’Donohue & Noll, 1995). The behavioral models emphasized maladaptive learning and self- sustaining behaviors as key to the maintenance of psychopathology. This made behavioral change the obvious target of treatment, an approach that was in stark contrast to the previously dominant psychoanalytic models. Under psychoanalysis, pathological behavior was seen to reflect dysfunc- tion in underlying psychic structures. Behavioral change was thus seen as surface-level “symptom reduction” that did not address underlying prob- lems. BTs proved very effective, particularly in the treatment of phobias and more circumscribed states of anxiety. Principles of associative learning were used to account for the efficacy of these interventions. To the behaviorists, learning had a 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 behavioral models featured theoretical accounts focused on associative learning, nonassociative learning, in- cluding habituation, was also seen as important. Newer behavioral models also focus on inhibitory learning (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 cognitive models of Ellis and Beck focused on inferential errors leading to maladaptive views of one’s self, world, and the future. According to Beck, cognitive biases and maladaptive cognitive content are the product of the activation of cognitive schemas that typically develop early in life. Unlike BTs, which were initially successful in specific phobias and circumscribed anxieties, CTs were focused on depressotypic pre- sentations and more generalized anxiety. Early in his writing, Beck recognized that his cognitive theory of psychopathology, which gave a central role to cognition in the etiology of disorder, contrasted with behavioral theories of psychopathology. In his highly cited article, “Cognitive Therapy: Nature and Relation to Behavioral Therapy,” Beck (1970) described important differences between the 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 in the present, are symptom-focused, and require active therapist contribution. Beck (1970) recognized differences betweenbehavioral and cognitive approaches. He applied the principles of his then nascent cognitive theory to account for the mechanisms of action of systematic desensitization, a BT. He concluded that the cog- nitive model “provides a greater range of concepts for explaining psychopathology as well as the mode of action of therapy.” That is, Beck made a distinction between the nature of the therapeutic interventions (i.e., cognitive vs. behavioral) and their working mechanisms in providing a cognitive account of the effects of a behavioral intervention. Beck’s paper would become one of the early reflec- tions on the relative contributions of cognitive to behavioral strategies and the relevant mechanisms of 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 the locus of the cognitive pathology and that cognitive change, regardless of how this change is achieved, is integral to symptom change.Cognitive Vulnerability to Depression and AnxietyBasic research supports the notion that cognitive vulnerabilities confer risk to the onset and main- tenance of psychopathology (see Mathews & MacLeod, 2005). Attentional biases to threateningCognitive Behavioral Theory Versus Rational Emotive Behavioral Theory Paper 787cb t: n at ur e an d r el at ion to non -c btstimuli, along with overestimation of threat, have been implicated in the etiology of anxiety disor- ders (Bar-Haim, Lamy, Pergamin, Bakermans- Kranenburg, & Van Ijzendoorn, 2007). Biases associated with depression include difficulties dis- engaging from negative material, sustained or sym- metrical attention to negative, relative to positive, stimuli (Kircanski & Gotlib, 2015), negative biases in the appraisal of life events (Mehu & Scherer, 2015), symmetric memory for negative vs. neutral or positive information (Kircanski & Gotlib, 2015), and negative schemas about the self that foster 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 consistently suggests that, on average, healthy individuals have a bias towards optimistic thinking that is not found in individuals who are depressed and who, instead, have a bias towards more negative thinking (Mezulis, Abramson, Hyde, & Hankin, 2004). Similarly, in a meta-analytic review of 172 studies examining 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). The causal role of these cognitive vulnerabilities, par- ticularly in depression, has been questioned partly because most of the early research on this matter was correlational in nature (see Ingram et al., 2006). Findings from prospective studies, however, also support cognitive models. For example, daily fluctuations in negative automatic thoughts have been found to predict subsequent negative mood, even controlling for prior levelsof automatic thoughts (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 one study, participants who were classified as being at high cognitive risk were almost 7 times more likely to report a major depressive episode at 2.5 years follow-up, relative to those at low risk (Alloy et al., 2006). Although prospective studies provide a strongerlevel of evidence for causality than correlational studies, findings from these studies are still subject to third variable confounds, making experimental designs preferable. Relatively few experiments manipulating cognitions and assessing the effects of the manipulation on mood have been conducted. The results of these experiments, however, are consistent with models of cognitive vulnerability (see Mathews & MacLeod, 2005). For example, in a series of experiments, Mathews and Mackintosh(2000) reported that inducing bias in the interpre- tation of ambiguous information as threatening leads to increases in state anxiety. In another study, MacLeod et al. (2002) manipulated attention to emotionally negative information. After a stressor task, participants who had had their attention manipulated towards negatively valenced stimuli showed 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 that address these biases should result in a reduction of risk. This hypothesis has support in basic research on emotion regulation. Webb, Miles, and Sheeran (2012) conducted a meta-analysis of 306 compar- isons of emotion regulation strategies. Strategies that focused on cognitive change were estimated to be the most consistently effective ways of regulating emotions (d = 0.36). Strategies aimed at helping individuals adopt more rational perspectives, as is encouraged in CT, were associated with the largest effect (d = 0.45). Providing even more support for cognitive theories, studies that examine the bio- logical vulnerabilities to negative emotional states suggest that, at the phenomenological level, biolog- ical vulnerabilities render individuals more likely to experience negative emotional states by interfering with their abilities to engage in cognitive reapprais- al strategies (Firk, Siep, & Markus, 2013; Lemogne et al., 2011). More research is needed that characterizes moreprecisely the nature of the cognitive biases impli- cated in depression and anxiety, especially research that is experimental. The relationship between affective 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 is a valid characterization of the etiology of affective disorders. Thus, one would expect considerable support for the hypothesis that change in cognition mediates symptom change in the context of psy- chotherapy. Instead, the literature contains ques- tions about whether “we need to challenge thoughts in cognitive behavior therapy?” (Longmore & Worrell, 2007) and assertions such as “whatever may be the basis of changes with CT, it does not seem to be the cognitions as originally proposed” (Kazdin, 2007). Why is this so?It’s Complicated Previously, we (Lorenzo-Luaces, German, & DeRubeis, 2015) have argued that disagreement among commentators (e.g., Kazdin, 2007; Longmore & Worrell, 2007) regarding the role of cognitiveCognitive Behavioral Theory Versus Rational Emotive Behavioral Theory Paper 788 l o re n zo – l ua c e s et a l .change in promoting symptom change in psycho- therapy for depression emerges from different assumptions regarding the inferences that can be drawn from treatment studies. Below we review some of these issues in psychotherapies for depres- sion and anxiety.experimental designs: additive and dismantling studies When two treatment packages are very different (e.g., psychoanalysis vs. exposure and response- prevention), it is easy and perhaps even appropriate to 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, when assessing treatments, such as CBT or eye-movement desensitization and reprocessing (EMDR), which combine 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 from outcome 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 about the differential utility of treatment elements. These component studies are often referred to as if they represent a single class of study design, but there are at least two different types of study designs, additive and dismantling designs, that fall under this rubric. As described by Bell, Marcus, and Goodlad (2013), they address different kinds of questions. In additive component studies, in one condition a component is added to and compared with an already-existing, simpler treatment. Butler, Cullington, Munby, Amies, and Gelder (1984) provide an early example of such a study. They examined the value of adding anxiety management to exposure for social anxiety by comparing the combined treatment to exposure only 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 a multicomponent treatment package is removed from the treatment and compared to the full treatment package or to the other components. For example, Foa, Steketee, Grayson, Turner, and Latimer (1984) dismantled exposure and response-prevention (ERP) and compared its effects with the effects of exposure only and response prevention only. Their findings suggested that ERP was superior to either of its single components 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 and concluded that it is uncommon, in studies that have used dismantling designs, for one component of a treatment to outperform another. However, in studies that have used additive designs, adding one treatment component to another enhances positive therapeutic outcomes, particularly in the longer term. A meta-analysis by Adams et al. (2015) addressedthe contribution of CT to BT and did not find an added benefit of CT to BT and CBT packages. However, this meta-analysis did not differentiate between additive and dismantling designs. Al- though, on the face of it the component studies in the meta-analysis by Adams et al. seem like they provide very conclusive answers about the superi- ority or equipotency of CT and BT, component studies, as they have been conducted and inter- preted, have been extremely problematic. Summar- ily reviewing some of the limitations of component studies, Bell et al. (2013) stated:… Null results [in component studies] do not directly address the issue of specific versus common factors because there is no group that received only common treatment components. […] Component designs may also under- estimate the contributions of the component. Rehm (2009) suggested that because much improvement typically occurs in the early stages of therapy, whichever component is presented first will appear to be the most effective. Thus, the dismantled component (which is never introduced) is likely to appear unnecessary. Component studies are also likely to be statistically underpowered (Kazdin & Whitley, 2003) to detect the relatively small effect sizes that are likely to occur with these types of designs. […]. [A] two-group component study with a presumed effect size of .24 (half the treatment vs. placebo effect size) would require over 250 patients in each condition to have a power of .80. Even Kazdin and Whitley’s (2003) higher estimate of an effect size of .45 for additive design studies would require 78 patients in each condition. In contrast, the average sample size for the studies included in the present meta-analysis was 23 participants in each condition, which would require a large effect size of .84 to have a power of .80.The component methodology evidenced a surge in popularity following a landmark study by Jacobson et al. (1996). Jacobson et al. conjectured that the full CBT for depression package could be divided into three components: (1) behavioral activation (BA); (2) challenging automatic thoughts (ATs); and (3) modifying core beliefs (CBs). To compare the relative efficacy of these procedures, and perceiving limitations in prior work suggesting that CT for depression was superior to BT (Shaw 1977), Jacobson et al. randomized participants to three conditions lasting a maximum of 20 sessions: (1) 100% BA; (2) a condition that could use all the elements of BA and could include AT work; and (3) a condition that could use all of the elements of  789cb t: n at ur e an d r el at ion to non -c btBA, work on ATs, with a required minimum of 8 sessions devoted to CB work. In this study, across