Blackwell Publishing Inc

Treatment of Depression and Mechanisms of Change: Strengthening the Links Among Theory, Research, and Practice

Lauren C. Haubert and Keith S. Dobson, University of Calgary

Greater knowledge of the mechanisms underlying cognitive change in the context of depression is an important goal of current clinical research. The thoughtful review by Garratt, Ingram, Rand, and Sawalani (2007) highlights the wealth of research that has been conducted in this area, while also drawing attention to the many complexities inherent in studying the cognitive mediation hypothesis in cognitive therapy. In this commentary, we use the review by Garratt et al. as a starting point from which to highlight some of the issues that we believe to be imperative to the advancement of knowledge in this eld of research. These issues include the need for strong connections between theories of cognitive mediation and depression, the deployment of appropriate research paradigms and methods to advance the eld, and the conduct of research in contexts that are relevant to clinical practice. Key words: cognitive mediation, cognitive processes, psychotherapy. [Clin Psychol Sci Prac 14: 247251, 2007]

of change in CT and other interventions, and the conclusions that may be drawn from the available research base. There is much to appreciate in the article by Garratt et al. This commentary is therefore not a critique of that work, but rather uses it as a springboard to address three issues that we deem to be particularly important in terms of advancing research in the area of mechanisms of change and cognitive mediation in therapy. These issues are related to (a) optimal design of tests of theories of depression and cognitive mediation, (b) a call for comprehensive, creative, and appropriate methods in the assessment of cognition, and (c) the extension of research into clinical practice, each of which is discussed in turn below. It is our hope that researchers involved in this area will consider these issues and work toward the development of methods that may address potential gaps or weaknesses in the existing literature.
OPTIMAL DESIGN OF TESTS OF THEORIES OF DEPRESSION AND COGNITIVE MEDIATION

Following a hiatus since Whismans (1993) review

article examining mechanisms of change in cognitive therapy (CT) of depression, Garratt, Ingram, Rand, and Sawalani (2007) have thoughtfully reviewed the body of literature addressing the cognitive mediational hypothesis in cognitive therapy for depression. In doing so, they also address whether cognitive mediation is specic to CT or is present in other noncognitive treatments for depression. Throughout their review, the authors raise a number of critical and timely issues relevant to understanding the current state of empirical research, theoretical and methodological aspects of research on mechanisms

Address correspondence to Keith S. Dobson, Department of Psychology, University of Calgary, 2500 University Drive NW, Calgary, AB T2N 3H6, Canada. E-mail: ksdobson@ucalgary.ca.

Cognition is not a unitary concept, but rather a complex system. For example, it has been proposed that cognition may be broken down into several components, including cognitive contents, processes, products, and structures/ organization (e.g., Ingram & Kendall, 1986). Conceptually, cognitive structures relate to organizational aspects of cognition, perhaps best seen in concepts such as schemas in long-term memory. Cognitive processes involve differential systems and their interactions that are associated with the processing of information from sensory input into short- and long-term memory, as well as the subsequent retrieval/memory of such inputs. Cognitive content refers to the actual manifest information that is being encoded or recalled, while cognitive products refers to the endpoint of cognitive processing, in the form of specic cognitions or cognitive outputs. The measurement of cognitive products often occurs through the use of self-report measures (e.g., Attributional Style Questionnaire, Peterson et al., 1982; Dysfunctional Attitudes Scale, Weissman & Beck, 1978; Automatic Thoughts Questionnaire, Hollon & Kendall, 1980) that have the benets of economy, ease of scoring and administration, standardization, and normative and psychometric data. However, it is quite possible that the study of cognitive products will not reveal information about the

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mediational processes that are important in symptom improvement. Certainly, the study of treatment outcome measures may not be the most productive way of examining the processes that affect cognitive and symptom change, as changes in products or symptoms do not necessarily directly reect changes in underlying cognitive processes and structures. While available evidence does reveal changes in cognitive products and content following CT (Garratt et al., 2007), the underlying changes in cognitive processes and structures remain relatively understudied, and researchers should be cautious in inferring causal mechanisms and mediators of change strictly from such measurement. A central theoretical principle in CT is that changes in cognitive processes mediate symptom improvement in depression; however, directly testing this hypothesis is extremely difcult. For example, the schema construct has been elusive to measure directly (Clark, Beck, & Alford, 1999), in part because it is hypothetically latent until activated by relevant life events or mood (Ingram, Miranda, & Segal, 1998), and in part because rm agreement on its core elements or properties has not yet been reached. As a consequence, researchers often rely on secondary constructs, such as self-reports of cognitive products, to indirectly evaluate cognitive models, and to infer the underlying structures and processes that led to these outcomes. Even more problematic, some authors have relied on the efcacy of treatment outcomes to infer causal processes. Such reliance on secondary constructs and treatment outcomes, however, is at best a weak test of theoretical models. It is imperative that depression researchers maintain links to theory. Garratt et al. appropriately raise this issue with regard to studying the nature of schema change during the course of therapy. Although self-report assessment may indicate that schematic products have been altered following treatment, it is important to assess whether underlying schematic structures have been modied in fundamental ways, or whether they have simply been deactivated. Some research, for example, has found virtually no differences on self-report measures of cognition (e.g., dysfunctional attitudes) among participants successfully treated with either pharmacotherapy or CT (Segal, Gemar, & Williams, 1999). However, one cannot infer from a lack of difference on cognitive variables at the end of treatment that CT did not achieve any