various metrics, no statistically significant between- conditon differences in outcome were reported. These findings have generally been misinterepreted as indicating that BA is the active component in CBT for depression and that the interventions provided in the cognitive components were inert, thus presenting a major challenge to Beck’s cogni- tive theory (Longmore & Worrell, 2007). Data from assessments of therapists’ adherencespeak to the construct validity of the experiment by Jacobson et al. (1996). Although, in terms of the absolute frequency with which techniques were conducted, behavioral work was nearly as frequent in the CB condition as they were in BA, the relative frequency of BA procedures was greater in BA than in AT and CB. In the follow-up analysis of the trial, Jacobson and colleagues went on further to note:Cognitive Behavioral Theory Versus Rational Emotive Behavioral Theory Paper… by definition, participants in the BA condition received more BA than did those in the other treatment conditions. Although one might be tempted to infer from this study that cognitive interventions are nonessential, our study does not directly address the validity of such an interpretation. All we can conclude is that adding cognitive interventions to BA is no more effective than using that time to add more BA. (Gortner, Gollan, Dobson, & Jacobson, 1998, p. 381, emphasis added)In other words, if the findings from Jacobson et al. (1996) are taken to mean that CT procedures are inert, a corollary emerges that was not tested in their design: that a BA condition that allowed only 6 or 7 sessions (one-third of the 20 sessions) should yield outcomes equivalent to a 20-session course of BA. Thus, per Gortner et al. (1998), the only hypotheses regarding behavioral treatment of de- pression that could have been tested with the study design were that BA is: (a) superior to, or (b) not inferior to, a cognitive-behavioral treatment. As there were no significant differences between the treatments, the most that can be said is that the BA condition, in the context of a study with low power, was not shown to be inferior to treatments that divided time between cognitive components and behavioral ones. Very few dismantling studies have directlycompared “pure” cognitive and behavioral inter- ventions. The handful of studies that have com- pared purely behavioral (e.g., activity scheduling) to purely cognitive (e.g., cognitive restructuring) treatments for depression have tended to find little if any difference in the acute effects of cognitive versus behavioral treatments (Mazzucchelli, Kane, & Rees, 2009). In one study comparing BA to CT (Dimidjian et al., 2006), although there were no statistically significant differences between the twotreatments, BA was more effective than CT or medications for individuals who were severely depressed. In the BA condition, 76% of more severely depressed participants met criteria for re- sponse or remission, compared to 48% of patients in CT and 49% in antidepressant medications. Among the less severely depressed patients, response rates on the BDI were 56% in CT, 60% in BA, and 40% in ADM. Coffman et al. (2007) identified patients from the Dimidjian et al. trial who exhibited a pattern of “extreme non-response” (ENR) in CT (approximately one-fourth of those assigned to CT) and noted that none of the patients assigned to BA evidenced an ENR. At baseline, the CT ENR patients were more severely depressed, evidenced more functional impairment, and reported more problems with their primary support group. They interpreted these findings to suggest that, relative to CT and medications, BA may be particularly effective for patients with severe depression that is accompanied by interpersonal dysfunction. However, it should be noted that the advantage of BA over CT dissipated entirely across the trial’s 2-year follow-up (Dobson et al., 2008). Moreover, to our knowledge, the findings of Dimidjian et al. (2006) have not been replicated. An attempt to replicate Coffman et al.’s ENR findings in a separate sample of depressed patients (Koenig, Jarrett, Gallop, Barrett, & Thase, 2014) treated with CT found a low (6%) rate of nonresponse, and severity, functional impairment, and interpersonal problems were not good predictors of nonresponse. Finally, Webb et al. (2013) found that the therapists in the Dimidjian et al. (2006) trial implemented CT with a relatively more behavioral than cognitive focus, compared to therapists from other CT trials. The effect of cognitive change strategies in Beck’sC(B)T for depression has also been questioned, on the basis that much of symptom change occurs early in treatment (Ilardi & Craighead, 1994). However, it has been shown in several studies that CBT therapists use cognitive change techniques as early as session one (Braun, Strunk, Sasso, & Cooper, 2015; Conklin & Strunk, 2015; Strunk, Brotman, & DeRubeis, 2010). In fact, at least one therapy manual (i.e., Muñoz & Miranda, 1986) addresses cognitive change exclusively for several sessions before addressing behavior. In anxiety disorders, among the studies includedin the meta-analyses of Adams et al. (2015) and Bell et al. (2013), only eight studies (Barlow, Rapee, Brown, 1992; Borkovec, Newman, Pincus, & Lytle, 2002; Emmelkamp & Beens, 1991; Marks, Lovell, Noshirvani, Livanou, & Thrasher, 1998; Mattick, Peters, & Clarke, 1989, Szymanski, & O’Donohue, 1995; White, Keenan, & Brooks, 1992; Williams,Cognitive Behavioral Theory Versus Rational Emotive Behavioral Theory Paper 790 l o re n zo – l ua c e s et a l .& Falbo, 1996) compared a purely cognitive treatment condition to a purely behavioral condi- tion. Among these eight studies, we conducted a random effects meta-analysis (settings as per IntHout, Ioannidis, & Borm, 2014). There was no statistically significant difference in end-state pri- mary outcomes between “pure” CT and “pure” BT (higher values indicate superiority for CT; g = 0.010 [95% CI: -0.203 to 0.222], SE = 0.090, t = 0.106, p = 0.919; see Fig. 1). There was minimal heterogeneity between effect sizes included in the meta-analysis (Cochrane’s Q = 3.371, df = 7, p = 0.849; 14.90% heterogeneity), consistent with an account that trial-level findings were generally equivocal, with few meaningful between-trial dif- ferences in effects. The results of these studies suggest that CTs can be as effective as BTs in the treatment of anxiety disorders. Although exposur- e-based treatments are considered the mainstay of CBTs for anxiety, other meta-analytic reviews also suggest that ERP, CBT, and CT are about equally effective across a range of anxiety disorders (Norton & Price, 2007; Ougrin, 2011). This led Arch and Craske (2008) to propose that cognitive restructuring is a form of exposure whose effects are possibly cognitively mediated. One exception to the pattern of equivalence in CT and BT is that, for OCD, ERP appears to be more effective than CTFIGURE 1 Meta-analytic plot of the comparative efficacy of “pure” C Adams et al. (2015) and Bell et al. (2013). Positive values indicate a super effect size of the end-scores of a trial primary outcome measure, sele prepared by LLL. No notable changes in effect size or statistical significanc meta-regressing the Hedge’s g of the pre-treatment score differences bet not detect the presence of a significantly asymmetrical funnel plot pot Copas’ (2010) test of publication bias proffered a similar between-grou(Fisher & Wells, 2005; McLean et al., 2001; but see Öst, Havnen, Hansen, & Kvale, 2015). Another exception is that, in social anxiety, the CT com- ponent appears to add to the efficacy of exposure (Hofmann, 2004; Mayo-Wilson et al., 2014; Ougrin, 2011; but see Chambless & Gillis, 1993). It has been suggested that, because with someanxiety disorders cognitive techniques may add little or nothing to the efficacy of BTs, exposure and other BTs are best conducted without the questioning of beliefs or the provision of other CT procedures (e.g., Arch & Craske, 2008). Indeed, a favored approach to the treatment of simple phobias has been and continues to be one that relies primarily or only on BT techniques (Wolitzky-Taylor, Horowitz, Powers, & Telch, 2008; but see Choy, Fyer, & Lipsitz, 2007). Some BTs, like the ones focused on relaxation, do not even directly address feared stimuli which may be taken to call into question the need to engage in cognitive work. There are at least two things to keep in mind regarding these comparisons. First, there is no evidence that these therapies lead to greater symptom reduction than CT (e.g., Borkevec et al., 2002; Mayo-Wilson et al., 2014). Second, the fact that these therapies, which do not directly address thinking, are effective does not directly inform about their mechanisms. Recall that Beck (1970) accounted for the efficacy ofT compared to “pure” BT in anxiety disorder RCTs identified by iority of CT over BT. Hedge’s g was calculated as a between-groups cted by RJD and JRK from a results-blinded list of trial outcomes e resulted from controlling for pre-treatment severity differences by ween treatments (analyses available upon request). Egger’s test did entially indicative of publication bias (p = 0.169), and Henmi and ps effect estimate (g = 0.017).Cognitive Behavioral Theory Versus Rational Emotive Behavioral Theory Paper 791cb t: n at ur e an d r el at ion to non -c btbehavioral therapies, giving the specific example of desensitization, in cognitive terms.techniques vs. mechanisms It appears to be a frequent misunderstanding of comparative psychotherapy research, including com- ponent trials, that outcome studies inform about the mechanisms of treatments. Various authors have cautioned against conflating the efficacy of thera- peutic procedures with their mechanisms of action (e.g., Hofmann, 2008; Lorenzo-Luaces et al., 2015), and the separation between therapeutic procedures and mechanisms has long been recognized (e.g., Beck, 1970; Foa & Rauch, 2004). Jacobson et al. (1996) explained it this way:Of course, it is also possible that BA-focused treatments are more effective ways of changing the way people think than treatments that explicitly attempt to alter thinking. Perhaps the exposure to naturally reinforcing contingencies produces changes in thinking more effectively than the explicitly cognitive interventions do. (p. 303)Although it may be tempting to assume that BT and CT produce symptom change via different theorized mechanisms (see DeRubeis, Brotman, & Gibbons, 2005), they may also do so by the same mechanisms (Hofmann, 2008). It is possible that both treatments work because they change think- ing. A pattern of findings that would be consistent with this hypothesis is that both therapies change cognition and that the cognitive changes lead to symptom change irrespective of how the cognitive changes are achieved. This latter point is one of contention in the research literature because some have erroneously assumed that a cognitive theory of change implies that change in cognition leads to symptom change uniquely in CBTs (see Hollon, DeRubeis, & Evans, 1987). To the contrary, cogni- tive theories highlight the mechanistic role of cog- nition in psychopathology (Lorenzo-Luaces et al., 2015). Given that findings from comparative outcomestudies can, at best, provide food for thought about mechanisms of change, what is needed is more research on the psychological changes that account for symptom change in psychotherapy. In the con- text of component designs (e.g., Hofmann, 2004), as well as in other kinds of randomized compari- sons, investigations of the mediation of the effects of psychotherapy promise to advance the under- standing of the workings of psychotherapy.temporality One of the greatest challenge to our understanding of how BT and CT work is that most studies that explore these questions have been unable to rule outreverse causality. Inferences about causality rest on the ascertainment of the correct temporal relation of the criterion and predictor variables. One must have confidence that change on the predictor variable preceded the change in the criterion. This has sometimes been interpreted to mean that pre- post changes in an outcome measure, regressed on an index of early change, establishes temporal precedence. However, it frequently is the case that substantial portions of pre to post changes in both proposed mediator and the outcome occur early in treatment, making early measurement of the medi- ator variable a crucial step in establishing causality. Changes in the criterion variable must be assessed subsequent to the assessment of change in the mediator if the aim is to rule out reverse causality. Only a small minority of tests of relations between symptom changes and proposed mediators of those changes has conformed to this pattern.third variable confounds Even in studies with the temporal features that allow reverse causality to be ruled out, third variable con- founds can limit the inferences that can be made. Third variable confounds can never be entirely ruled out because the multitude of variables that may be confounding the relation between