clinical effects through cognitive change mechanisms. Such ndings highlight the importance of using priming methods (e.g., cognitive reactivity paradigms) to examine schematic change that may not be detectable through self-report. Continued innovative work in this area (e.g., Scher, Ingram, & Segal, 2005; Segal et al., 2006) will be important in answering questions regarding the degree to which underlying depressogenic structures are altered during treatment, and the mechanisms involved in depressive relapse. Improved methodological and statistical methods may help tease apart the underlying processes and mechanisms of change in CT. For example, Garratt et al. suggested that studies with higher power are needed, perhaps employing more current and powerful statistical methods (e.g., structural equation modeling). We concur with these suggestions. For example, given a research focus on processes, structural equation modeling may well be a helpful statistical tool in determining causal pathways leading to cognitive change. In addition, it is important to note that none of the studies presented in the review by Garratt et al. met all four of the cognitive mediation criteria proposed by DeRubeis et al. (1990). Because those criteria are additive and not mutually exclusive, we would therefore suggest that none of the studies presented in the review comprised a complete examination of mechanisms of cognitive change. As such, it may be argued that many conclusions that may currently be drawn based on available research are tenuous, at best.
ASSESSMENT OF COGNITION: A CALL FOR COMPREHENSIVE, CREATIVE, AND APPROPRIATE METHODS

Self-report measures are based on the assumption that the cognitive products are an accurate reection of changes in cognitive structures and/or processes. This assumption raises the issue of construct validity of cognitive assessment; that is, the ability of an assessment tool to measure the cognitive domain of interest. In addition, these measures may be subject to response biases or social desirability responses that are consistent with the therapists beliefs about the clients problem. It also remains questionable whether underlying cognitive structures are fully accessible through self-report methods, or whether more implicit assessment techniques may better capture changes in underlying cognitive structure.

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While we believe that some progress has been made in terms of designing research paradigms to account for the potentially latent nature of cognitive structures (e.g., cognitive reactivity), the use of self-report measures continues to be widespread. While self-report measurement of cognitions certainly has merit, we suggest that using these measures exclusively as measures of change in cognitive processes and structures/organization is potentially problematic. In addition, most studies typically employ only one or two measures of cognition at treatment outcome, and it is important to carefully consider whether the selected measures reect the cognitive change domains of interest. Much of the available research not only uses self-report, but also uses group changes following treatment. Paradoxically, the use of total group scores on self-report measures may actually obscure some of the treatment effects, which more ne-grained analyses might elucidate. For example, Teasdale et al. (2001) found no differences on cognitive measures between treatment groups at posttreatment, but found that extreme responses were endorsed less in CT than the other treatment groups. Furthermore, the use of group changes at the end of treatment may not be as rich as within-session evaluations of cognitive and symptomatic change. Whisman (1993), for example, urged an increase in research paradigms that provide an intensive analysis of critical change events in psychotherapy (p. 260), in order to better understand variability in patterns of change across individuals and situations. Such an approach might provide a more detailed examination of the linkages between processes and techniques used in CT. For instance, relatively recent studies of sudden gains in CT (e.g., Tang & DeRubeis, 1999; Tang, DeRubeis, Beberman, & Pham, 2005) provide valuable insights into the aspects of CT that produce changes in cognitions on a session-by-session basis. We would also advocate the use of ongoing measurement of cognitive change throughout the course of therapy, not just at the end of treatment. As noted by Garratt et al., all cognitive therapies are not created equal and, therefore, the precise techniques and interventions used across different studies and individuals almost certainly affect different aspects of depressogenic thinking and schemata. Researchers should be encouraged to engage in ongoing assessment of cognitive variables over the course of therapy, on a session-by-session basis when

possible, in order to better map the aspects of CT onto cognitive changes in the individuals being treated. In doing so, underlying processes of cognitive change may be better elucidated. In addition, the ongoing examination and coding of client verbalizations of cognitions (e.g., McNamara & Horan, 1986) during the course of therapy may be an underutilized paradigm for studying session-by-session change. Only a small number of studies have compared noncognitive psychosocial treatments to CT in terms of examining the cognitive mediation hypothesis. However, research evidence suggests that therapies that do not involve direct cognitive intervention strategies may also lead to cognitive change and depressive symptom reduction. For example, it has been demonstrated that behavioural activation also affects depressogenic cognitions, and at levels consistent with CT (Jacobson et al., 1996). What is not yet clear, however, is whether different processes are responsible for producing cognitive change across CT and other psychosocial interventions. Given that the majority of research has explored cognitive mediation in the context of traditional CT, future studies should address how cognitive processes unfold across CT and other noncognitive interventions that may also have a strong inuence on cognitions. It is also important to note that the mechanisms underlying onset, maintenance, and relapse of depression may not necessarily be the same. For instance, the research on mindfulness-based cognitive therapy for depression (Segal, Williams, & Teasdale, 2002) suggests that this intervention is particularly benecial for preventing relapse for individuals who have experienced three or more episodes of past depression (although mindfulnessbased cognitive therapy has less benet for preventing relapse in individuals with two or fewer episodes; Ma & Teasdale, 2004). Therefore, it seems plausible that rather than directly targeting negative thinking as in traditional CT approaches, the use of more mindful and indirect treatment of thoughts may be a particularly important mechanism of cognitive change for individuals suffering from chronic, recurrent depression. Issues related to relapse and recurrence may also require the consideration of alternative methods, more appropriate to longitudinal studies. Such studies might also benet from the use of different populations (e.g., community or high-risk samples), in addition to clinical samples.