a therapeutic procedure, a mechanism, and symptom change are unknown and potentially unknowable. With obser- vational studies the best one can do is to test for the most plausible confounds, using the best available measures of the potentially confounding construct. Experimental designs can protect against many of the third variable confounds, but unobserved vari- ables may still act as proxies for the purported mediating construct. Yet, as noted by Kazdin (2007), most of the experimental designs in psychotherapy are manipulations of the therapy, not of the proposed mediator. In the study of change in psychotherapy, thedomains most commonly hypothesized to account for symptom change have been: common factors, especially the therapeutic alliance; cognitive change; and behavioral changes. Ideally, a study that was attempting to address questions about causality in psychotherapy would include measures or manipu- lations of these phenomena. Given that the literature is replete with studies that measure only one or two of these variables, any conclusion that can be drawn about common factors, cognitive change, and be- havioral change is necessarily tentative.statistics and mediation Another conceptual hurdle in the understanding of the relationship between therapeutic procedures,Cognitive Behavioral Theory Versus Rational Emotive Behavioral Theory Paper 792 l o re n zo – l ua c e s et a l .cognitive change, and symptom change regards the role of statistical analyses. Statistical tests cannot determine causality. It does not matter how robust the test’s statistic is or whether the test is conducted in the context of so-called “causal modeling.” The crucial matter is whether the structure of the data, which is dependent on the assessment schedule, meets the assumptions of causal models. In addi- tion, plausible third variables confounds must be ruled out. Thus, a series of carefully planned single- case studies, in which mediators are experimentally manipulated, and temporal order and third variable issues are addressed, may provide stronger evidence concerning the causal status of a mediator than would the use of more seemingly sophisticated data analyses developed in a large sample (if there is overlap in the time periods referenced in the mediator and outcome assessments). Furthermore, an assumption in the writing ofseveral commentators is that mediational tests are the sine qua non for establishing causality (see Hundt, Mignogna, Underhill, & Cully, 2013; Kazdin, 2007). As it relates to cognitive change procedures and cognitive change, in the mediation framework proposed by Baron and Kenny (1986), evidence concerning cognitive change as a mediator of symptom change is given by answers to the following questions:1. Are cognitive change procedures more effica- cious than (at least some) other procedures?2. Do cognitive change procedures generate more cognitive change than those other procedures?3. Does superiority in cognitive change account for superior symptom change in the context of cognitive change procedures vs. those other procedures?This framework for conducting tests of media- tion is widely accepted, but can easily be mis- applied. Two change procedures can result in equivalent magnitudes of changes both on the outcome variable and on a putative mediator variable. For example, when cognitive and be- havioral techniques produce equivalent outcomes, they may do so because they are equally effective at changing cognitions (or behavior). A study may find that cognitive and behavioral techniques are equally effective in changing symptoms, cogni- tion, and behavior. However, a traditional medi- ational analysis will not be informative unless a condition is included in the design and analysis that produces less change in the mediator(s) and the symptoms because there would be no effect to mediate. As regards the role of cognitive change inproducing symptom change, there are four guid- ing questions:1. Are cognitive change procedures more effica- cious in reducing symptoms than other procedures?2. Do cognitive change procedures generate more cognitive change than other procedures?3. Does cognitive change lead to symptom change?Cognitive Behavioral Theory Versus Rational Emotive Behavioral Theory Paper4. Is cognitive change a specific predictor of symptom change only in the context of cog- nitive change interventions?Although some writers have assumed that the cognitive change model implies that the answer to all of these questions should be affirmative (e.g., Longmore & Worrell, 2007), we have argued that only the third question is a test of the cognitive theory of change (Lorenzo-Luaces et al., 2015). In agreement with Jacobson et al. (1996) it is even possible that a noncognitive procedure will produce more cognitive change than an explicit cognitive focus. The question is whether cognitive change, once it has been produced, leads to symptom change.Behavioral Change Strategies, Cognitive Change, and Symptom ChangeExisting evidence largely supports cognitive chang- es as mechanisms of change in cognitive, behavior- al, and cognitive behavioral therapies. Most of this research has been conducted in the context of social anxiety, panic disorder (Smits et al., 2012), and depression (Lorenzo-Luaces et al., 2015). Below, we review evidence for the role of cognitive change in symptom change in CT, BT, and anxiety Cognitive models of social anxiety highlight the etiological role of cognitive biases in the perceived likelihood that negative social events will occur (Smits, Rosenfield, McDonald, & Telch, 2006), as well as in the overestimation of costs associated with these events (Clark & Wells, 1995). Moreover, it has been suggested that individuals with social anxiety tend to believe they are less socially desirable than they actually are (Moscovitch, 2009). The proposed cognitive mediators of outcomes insocial anxiety co-vary with symptom change in CBTs (Hofmann, 2008; Wilson & Rapee, 2005). For example, Boden et al. (2012) reported that changes in maladaptive interpersonal beliefs fully accounted for changes in social anxiety over the course of CBT for social anxiety. Hoffart, Borge, Sexton, and Clark (2009) explored four cognitive-  793cb t: n at ur e an d r el at ion to non -c btbehavioral and four interpersonal processes of change in CBT and interpersonal psychotherapy (IPT) for social phobia. The lone IPT variable that predicted symptom change, perceived acceptance by others, is arguably a cognitive construct. By con- trast, change in each of the four cognitive-behavioral variables—self-focus, estimated probability of nega- tive social events, estimated cost of negative social events, and safety behaviors—predicted changes in social anxiety. Changes in positive, but not negative, self-view have been reported to co-vary with the reduction of social anxiety symptoms following acute CBT and over a 1-year follow-up (Goldin et al., 2013). Changes in self-focused attention have also been reported to account for treatment out- comes in individual CT and in group-based CBT (Hedman et al., 2013), whereas change in negative and positive self-statements predict outcomes in ACT and CBT (Niles et al., 2014). Thus, a variety of cognitive constructs have shownassociations with symptom improvement in CT, CBT, IPT, and ACT. An issue with many of these studies, however, is that the measurement of the predictor and criterion variables is contemporane- ous. In one study that accounted for the temporal order of change in a mediator and change in out- come, Goldin et al. (2014) reported that the success (but not the frequency of use) of cognitive reappraisal strategies predicted subsequent decreases in social anxiety symptom. Decreases in social anxiety did not predict the successful use of cognitive reappraisal strategies. This study is encouraging in suggesting that cognitive process variables predict symptom change in social anxiety. However, given the large number of cognitive constructs that have been reported to co-vary with outcomes in social anxiety, it is likely that at least some of them are products rather than predictors of symptom change. Illustrat- ing this point, Smits et al. (2006) found that changes in probability biases for negative social events predicted changes in social anxiety. However, after symptoms improved, there was a reduction in patients’ estimates of the costs attributed to negative social events. This pattern of results suggests that whereas changes in probability biases were causally related to symptom change, changes in cost estimates were the consequence of symptom change. These findings were replicated successfully and tested against the therapeutic alliance as a competing predictor of change (Calamaras, Tully, Tone, Price, & Anderson, 2015). In this study, the alliance was not found to predict symptom change.Cognitive Behavioral Theory Versus Rational Emotive Behavioral Theory Paperpanic In cognitive models of panic disorder, catastrophic misinterpretations of interoceptive cues are implicat-ed in the etiology and maintenance of the pathology (Clark, 1986). Anxiety sensitivity, the attribution of negative somatic, cognitive, and social consequences to anxiety, has been specifically reported to render individuals vulnerable to panic disorder (Reiss, 1991). Additionally, panic self-efficacy, the percep- tion of one’s ability to cope with panic attacks, has also been implicated in the maintenance of the disorder (Casey, Oei, & Newcombe, 2004). In one study, fear of bodily sensations and anxietysensitivity, jointly “fear of fear,” were reported to mediate the superiority of exposure relative to a wait-list control (Smits, Powers, Cho, & Telch, 2004). Casey, Oei, Newcombe, and Kenardy (2004) reported that changes in catastrophic misinterpreta- tions, as well as changes in self-efficacy, co-varied with symptom change in CBT. Others, however, have reported that changes in self-efficacy, but not in catastrophic beliefs, correlate with symptom change (Fentz et al., 2013; Hoffart, 1995). Attending to the temporal order of cognitive andsymptom change, Teachman, Marker, and col- leagues have reported that cognitive change pre- cedes and predicts symptom change in CBT for panic (Teachman, Marker, & Clerkin, 2010; Teachman, Marker, & Smith-Janik, 2008). In one study, changes in automatic panic associations predicted changes in symptom severity (Teachman et al., 2008). In another study, changes in cata- strophic misinterpretations predicted subsequent change in overall symptom severity, panic attack frequency, panic apprehension, and avoidance behavior (Teachman et al., 2010). Gallagher et al. (2013) also provided evidence for the temporal precedence of changes in anxiety sensitivity and also found changes in self-efficacy to precede symptom change. These authors observed that overall change in anxiety sensitivity was greater than change in self-efficacy, and that changes in self-efficacy oc- curred later in treatment than changes in anxiety sensitivity. Taken together, these studies support the mediational roles of anxiety sensitivity, catastrophic misinterpretations, and panic self-efficacy as cogni- tive mediators of treatment effects in CBTs for panic disorder (Sandin et al., 2015).ptsd Current theories of posttraumatic disorder (PTSD) highlight the causal role of associations between threatening (unconditioned fear stimuli) and non- threatening (i.e., conditioned) stimuli in fear struc- tures of traumatic memories (Cahill & Foa, 2007). Additionally, trauma-related cognitions about the self, others, and the world—most commonly mea- sured with the Post-Traumatic Cognitions Inventory (PCTI; Foa, Ehlers, Clark, Tolin, & Orsillo, 1999)— Cognitive Behavioral Theory Versus Rational Emotive Behavioral Theory Paper794 l o re n zo – l ua c e s et a l .have also been implicated in the etiology and main- tenance of the disorder. In prolonged exposure (PE), changes in negativecognitions about the self have been reported to co-vary with changes in PTSD symptoms, whether or not the intervention includes cognitive restruc- turing (Foa & Rauch, 2004). In a sample of patients with a severe mental illness comorbid with PTSD, changes in posttraumatic cognitions were found to mediate the superiority of CBT relative to treatment as usual (Mueser et al., 2008). Research attending to the temporality of cognitive change and symp- tom change suggests that these findings do not reflect an epiphenomenal status for the cognitive changes. In patients who received trauma-focused CT for PTSD, weekly changes in trauma-related cognitions predicted subsequent reduction in symp- toms (Kleim et al., 2013). Similarly, using data from a sample of patients who received PE, Zalta et al. (2014) reported that session-to-session changes in trauma-related cognitions predicted subsequent changes in PTSD symptoms, but not the other way around. Thus, there is support for the cognitive model of symptom change in treatments for PTSD, although more research, with tests of additional measures of trauma-relevant cognition, would help advance our understanding of how treatments for PTSD work.ocd Cognitive theories of obsessive–compulsive disor- der (OCD) highlight the role of various cognitive variables. Overly attaching significance to one’s thoughts is central to Rachman’s influential cogni- tive theory (Rachman, 1997). Intolerance of uncer- tainty, overestimation of threat, the belief that thoughts should be controlled, inflated sense of responsibility, and perfectionism have also been implicated (Obsessive Compulsive Cognitions Working Group, 2003), with disagreement among the authors as to which cognitions are key to the etiology of OCD (Grayson, 2010; Gwilliam, Wells, & Cartwright-Hatton, 2004). There are few studies that have explored medi-ators of change in psychotherapy for OCD, a surprising state of affairs given the number of purported cognitive mediators. Interestingly, many of the studies that have been conducted have ade- quately addressed the temporal relation between the purported mediators and outcomes, with mixed results. Woody, Whittal, and McLean (2011) reported that mediational tests conducted in a pre-post fashion suggested that the superiority of CBT relative to stress training were mediated by changes in negative cognitions. However, when these authors utilized the full session-by-sessiondata available to them, changes in cognition were actually predicted by changes in symptoms rather than vice versa. An almost identical pattern of results was reported by Olatunji et al. (2013): it was symptom change that preceded and predicted changes in cognition and in avoidance behavior. Interestingly, changes in depression preceded chang- es in OCD symptoms. In a recent trial, Wilhelm, Berman, Keshaviah, Schwartz, and Steketee (2015) reported that, in CT for OCD, changes in perfec- tionism and certainty beliefs predicted subsequent change. These authors also reported that changes in maladaptive schemas related to dependency and incompetence predicted symptom improvement. Taken together, these studies do not providestrong support for a causal role of any cognitive change variable in OCD treatment. An alternative mediator to cognitive change—such as behavioral change—has not successfully emerged as a predictor of change. It is possible that a cognitive mediator accounts for change in OCD but it not well captured by existing measures. The findings that changes in depression precede changes in OCD, along with the findings that changes in thoughts of dependency and incompetence predict symptom change, may be taken to suggest that cognitions that have been more typically thought of as depressotypic may func- tion as one of the mechanisms of change in OCD treatments.Cognitive Behavioral Theory Versus Rational Emotive Behavioral Theory Papermajor depression Cognitive models of major depression highlight the role of negatively biased cognitive processes (e.g., overgeneral memory style) and content (e.g., negative schemata, dysfunctional attitudes), as well as deficiencies in the ability to use cognitive reappraisal to modulate negative moods. This liter- ature has been reviewed elsewhere (see Lorenzo- Luaces et al., 2015). Contemporaneous associations between cognitive change and symptom change during treatments for depression have been observed in numerous investigations (e.g., Cristea et al., 2015; Hundt et al., 2013). In a recent meta-analysis, for example, Cristea et al. (2015) reported a very strong correlation between symptom change and cognitive change in treatments for depression (r = 0.77). Although these findings are consistent with the proposal that cognitive change produces symptom change, they are also consistent with the converse. Support for cognitive mediation models has been obtained in studies that have attempted to address reverse causality by modeling subsequent change in depression using prior cognitive change (Forman et al., 2012; Segal et al., 1999; Segal et al., 2006; Strunk, DeRubeis, Chiu, & Alvarez, 2007; Tang & DeRubeis, 1999; Tang, DeRubeis, Beberman, &  795cb t: n at ur e an d r el at ion to non -c btPham, 2005). Although these studies provide general support for cognitive theories of change in symp- toms, no one variable has emerged as the clear predictor of symptom change in therapy. For example, Strunk et al. (2007) found that patients’ competence in behavioral strategies, automatic thoughts, and core schematic work predicted a lower risk of relapse. Given how heterogeneous depression is, it is likelythat patients differentially benefit from different interventions. Adding support for this hypothesis, Sasso et al. (2015) found that more anxious patients and those with less recurrent depression benefitted more therapists’ use of behavioral strategies than cognitive ones. By contrast, Keefe, Webb, and DeRubeis (2016) found that patients with depres- sion and personality disorders benefitted from a focus on maladaptive core beliefs but did not experience benefit from other techniques such as a focus on automatic thoughts and behavioral change.Cognitive Behavioral Theory Versus Rational Emotive Behavioral Theory Papergeneralized anxiety and specific phobias There have been relatively few investigations of the mediation of change in treatments of generalized anxiety disorder (GAD) and specific phobias. Current etiological models of GAD highlight the causal roles of intolerance of uncertainty, positive beliefs about worry, and the avoidance of emotion- al/internal experiences (including emotional con- trasts). Few studies have explored these constructs as mediators or explanatory variables in CBTs for GAD, although they each have some support in basic research (see Newman, Llera, Erickson, Przeworski, & Castonguay, 2013). Goldman et al. (2007) reported that decreases in intolerance of uncertainty preceded changes in worry over the course of treatment. Similarly, Bomyea et al. (2015) reported that changes in intolerance of uncertainty preceded and predicted change in GAD symptoms. Cognitive models of specific phobias highlightthe role of exaggerated judgments of dangerous- ness, disgust, unpredictability, and uncontrollabil- ity associated with feared stimuli (see Armfield, 2006). Additionally, these models highlight the role of low expectations for the capacity to cope with the consequences of coming into contact with the feared stimuli, which may include the ability to tolerate uncomfortable physiological sensations. In one study examining behavioral exposures vs. behavioral experiments designed to test maladap- tive beliefs, both treatments showed substantial symptom and cognitive change, and cognitive change was associated with symptom levels at posttreatment and follow-up (Raes et al., 2011).cognitive specificity There is much excitement regarding the possibility that different treatments could work via different hypothesized mechanism. Statistical tests that reveal the moderation of a predictive effect (e.g., tests of moderated mediation) may be taken as evidence for this. Although the interpretation of mediators and predictors within a treatment has been widely discussed, moderated mediation and related findings have received relatively less attention and are conse- quently less well-understood (Gelfand & DeRubeis, 2015). Various findings of this nature, however, have been reported (e.g., Cottraux et al., 2001; Hedman et al., 2013; Niles et al., 2014). Here we focus on the interpretation of moderated relations between cog- nitive change and symptom change across treatments for panic disorder. Arntz (2002) reported equal amounts of changein catastrophic interpretations following CT and BT for panic. However, posttreatment beliefs cor- related with severity of symptoms at a follow-up in CT but not in BT. In a sample of patients receiving CBT, imipramine, or combined treatment, analy- ses suggested that changes in panic-related cogni- tions, which were equal across conditions, co- varied with changes in panic severity in CBT or combined treatment but not imipramine mono- therapy (Hofmann et al., 2007). In a comparisons of capnometry-assisted respiratory training (CART) versus training in CT strategies, Meuret, Rosenfield, Seidel, Bhaskara, and Hofmann (2010) found sup- port for the therapy-specific mediators. In CART, reduced carbon dioxide in the bloodstream from hyperventilation (hypocapnia), but not cognitive reappraisal, predicted symptom change. In cognitive training, the opposite pattern was obtained; cog- nitive reappraisal, but not hypocapnia, predicted symptom change. Thus, in several studies of treatments for panicdisorder, a “non-cognitive” intervention produced similar amounts of cognitive and symptom change relative to an explicitly cognitive intervention, yet the relation of cognitive change to symptom change was only found in the cognitive intervention. It is difficult to reconcile these findings with cognitive theories of panic, or cognitive theories of psycho- pathology more broadly, because these models assume that changes in cognitive variables are mechanisms of symptom change across treatment modalities (Lorenzo-Luaces et al., 2015). One possibility is that the cognitive change variables examined play a causal role only in interactions with another variable that is present only in the treatments in which cognitive change was predic- tive of symptom change (see DeRubeis et al., 1990). For example, catastrophic misinterpretations of  796 l o re n zo – l ua c e s et a l .panic, in conjunction with increased self-efficacy, might mediate changes in both CT and respiratory training. A further possibility is that the treat- ments intervene at different stages of the patho- logical process. For example, one account of panic disorder could be that hyperventilation leads to hypocapnia, which produces dizziness and dis- comfort, which is misinterpreted, resulting in more severe panic symptoms. Breathing retraining might intervene “early” in this cycle, whereas cognitive interventions address the appraisal of bodily sensations have already been experienced. In such a case, the cognitive changes observed in breathing retraining are only a product of reduced symptoms.Cognitive Behavioral Theory Versus Rational Emotive Behavioral Theory PaperDistinguishing Cognition and Behavior Thus far in this review we have used “cognition,” “behavior,” and their adjectival forms to reflect the way previous authors have used them in discussions of therapeutic techniques or mechanisms. However, clear, consensually-agreed-upon definitions of these terms do not exist. In some cases, therapeutic procedures or mechanisms are easy to characterize as cognitive or behavioral. For example, searching for evidence for or against a belief in the context of therapy is readily seen as a cognitive procedure, just as engaging in in vivo exposure following a habituation rationale is easily seen as behavioral. However, cognitive techniques may be used to facilitate exposure (Arch & Craske, 2008), and cognitive therapists use behavioral techniques to facilitate tests of patients’ beliefs (McManus, Van Doorn, & Yiend, 2012). Thus, it behooves inves- tigators to specify what counts as cognitive or behavioral vs. what does not. Similarly, cognitive and behavioral mechanisms of therapy must be operationalized in a way that allows for falsifica- tion. Arguing that all behavioral changes must, by definition, entail cognitive changes, or that all cognition is behavior, is unlikely to lead to more valid models of psychopathology. A related issue to the conceptualization of cog-nition and behavior is their measurement. Measur- ing cognitive and behavioral activity objectively in the context of psychotherapy is a difficult enter- prise. Although self-reported measures are the most convenient way of measuring cognitive or behav- ioral change, they are subject to various biases that have been well-articulated in the research literature. It remains to be ascertained whether self-report measures are more valid ways of ascertaining cog- nitive change than behavioral change or vice-versa. Moreover, as avoidance behaviors and maladaptive cognitions are symptoms of psychopathology, assessments of both behaviors and cognitions aredifficult to disentangle, conceptually and practical- ly, from symptom measures.Recommendations for Future Research Although the existing literature allows one to draw conclusions regarding the status of cognitive and behavioral techniques, as well as the mediational role of cognitive change, more research is clearly needed, particularly research employing experimen- tal methods. Dismantling studies and randomized comparative trials only infrequently are comple- mented by mediational analyses that could help to clarify what drives change in the interventions. It will be important to conduct more experiments where interventions are compared and mediational hypotheses are tested. As Kazdin (2007) has noted, however, it is important for research to test the effects of the manipulations of mechanisms, rather than continuing a focus on the manipulation of techniques or packages of techniques. Researchers who conduct work on mediators ofchange in nonexperimental contexts should ensure that third variables and competing mediators