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EXTENDING RESEARCH INTO CLINICAL PRACTICE

As noted by Garratt et al., all cognitive therapies for depression are not created equal, and cognitive therapists themselves vary in terms of levels of ability and experience, and tend to have unique and diverse approaches to their application of cognitive techniques. In terms of clinical practice, we know that CT works (Hollon, 2006; Hollon, Stewart, & Strunk, 2006); however, the translation of research ndings into the clinical practice context lags behind. Despite the progress that has been made in understanding mechanisms of cognitive change, several fundamental questions about the practical applications of research ndings for depression have yet to be answered. For example, relatively little research speaks to how cognitive mechanisms of change unfold in clinical settings outside of research laboratories (i.e., effectiveness studies). As demonstrated through the review of the research base by Garratt et al., identication of cognitive mechanisms of change can be challenging, at best, to accomplish under highly controlled research settings. When the creativity and individualistic styles of therapists are added to the mix, the conclusions regarding therapeutic mechanisms of cognitive change likely become even more complex and speculative. Consequently, we encourage researchers to extend research into practice settings, while also taking into account the methodological challenges (and potential suggestions for improvement) inherent in studying mechanisms and processes of change. Whisman (1993) noted that testing of the theoretical underpinnings of CT requires the identication of CTs active ingredients, which also has implications for improving the efcacy of therapist training. For instance, knowledge about the processes by which particular techniques bring about changes in depressogenic schemas, and the most effective sequencing of therapeutic interventions for eliciting changes in the client, would be benecial for clinicians to incorporate into their practice. Unfortunately, the research ndings do not always reach the clinicians whose work will ultimately have a considerable impact on the well-being of depressed individuals. It is our hope that researchers will continue to disseminate their ndings, and that clinicians will seek out current information through such available learning opportunities. Although not reviewed in the article by Garratt et al., the investigation of moderator variables is also an important avenue of research that may yield some insights that

can be readily applied in clinical practice contexts. For example, it has been suggested that nonspecic variables (e.g., therapist, client, and relationship variables) may account for some of the positive benets that are observed in CT for depression. In terms of understanding cognitive change in psychosocial treatments other than CT, it is important to examine whether cognitive change results from the use of specic procedures, or whether some of the change may be accounted for by nonspecic treatment factors. This line of research may help to elucidate how common factors moderate the underlying change processes in both cognitive and noncognitive treatments. Equally important to studying the success of interventions in producing cognitive change is the examination of treatment failures; that is, under what conditions do cognitive change and symptomatic reduction not occur, and what variables are associated with a lack of therapeutic benets? Research addressing cognitive processes of change likely paints a picture of the typical process of change during the course of CT; however, it is possible that multiple pathways to change exist, and that not all of these pathways are adequately captured by the research ndings. Given that a combination of variables and multiple causal pathways lead to the onset and/or relapse of depression (e.g., diathesis-stress models), different pathways may also be responsible for the cognitive and symptom change that occur following treatments.
CONCLUSIONS

As evidenced by the review by Garratt et al., considerable progress has been made in terms of elucidating the underlying mechanisms of change in CT. Based on the existing evidence, it is clear that cognitive changes do tend to be associated with therapeutic benets (and are generally predictive of symptom change), lending support to the mediation hypothesis. In terms of the specicity of cognitive change in CT, the authors suggest that it is too early to disconrm this hypothesis, as the evidence is fairly mixed. However, we would argue that the evidence is fairly strong in favour of nonspecicity for change in cognitive products following treatment. We do agree that further research examining cognitive processes and structural change is necessary before any rm conclusions may be made regarding specicity of cognitive mediation and mechanisms of change in CT. In addition, more research is needed to explore underlying

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processes and structures in greater depth, and whether changes in cognition are more supercial in noncognitive and psychosocial treatments other than CT. The review by Garratt et al. clearly highlights some of the gaps that still remain in terms of the available empirical literature. We endorse this concern, and have emphasized the need for optimal design of tests of theories of depression and cognitive mediation, the use of optimal methods in cognitive assessment, and the extension of research into clinical practice. We look forward to advances in the eld, to the extent that these ideas are embraced in research and practice.
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