are measured. Given that behavioral change, cognitive change, and common factors are the most frequent- ly cited mediators of symptom change, it will be important to measure and model these variables concurrently. Moreover, it might also be important to measure multiple aspects of a given construct. For example, in the behavioral domain, a reduction in safety behaviors along with behavioral exposures are both purported mechanisms of symptom change. In the cognitive domain, the multiplicity of cognitive variables that have been implicated should also be measured, particularly for disorders like depression and OCD, where multiple cognitive vulnerabilities are hypothesized to be at play. Additionally, the role of emotions and emotional arousal, whether by themselves or in interactions with other variables, needs to explored. Although non-CBT treatments have traditionally focused more on emotional experiences than CBTs (Whelton, 2004), there is evidence that clients’ in-session emo- tional involvement relates to outcomes, at least in CT for depression (Castonguay, Goldfried, Wiser, Raue, & Hayes, 1996). Hayes and colleagues (Grosse Holtforth et al., 2012; Hayes, Beevers, Feldman, Laurenceau, & Perlman, 2005; Hayes et al., 2007) have proposed, and found evidence for, a model of change in depression treatment where behavioral interventions foster emotional arousal that, when combined with cognitive processing, leads to symptom change. These findings, which can be conceptualized using the concept of cognitive- affective schemata (Beck & Haigh, 2014), warrant further exploration. Cognitive Behavioral Theory Versus Rational Emotive Behavioral Theory Paper797cb t: n at ur e an d r el at ion to non -c btMechanisms of Change: Cognitive and Behavioral TreatmentsThe suggestion that behavioral exposure is superior to cognitive restructuring alone for OCD and that cognitive restructuring adds to behavioral expo- sures for social anxiety may be dismissed, given that these are not universal observations. However, it is noteworthy that in a disorder in which cognitive procedures appear to be especially potent—social anxiety—strong evidence has been obtained for cognitive change as a mechanism of symptom change (see McMillan & Lee, 2010). By contrast, in a disorder in which cognitive procedures appear to be less potent (OCD), there is little if any evi- dence for a cognitive mechanism of symptom change. (These observations, however, should not be taken to imply that efficacy findings allow one to make claims about causal mechanisms.) Much is made and little is done about the potential for knowledge of mediator variables to inform treat- ment research, but the existing data on the cognitive mediators in mood and anxiety disorders could be used to inform treatment. For example, in the context of treatment for social phobia, treatment could be targeted especially to the perception that negative social events are likely to occur, as op- posed to treating symptoms or functioning as the targets. In broad terms, research supports cognitive vul-nerability models of depression and anxiety disor- ders. Additionally, cognitive changes appear to correlate with and predict symptom change in therapy for depressive and anxiety disorders. Given this state of the literature, it behooves researchers to characterize the exact nature of the cognitive vulnerability to psychopathology, as well as the nature of the cognitive variables implicated in symptom change. Often the differences between different cognitive vulnerability theories lie in the stage of information processing that they focus on. For example, whereas some investigators have emphasized individual differences in the propensity to attend to negative stimuli (MacLeod et al., 2002), others have focused on individual differences in interpretation of life events (Abramson, Metalsky, & Alloy, 1989). The latest characterization of the cognitive model provided by Beck attempts to represent a more integrative picture of the cognitive vulnerabilities to psychopathology (Beck & Haigh, 2014), highlighting the roles of attention, memory, interpretative biases, emotional processing, and cognitive schemata in the development of psycho- pathology. However, it may be that vulnerabilities in different stages of information processing lead to different types of psychopathology. Reviewingthe literature on cognitive biases and cognitive bias modification, Hallion and Ruscio (2011) asserted that:anxiety is associated with biases in the early, automatic stages as well as the later, strategic stages of attention (Bar-Haim et al., 2007), whereas depression is associated with [cognitive] biases only in the later stages. (e.g., Gotlib et al., 2004; Joormann, 2004)Temporal precedence of cognitive change has been easier to establish in anxiety disorders than in depressive disorders. It is possible that this reflects the temporal precedence of cognitive biases in anxiety relative to depression, thought this question merits further exploration.Conclusions As has been noted extensively (DeRubeis et al., 2005; Haaga, 2007; Kazdin, 2007), characterizing the process of change in psychotherapy is extremely challenging. Within a therapeutic orientation, a given therapeutic package will encourage a set of therapeutic procedures, such as enhancing motiva- tion for behavioral change, some of which may overlap with those of therapeutic packages, within or outside of that orientation. Factors common to different interventions may also drive symptom change, confounding the relation between specific procedures and improvement. Furthermore, a given procedure might not affect the psychological mechanism(s) it is intended to target, and might instead affect a mechanism that is not its intended target. As noted by Beck (1991), a psychotherapeuticapproach is not a dissociated collection of tech- niques, but rather a set of procedures that follow from “a comprehensive theory of psychopathology that articulates with the structure of psychothera- py” (p. 368). Thus, productive considerations of the effectiveness or validity of a procedure or mecha- nism should be linked to the theory of the disorder or pathological process in question. Critiques of a cognitive model of the development, maintenance, and resolution of psychopathology will advance the discussion insofar as they are accompanied by an alternative theory, along with proposals, and evidence, regarding alternative noncognitive mech- anisms of change. In our view, oft-cited critiques of the theoretical model that underlie CBTs (Kazdin, 2007; Hayes, 2004; Longmore & Worrell, 2007) have employed oversimplifications of the CBT model. The available data across the sciences supports cognitive models (Beck & Haigh, 2014; Hofmann et al., 2013) in suggesting that some individuals are more likely than others to be ex- posed to negative environmental stimuli, less likely to be exposed to positive stimuli, or more likely to Cognitive Behavioral Theory Versus Rational Emotive Behavioral Theory Paper798 l o re n zo – l ua c e s et a l .attend preferentially to negative information. In the contexts of stress, these individuals are more likely to experience distress and less likely to engage the kinds of reappraisal and coping strategies that would produce naturalistic recovery. Cognitive and behavioral therapies represent an attempt to activate these resources. The distinctions between behavioral and cognitive change strategies and procedures are, to some degree, artificial inasmuch as CT procedures are often used before and after behavioral exercises, and vice-versa. Moreover, the relative efficacy of these procedures, even when considered in specific contexts, does not provide dispositive evidence concerning mechanisms. To date, the most parsimonious account of change produced in psychotherapy is one that invokes the importance of changes in cognitive systems or contents. Although the research literature is limited in its ability to provide strong confirmations of the causal hypotheses embedded in cognitive theories of change, a compelling, evidence-based competing theory of change has yet to emerge.Conflict of Interest Statement The authors declare that there are no conflicts of interest.ReferencesAbramson, L. Y., Metalsky, G. I., & Alloy, L. B. (1989). Hopelessness depression: A theory-based subtype of depres- sion. Psychological Review, 96, 358–372. 10.1037/0033-295X.96.2.358Adams, T. G., Brady, R. E., Lohr, J. M., & Jacobs, W. J. (2015). A meta-analysis of CBT components for anxiety disorders. the Behavior Therapist, 38, 87–97.Alloy, L. 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August 9, 2015 ACCEPTED: February 25, 2016 AVAILABLE ONLINE: 4 March 2016 Cognitive-Behavioral Therapy: Nature and Relation to Non-Cognitive Behavioral TherapyCognitive Therapy: Nature and Relation to Behavioral TherapyCognitive Vulnerability to Depression and�AnxietyIt’s ComplicatedExperimental Designs: Additive and Dismantling StudiesTechniques vs. MechanismsTemporalityThird Variable ConfoundsStatistics and MediationBehavioral Change Strategies, Cognitive Change, and Symptom ChangeSocial AnxietyPanicPTSDOCDMajor DepressionGeneralized Anxiety and Specific PhobiasCognitive SpecificityDistinguishing Cognition and BehaviorRecommendations for Future ResearchMechanisms of Change: Cognitive and �Behavioral TreatmentsConclusionsConflict of Interest StatementReferencesCognitive Therapy: Nature and Relation to Behavior Therapy – Republished ArticleAaron T. Beck University of PennsylvaniaRecent innovations in behavior modification have, for the most part, detoured around the role of cognitive processes in the production and alleviation of symptomatology. Although self-reports of private experiences are not verifiable by other observers, these introspective data provide awealth of testable hypotheses. Repeated correlations of measures of inferred constructs with observable behaviors have yielded consistent findings in the predicted direction. Systematic study of self-reports suggests that an individual’s belief systems, expectancies, and assumptions exert a strong influence on his state of well-being, as well as on his directly observable behavior. Applying a cognitive model, the clinician may usefully construe neurotic behavior in terms of the patient’s idiosyncratic concepts of himself and of his animate and inanimate environment. The individual’s belief systems may be grossly contradictory; i.e., he may simulta- neously attach credence to both realistic and unrealistic conceptualizations of the same event or object. This inconsis- tency in beliefs may explain, for example, why an individual may react with fear to an innocuous situation even though he may concomitantly acknowledge that this fear is unrealistic. Cognitive therapy, based on cognitive theory, is designed to modify the individual’s idiosyncratic, maladaptive ideation. The basic cognitive technique consists of delineating the individual’s specific misconceptions, distortions, and maladaptive assumptions, and of testing their validity and reasonableness. By loosening the grip of his perseverative, distorted ideation, the patient is enabled to formulate hisThe preparation of this report was supported by a grant from the Marsh Foundation. Reprint requests should be sent to 202 Piersol, Hospital of University of Pennsylvania.Cognitive Behavioral Theory Versus Rational Emotive Behavioral Theory PaperThis article is a reprint of a previously published article. For citation purposes, please use the original publication details; Behavior Therapy, 1 (1970), pp 184-200.DOI of original item: 7894(70)80030-2.0005-7894/© 2016 Association for Behavioral and Cognitive Therapies. Published by Elsevier Ltd. All rights reserved.experiences more realistically. Clinical experience, as well as some experimental studies, indicate that such cognitive restructuring leads to symptom relief.TWO SYSTEMS OF PSYCHOTHERAPY that have recently gained prominence have been the subject of a rapidly increasing number of clinical and experimental studies. Cognitive therapy,1 the more recent entry into the field of psychotherapy, and behavior therapy already show signs of becoming institutionalized. Although behavior therapy has been publicized ina large number of articles andmonographs, cognitive therapy has received much less recognition. Despite the fact that behavior therapy is based primarily on learning theory whereas cognitive therapy is rooted more in cognitive theory, the two systems of psychotherapy have much in common.First, in both systems of psychotherapy the therapeutic interview is more overtly structured and the therapist more active than in other psychotherapies. After the preliminary diagnostic interviews in which a systematic and highly detailed description of the patient’s problems is obtained, both the cognitive and the behavior therapists formulate the patient’s presenting symptoms (in cognitive or behavioral terms, respectively) and design specific sets of operations for the particular problem areas. After mapping out the areas for therapeuticwork, the therapist explicitly coaches the patient regarding the kinds of responses and behaviors that are useful with this particular form of therapy. Detailed instructions are presented to the patient,1 Ellis (1957) used the label “Rational Therapy” which he later changed to “Rational-Emotive Therapy.”Cognitive Behavioral Theory Versus Rational Emotive Behavioral Theory PaperUnlabelled image 777ct : nature and relat ion to behav ior therapyfor example, to stimulate pictorial fantasies (system- atic desensitization) or to facilitate his awareness and recognition of his cognitions (cognitive therapy). The goals of these therapies are circumscribed, in contrast to the evocative therapies whose goals are open ended (Frank, 1961). Second, both the cognitive and behavior therapistsaim their therapeutic techniques at the overt symptom or behavior problem, such as a particular phobia, obsession, or hysterical symptom. However, the target differs somewhat. The cognitive therapist focuses more on the ideational content involved in the symptom, viz., the irrational inferences and premises. The behavior therapist focuses more on the overt behavior, e.g., the maladaptive avoidance responses. Both psychotherapeutic systems concep- tualize symptom formation in termsof constructs that are accessible either to behavioral observation or to introspection, in contrast to psychoanalysis, which views most symptoms as the disguised derivatives of unconscious conflicts. Third, in further contrast to psychoanalytic therapy,neither cognitive therapy nor behavior therapy draws substantially on recollections or reconstructions of the patient’s childhood experiences and early family relationships. The emphasis on correlating present problems with developmental events, furthermore, is much less prominent than in psychoanalytic psycho- therapy. A fourth point in common between these twosystems is that their theoretical paradigms exclude many traditional psychoanalytic assumptions such as infantile sexuality, fixations, the unconscious, and mechanisms of defense. The behavior and cognitive therapists may devise their therapeutic strategies on the basis of introspective data provided by the patient; however, they generally take the patients’ self-reports at face value2 and do not make the kind of high-level abstractions characteristic of psycho- analytic formulations. Finally, a major assumption of both cognitivetherapy and behavior therapy is that the patient has acquired maladaptive reaction patterns that can be “unlearned” without the absolute requirement that he obtain insight into the origin of the symptom. One of the major assets of behavior therapy hasbeen the large number of well-designed experiments that support certain of its basic assumptions. Although of more recent vintage, several systematic studies supporting the underpinnings of cognitive2 Although the patient may not be immediately aware of the content of his maladaptive attitudes and patterns, this concept is not “unconscious” in the psychoanalytic sense and is accessible to the patient’s introspection. Furthermore, unlike many psycho- analytic formulations, the inferences can be tested by currently available research techniques.therapy have also been reported (Carlson, Travers, & Schwab, 1969; Jones, 1968; Krippner, 1964; Loeb, Beck, Diggory, & Tuthill, 1967; Rimm & Litvak, 1969; Velten, 1968). The few controlled- outcome studies of cognitive therapy (Ellis, 1957; Trexler&Karst, 1969) provide preliminary evidence of the effectiveness of this therapy. There are obvious differences in the techniquesused in behavior therapy and cognitive therapy. In systematic desensitization, for example, the behavior therapist induces a predetermined sequence of picto- rial images alternatingwith periods of relaxation. The cognitive therapist, on the other hand, relies more on the patient’s spontaneously experienced and reported thoughts. These cognitions, whether in pictorial or verbal form, are the target for therapeutic work. The technical distinctions between the two systems of psychotherapy are often blurred, however. For example, the cognitive therapist uses induced images to clarify problems (Beck, 1967; 1970), and the behavior therapist uses verbal techniques such as “thought-stoppage” (Wolpe & Lazarus, 1966). The most striking theoretical difference betweencognitive and behavior therapy lies in the concepts used to explain the dissolution of maladaptive responses through therapy. Wolpe, for example, utilizes behavioral or neurophysiological explanations such as counterconditioning or reciprocal inhibition; the cognitivists postulate the modification of con- ceptual systems, i.e., changes in attitudes ormodes of thinking. As will be discussed later, many behavior therapists implicitly or explicitly recognize the importance of cognitive factors in therapy, although they donot expandon these in detail (Davison, 1968; Lazarus, 1968).Cognitive Behavioral Theory Versus Rational Emotive Behavioral Theory PaperTechniques of Cognitive Therapy Cognitive therapy may be defined in two ways: In a broad sense, any technique whose major mode of action is the modification of faulty patterns of thinking can be regarded as cognitive therapy. This definition embraces all therapeutic operations that indirectly affect the cognitive patterns, as well as those that directly affect them (Frank, 1961). An individual’s distorted views of himself and his world, for example, may be corrected through insight into the historical antecedents of his misinterpretations (as in dynamic psychotherapy), through greater congruence between the concept of the self and the ideal (as in Rogerian therapy), and through increas- ingly sharp recognition of the unreality of fears (as in systematic desensitization). However, cognitive therapy may be definedmore narrowly as a set of operations focused on a patient’s cognitions (verbal or pictorial) and on the premises, assumptions, and attitudes underlying  778 beckthese cognitions. This section will describe the specific techniques of cognitive therapy.Recognizing Idiosyncratic Cognitions One of the main cognitive techniques consists of training the patient to recognize his idiosyncratic cognitions or “automatic thoughts” (beck, 1963). ellis (1962) refers to these cognitions as “internalized statements” or “self-statements,” and explains them to the patient as “things that you tell yourself.” these cognitions are termed idiosyncratic because they reflect a faulty appraisal, ranging from a mild distortion to a complete misinterpretation, and because they fall into a pattern that is peculiar to a given individual or to a particular psychopathological state. In the acutely disturbed patient, the distortedideation is frequently in the center of the patient’s phenomenal field. In such cases, the patient is very much aware of these idiosyncratic thoughts and can easily describe them. The acutely paranoid patient, for instance, is bombarded with thoughts relevant to his being persecuted, abused, or discriminated against by other people. In the mild or moderate neurotic, the distorted ideas are generally at the periphery of awareness.3 It is therefore necessary to motivate and to train the patient to attend to these thoughts. Manypatients reporting unpleasant affects describea sequence consisting of a specific event (external stimulus) leading to an unpleasant affect. For instance, the patient may outline the sequence of (a) seeing an old friend and then (b) experiencing a feeling of sadness. Oftentimes, the sadness is inexpli- cable to the patient. Another person (a) hears about somebody having been killed in an automobile accident and (b) feels anxiety. However, he cannot make a direct connection between these two phe- nomena; e.g., there is a missing link in the sequence. In these instances of a particular event leading toan unpleasant affect, it is possible to discern an intervening variable, namely, a cognition, which forms the bridge between the external stimulus and the subjective feeling. Seeing an old friend stimulates cognitions such as “It won’t be like old times,” or “He won’t accept me as he used to.” The cognition then generates the sadness. The report of an automobile accident stimulates a pictorial image in which the patient himself is the victim of an automobile accident. The image then leads to the anxiety. This paradigm can be further illustrated by anumber of examples. A patient treated by the writer3 In obsessional neurosis, of course, the idiosyncratic ideas are central and the patient has difficulty in ignoring them.complained that he experienced anxiety whenever he saw a dog.4 He was puzzled by the fact that he experienced anxiety even when the dog was chained or caged or else was obviously harmless. The patient was instructed: “Notice what thoughts go through yourmind the next time you see a dog—any dog.”At the next interview, the patient reported that during numerous encounters with dogs between appoint- ments, he had recognized a phenomenon that he had not noticed previously; namely, that each time he saw the dog he had a thought such as “It’s going to bite me.” By being able to detect the intervening cognitions,the patient was able to understand why he felt anxious, namely, he indiscriminately regarded every dog as dangerous.He stated, “I even got that thought when I saw a small poodle. Then I realized how ridiculous it was to think that a poodle could hurt me.”He also recognized that when he saw a big dog on a leash, he thought of the most deleterious consequences: “The dog will jump up and bite out one of my eyes,” or “It will jump up and bite my jugular vein and kill me.” Within 2 or 3 weeks, the patient was able to overcome completely his long- standing dog phobia simply by recognizing his cognitions when exposed to a dog. Another examplewas providedby a college studentwho experienced inexplicable anxiety in a social situation. After being trained to examine and write down his cognitions, he reported that in social situations he would have thoughts such as, “They think I look pathetic,” or “Nobody will want to talk to me,” or “I’m just a misfit.” These thoughts were followed by anxiety. A patient complained that he was chronically angryat practically everybody whom he saw, but could not account for his angry response to these people. After some training at recognizing his cognitions, he reported having such thoughts as “He’s pushing me around,” “He thinks I’ma pushover,” “He’s trying to take advantage of me.” Immediately after experienc- ing these thoughts, he would feel angry at the individual towards whom they were directed. He also realized that there was no realistic basis for his appraising people in this negative way. Sometimes, the cognitionmay take a pictorial forminstead of, or in addition to, the verbal form (Beck, 1970). A woman who experienced spurts of anxiety when riding across a bridge was able to recognize that the anxiety was preceded by a pictorial image of her car breaking through the guard rail and falling off the bridge. Another woman, with a fear of walking alone, found that her spells of anxiety followed images of her having a heart attack and being left4 Ellis (1962) described a similar case.Cognitive Behavioral Theory Versus Rational Emotive Behavioral Theory Paper 779ct : nature and relat ion to behav ior therapyhelpless and dying on the street. A college student discovered that his anxiety at leaving his dormitory at night was triggered by visual fantasies of being attacked. The idiosyncratic cognitions (whether pictorial orverbal) are very rapid and often may contain an elaborate idea compressed into a very short period of time, even into a split second. These cognitions are experienced as though they are automatic; i.e., they seem to arise as if by reflex rather than through reasoning or deliberation. They also seem to have an involuntary quality. A severely anxious or depressed or paranoid person, for example, may continually experience the idiosyncratic cognitions, even though he may try to ward them off. Further- more, these cognitions tend to appear completely plausible to the patient.Distancing Even after a patient has learned to identify his idiosyncratic ideas, he may have difficulty in examining these ideas objectively. the thought often has the same kind of salience as the perception of an external stimulus. “distancing” refers to the process of gaining objectivity towards these cogni- tions. since the individual with a neurosis tends to accept the validity of his idiosyncratic thoughts without subjecting them to any kind of critical evaluation, it is essential to train him to make a distinction between thought and external reality, between hypothesis and fact. patients are often surprised to discover that they have been equating an inferencewith reality and that theyhave attacheda high degree of truth-value to their distorted concepts. The therapeutic dictum communicated to thepatient is as follows: Simply because he thinks something does notnecessarily mean that it is true. While such a dictum may seem to be a platitude, the writer has foundwith surprising regularity that patients have benefited from the repeated reminder that thoughts are not equivalent to external reality. Once the patient is able to“objectify”his thoughts,he is ready for the later stages of reality testing: applying rules of evidence and logic and considering alternative explanations.Correcting Cognitive Distortions and Deficiencies The writer has already indicated that patients show faulty or disordered thinking in certain circumscribed areas of experience. in these particular sectors, they have a reduced ability to make fine discriminations and tend tomake global, undifferentiated judgments. part of the task of cognitive therapy is to help the patient to recognize faulty thinking and to make appropriate corrections. it is often very useful for thepatient to specify the kind of fallacious thinking involved in his cognitive responses. Arbitrary inference refers to the process of drawinga conclusion when evidence is lacking or is actually contrary to the conclusion. This type of deviant thinking usually takes the formof personalization (or self-reference). A depressed patient, who sawa frown on the face of a passerby, thought, “He is disgusted with me.” A phobic girl of 21, reading about a womanwho had had a heart attack, got the thought, “I probably have heart disease.” A depressed woman, who was kept waiting for a few minutes by the therapist, thought, “He has deliberately left in order to avoid seeing me,” Overgeneralization refers to the process ofmaking an unjustified generalization on the basis of a single incident. This may take the form that was described in the case of the man with the dog phobia, who generalized from a particular dog that might attack him to all dogs. Another example is a patient who thinks, “I never succeed at anything” when he has a single isolated failure. Magnification refers to the propensity to exaggeratethe meaning or significance of a particular event. A person with a fear of dying, for instance, interpreted every unpleasant sensation or pain in his body as a sign of some fatal disease such as cancer, heart attack, or cerebral hemorrhage. Ellis (1962) applied the label “castrophizing” to this kind of reaction. As noted above, it is often helpful for the patientto label the particular aberration involved in his maladaptive cognition. Once the patient has firmly established that a particular type of cognition, such as “That dog is going to bite me,” is invalid, he will be equipped to correct this cognition on subsequent occasions. For example, his planned, rational response to the stimulus of a toy poodle would be, “Actually, it is just a harmless poodle and there is only a remote chance that it would bite me. And even if it did, it could not really injure me.” Cognitive deficiency refers to the disregard for animportant aspect of a life situation. Patients with this defect ignore, fail to integrate, or do not utilize information derived from experience. Such a patient, consequently, behaves as though he has a defect in his system of expectations: He consistently engages in behavior which he realizes, in retrospect, is self-defeating. This class of patients includes those who “act out,” e.g., psychopaths, as well as those whose overt behavior sabotages important personal goals. These individuals sacrifice long-range satisfac- tion or expose themselves to later pain or danger in favor of immediate satisfactions. This category includes problems such as alcoholism, obesity, drug addition, sexual deviation, and compulsion gambling.Cognitive Behavioral Theory Versus Rational Emotive Behavioral Theory Paper 780 beckThe deficient-anticipation patients show two major characteristics: First, when they yield to their wishes to engage in self-defeating, dangerous, or antisocial activities, they are oblivious of the probable consequences of their actions. At these times, they avoid thinking about the consequences by concentrating only on the present activity. They may fortify this modus operandi through an elaborate system of self-deceptions, such as “It can’t do any harm to cut loose, now.” Secondly, irrespective of howoften the individual is “burned” as a result of his maladaptive actions, he does not seem to integrate knowledge of the cause-and-effect relationships into his behavior. Therapy of such cases consists of training thepatient to think of the consequences as soon as his self-defeating wish arises. Consideration of the long-range loss must be forced into the interval between impulse and action. A patient, for instance, who continually operated his car beyond the speed limit or drove through stoplights was surprised each timehewas stoppedby a traffic officer.On interview, it was discovered that the patient was generally absorbed in a fantasy while driving—he imaged himself as a famous racing-car driver engaged in a race. Therapy at first consisted of trying to get him to watch the odometer—but without success. The next approach consisted of inducing fantasies of speeding, getting caught, and receiving punishment. At first, the patient had great difficulty in visualizing getting caught even though, in general, he could fantasize almost everything. However, after several sessions of induced fantasies, he was able to incorporate a negative outcome into his fantasy. Subsequently, he stopped daydreaming while driving and was able to observe traffic regulations. In the following case report, several cognitivetechniques directed at modifying anxiety proneness are illustrated.Cognitive Behavioral Theory Versus Rational Emotive Behavioral Theory PaperCase Report 5Mrs. G. was an attractive 27-year-old mother of three children. When first seen by the writer, she complained ofDyperiods of anxiety lasting up to 6 or 7 hr a day and recurring repeatedly over a 4-year period. She had consulted her family physician, who had prescribed a variety of sedatives, including Thorazine, without any apparent improvement. In an analysis of the cause-and-effect sequence of her anxiety, the following facts were elicited. The first anxiety episode occurred about 2 weeks after she had had a miscarriage. At that time she was bending over to bathe her 1-year-old son, and she suddenly began to feel faint. Following this episode, she had her first anxiety attack which lasted several hours. The patient could not find any explanation for her anxiety. However, when the writer5 This patient was treated in collaboration with Dr. William son.asked whether she had had any thought at the time she felt dizzy, she recalled having had the thought, “Suppose I should pass out and injure the baby.” It seemed plausible that her dizziness, which was probably the result of a postpartum anemia, led to the fear she might faint and drop the baby. This fear then produced anxiety, which she interpreted as a sign that she was “going to pieces.” Until the time of her miscarriage, the patient had been reasonably carefree and had not experienced any episodes of anxiety. However, after her miscarriage, she periodically had the thought, “Bad things can happen to me.” Subsequently, when she heard of somebody’s becoming sick, she often would have the thought, “This can happen to me,” and she would begin to feel anxious. The patient was instructed to try to pinpoint any thoughts that preceded further episodes of anxiety. At the next interview, she reported the following events:1. One evening, she heard that the husband of one of her friends was sick with a severe pulmonary infection. She then had an anxiety attack lasting several hours. In accordance with the instructions, she tried to recall the preceding cognition, which was, “Tom could get sick like that and maybe die.”2. She had considerable anxiety just before starting a trip to her sister’s house. She focused on her thoughts and realized she had the repetitive thought that she might get sick on the trip. She had had a serious episode of gastroenteritis during a previous trip to her sister’s house. She evidently believed that such a sickness could happen to her again.3. On another occasion, she was feeling uneasy and objects seemed somewhat unreal to her. She then had the thought that she might be losing her mind and immediately experienced an anxiety attack.4. One of her friends was committed to a state hospital because of a psychiatric illness. The patient had the thought, “This could happen to me. I could lose my mind.”When questioned about why she was afraid of losing her mind, she stated that she was afraid that if she went crazy, she would do something that would harm either her children or herself.It was evident that the patient’s crucial fear was the anticipation of loss of control, whether by fainting or by becoming psychotic. The patient was reassured that there were no signs that she was going psychotic. She was also provided with an explanation of the arousal of her anxiety and of her secondary elaboration of the meaning of these attacks. The major therapeutic thrust in this case was coaching the patient to recall and reflect on the thoughts that preceded her anxiety attacks. The realization that these attacks were initiated by a cognition rather than by some vague mysterious force convinced her she was neither totally vulnerable nor unable to control her reactions. Furthermore, by learning to pinpoint the anxiety-reducing thoughts, she was able to gain some detach- ment and to subject them to reality testing. Consequently, she was able to nullify the effects of those thoughts. During the next few weeks, her anxiety attacks became less frequent and less intense and, by the endof 4weeks, they disappeared completely.Cognitive Behavioral Theory Versus Rational Emotive Behavioral Theory PaperDifferences in Conceptual Framework between Behavior Therapy and Cognitive TherapyBehavior therapists conceptualize disorders of behavior and procedures for their amelioration  781ct : nature and relat ion to behav ior therapywithin a theoretical framework borrowed from the field of psychological learning theory and especially by means of concepts of classical and operant conditioning. Since these concepts are derived mainly from experiments with animals, they focus on the observable behavior of the organism. In fact, most of the published writings on behavior therapy tend to eschew inferred or hypothesized psychological states which cannot be directly observed and measured. Concepts andprinciples basedon immediate referents in the organism’s environment have advantages of parsimony, testability, quantifiability, and reliability. However, this framework does not readily accom- modate notions of internal psychological states such as thoughts, attitudes, and the like, which we commonly use to understand ourselves and other people. Cognitive therapists are more willing to use these inferred psychological states, collectively called “cognitions,” as clinical data. Consequently, large and useful sets of variables are directly taken into account. In recent years, several writers in the area ofbehavior therapy have acknowledged the importance of mediational constructs or cognitive processes in behavior therapy (Brady, 1967; Davison, 1968; Folkins, Lawson, Opton, & Lazarus, 1968; Lazarus, 1968; Leitenberg, Agras, Barlow, & Oliveau, 1969; London, 1964; Mischel, 1968; Murray & Jacobson, 1969; Sloane, 1969; Valins&Ray, 1967;Weitzman, 1967). Their cognitive formulations, however, have for the most part been brief. Substantial amplifica- tion of the nature of cognitive processes is necessary to account adequately for clinical phenomena and for the effects of therapeutic intervention (see Weitzman, 1967). A greater emphasis on the individual’s descriptionsof internal events can lead to amore complete viewof human psychopathology and the mechanisms of behavioral change. By using introspective data, the cognitive theorist has access to the patient’s thoughts, ideas, attitudes, dreams, and daydreams. These ideational productions provide the cognitive theorist with the raw materials with which he can form concepts andmodels. Such concepts are also capable of generating hypotheses amenable to controlled experiments on psychiatric patients (Loeb et al., 1967). Also, introspective data, such as dreams and cognitions, have been adapted to systematic investi- gation (Beck, 1967). Study andanalysis of the introspective data suggestthat the cognitive organization, far frombeing amere link in the stimulus response chain, is a quasi- autonomous system in its own right. Although this system generally interacts with the environment to a large extent, it may at other times be relatively independent of the environment; for example, whenthe patient is daydreaming or in the grip of an abnormal state such as depression. By getting inside the psychological matrix, as itwere, the cognitive theorist gains a glimpse of considerable activity. Introspective data indicate the existence of complex organizations of cognitive structures involved in the processes of screening external stimuli, interpreting experiences, storing and selectively recalling memories, and setting goals and plans (Harvey, Hunt & Schroder, 1961). Data suggest that cognitive organizations are highly active and are much more than a simple conduit between stimulus and response.A Cognitive Model of Psychopathology The total cognitive organization appears to be composed of primitive systems consisting of relatively crude cognitive structures (corresponding to Freud’s notion of Primary Process), and of more mature systems composed of refined and elastic structures (corresponding to the Secondary Process). Someof the conceptual elements may be predominantly verbal, whereas others may be predominantly pictorial. Many of the primitive concepts are idiosyncraticand unrealistic. Under ordinary waking conditions, these idiosyncratic concepts appear to exert only minimal or sporadic effects on the integrated thinking of the individual. Peculiar or irrational cognitions emanating from the primitive system are generally tested, authenticated, and rejected by the higher centers. However, when the cognitive organization is dislocated, as in depression, anxiety, or paranoid states, these idiosyncratic concepts are hyperactive. In such circumstances, the conceptual systems grind out a powerful stream of depressing, frightening, or paranoid thoughts. As these idiosyncratic ideas become hyperactive, they tend to supersede the more realistic conceptualizations and to become more refractory to reality testing and judgment. The form of psychiatric disorder is related tothe content of the predominant, perseverating verbal cognitions or fantasies. Depressed patients, for example, report a high frequency of themes of deprivation or of self-debasement in their waking thoughts, daydreams, and dreams. Anxious patients are dominated by the concept of specific or general- izedpersonal danger. Paranoidpatients are controlled by patterns relevant to unjustified abuse or persecu- tion. The phobic patient has a disproportionate or unrealistic notion of personal danger in specific and avoidable situations. (When forced into these situa- tions, he experiences anxiety inmuch the sameway as does the anxiety neurotic.) The compulsive patient is dominated by doubts or by fears of some danger to himself or others and he seeks to put an end to the doubts or fears through rituals.Cognitive Behavioral Theory Versus Rational Emotive Behavioral Theory Paper 782 beckExplanation of Therapeutic ChangeHowdoes the cognitivemodel provide an explanation for the therapeutic effects of cognitive or behavior therapy in states such as depressions, anxiety reac- tions, or phobias? First, the therapeutic situation produces a quietingdown of the hyperactive organization (Rachman, 1968). The quieting down may be the result of either the therapist’s empathy and acceptance (Truax & Carkhuff, 1967), his specific relaxation instructions (Wolpe & Lazarus, 1966), or his explicitly stated verbal approval (Wagner & Cauthen, 1968). The quieting effects may also be produced by automated relaxation instructions (Lang, 1969). In the treatment of phobias, the quieting effect is introduced after the schemas relevant to the phobia have been artificially stimulated by the imagery instruction. As Lader and Mathews (1968) have pointed out, reducing the level of arousal below a certain critical point tends to facilitate habituation (or desensitization). Second, the therapeutic session affords anopportunity for the patient to experience and to reality-test verbal or pictorial cognitions that are causally connected to his depressed or anxious affect. This mode of operation may be illustrated by thetreatment of a phobia through systematic desensi- tization. In this procedure, the patient reproduces the phobic situation in his fantasies, and experi- ences the same type of anxiety (but in lesser degree) that would occur if he actually were in the phobic situation. Whether he is actually in the phobic situation or is simply fantasizing himself in that situation, he believes to some degree that he is in danger. The more he believes in the reality of the danger, the greater is his anxiety. At times the fantasy may be so strong that the patient may lose cognizance of the fact that he is not actually in the phobic situation, and he may even scream for help. Many patients report that their fantasy experi-ences are almost identical with the actual situational experiences. The patient may live through the frightening event in much the same way that a patient with a combat neurosis relives (abreacts) a combat experience under hypnosis or Amytal. In systematic desensitization, the patient canexperience the problem in graded doses. This process enables him, first, to experience the unpleasant event (via imagery) and, second, to reality test his reactions in status nascendi. Since the anxiety is not allowed to mount up, the patient is able to regard the event objectively. Even when flooding or implosive tech- nique (Stampfl and Levis, 1968) is employed, the patient still has the opportunity,when the fantasy hasbeen completed, to examine his reaction, and he soon realizes that he has been reacting to a fantasy and not to a real danger. Another way of viewing the process of desensi-tization is that the patient is enabled to increase his objectivity, i.e., to discriminate between a real danger and a fantasied danger as he proceeds in a stepwise progression up the desensitization hierarchy. With increasing objectivity, he is less prone to misread the situation or to accept his unrealistic conceptualization of a situation. His increased objectivity is reflected in a reduction in his anxiety arousal by the imaged or the real situation (London, 1964). Patients who are questioned at the termination ofan induced fantasy generally construe the threatening situation differently and more realistically than previously (Beck, 1970). The operation of cognitive factors in desensitization has also been illustrated in case material cited by Brown (1967) and Weitzman (1967). It could be argued that the phobic patient reallyknows that there is no danger. However, his belief that his fear is irrational exists only when the patient is “safely” removed from the phobic situation.When he is in the situation, he believes to some degree that he is in danger. Desensitization is effective because it provides a practice session inwhich the patient is able to experience his reactions to the feared situation, label them as inappropriate, and gain some inner conviction that the phobic reaction is irrational. The same mode of operation described in relationto systematic desensitization may be observed in the techniques of cognitive therapy. In cognitive psycho- therapy, the patient examines his distorted ideas and is trained to discriminate between rational and irrational ideas, between objective reality and internal embroidery. He is enabled to bring his reality testing to bear and to apply judgment. He is thus able to realize with conviction that his idiosyncratic ideas are irrational.Often the ideation is in the formof pictorial fantasy, and the patient is able to view the fantasy as a product of his mind and not as a veridical represen- tation of a reality situation. According to this analysis, a crucial mechanism inthe psychotherapeutic chain is amodification or shift in the patient’s ideational system. As his irrational concept that he is paralyzed (hysteria), helpless and hopeless (depression), in danger (anxiety or phobia), persecuted (paranoid state), or superhuman (mania) becomes deactivated, the abnormal clinical picture recedes.Mechanism of Transfer or Generalization Transfer of the desensitization to the phobic situation can be explained readily using cognitive  783ct : nature and relat ion to behav ior therapyconcepts. When the untreated patient is placed in the phobic situation (for example, an elevator, tunnel, or bridge), he reacts as if there were a clear and present danger to his life. His emotional reaction, namely anxiety, is the same that would be aroused if such a highly probable danger actually did exist. For example, a woman with an elevator phobiawould get the ideawhenever she entered the elevator, “There won’t be enough air in here and I will suffocate.” Sometimes shewould have a visual image of herself gasping for air and suffocating. In addition, shewould experience a feeling of shortness of breath. This experience occurred even when she was the only passenger in a large, airy elevator. (The fear of elevators has a different content from patient to patient. Other patients believe that the elevator cables will break during the ascent or descent, or that the elevator will get stuck and they will starve to death, or that theywill be attacked by other people in the elevator.) When away from the elevator, however, the patient believed that her expectation of suffocation was highly unreasonable. In the therapy session the patient imagines that heis in a phobic situation. The patient with an elevator phobia, for instance, started to gasp for breath when she was asked to imagine herself in the elevator. It appears, both from the patients’ descriptions and from external observation, that during the fantasy the patient actually relives the situation as though it were actually happening. In other words, the woman with the elevator phobia who is simply imagining herself in the elevator to some degree gets carried away by the fantasy and to some degree perceives herself as in the elevator at that time. Hence the fear of being suffocated is stimulated even though she is in the safety of the consultation room. As the patient experiences her inappropriatereaction during the desensitization procedure, she is able to practice viewing her fears more objectively. The transfer or the generalization to the real-lifesituation may be explained in two ways: (a) The rehearsal effect: The patient gains experience in attacking the frightening ideas and therefore, as a result of this practice, is able to counteract the irrational ideas in the phobic situation; and (b) The desensitization procedure produces a significant modification in the patient’s concept of the phobic situation so that the latent fear of being suffocated, etc., is obliterated.Conclusions A question could be legitimately raised whether introducing another system of psychotherapy is warranted. The justification is twofold. First, the theoretical framework of cognitive therapy is broaderthan that of behavior therapy and of some of the more traditional psychotherapies. This theoretical framework is congruent with many of the assump- tions of behavior therapy, but provides a greater range of concepts for explaining psychopathology as well as the mode of action of therapy. Moreover, the theoretical structure of cognitive therapy yields hypotheses that can be (and have been) readily tested through the experimental techniques currently available. Secondly, the cognitive theories provide a frame-work for the development of a number of therapeutic strategies that are not derivable from the predomi- nantly extrinsic concepts of the conditioning model. Since these cognitive techniques, as well as the behavior techniques, are easily defined and have demonstrated some preliminary evidence of their efficacy in clinical practice, further exposition seems warranted. Ultimately, the strategies of psychological modifi-cation may be usefully regrouped into the cognition- oriented techniques and the behavior-oriented techniques. The cognitive techniques would include the methods making direct use of ideational material such as systematic desensitization and other forms of induced imagery and in the direct attempts tomodify idiosyncratic cognitions. The behavioral techniques would include those operations of a nonintrospective nature, such as in operant conditioning, exposure therapy, graded task assignments, roleplaying, and assertive training.ReferencesBeck, A. T. (1963). Thinking and depression; I. Idiosyncratic content and cognitive distortions. Archives of General Psychiatry, 9, 324–333.Beck, A. T. (1967). Depression: Clinical, experimental, and theoretical aspects. New York: Hoeber.Beck, A. T. (1970). Role of fantasies in psychotherapy and psychopathology. Journal of Nervous and Mental Disease, 150, 3–17.Brady, J. P. (1967). Psychotherapy, learning theory, and insight. Archives of General Psychiatry, 16, 304–311.Brown, B. M. (1967). Cognitive aspects of Wolpe’s behavior therapy. American Journal of Psychiatry, 124, 162–167.Carlson,W. A., Travers, R.M.W., & Schwab, E. A., Jr. (March 1969). A laboratory approach to the cognitive control of anxiety. Paper presented at the meeting of the American Personnel and Guidance Association, Las Vegas.Davison, G. C. (1968). Systematic desensitization as a counter- conditioning process. Journal of Abnormal Psychology, 73, 91–99.Ellis, A. (1957). Outcome of employing three techniques of psychotherapy. Journal of Clinical Psychology, 13, 344–350.Ellis, A. (1962). Reason and emotion in psychotherapy. New York: Lyle Stuart.Folkins, C. H., Lawson, K. D., Opton, E. M., & Lazarus, R. S. (1968). Desensitization of the experimental reduction of threat. Journal of Abnormal Psychology, 73, 100–113Cognitive Behavioral Theory Versus Rational Emotive Behavioral Theory Paper

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