cognitive models of depression from a psychobiological perspective

Cognitive Models of Depression from a Psychobiological PerspectiveAuthor(s): Steven D. HollonSource: Psychological Inquiry, Vol. 3, No. 3 (1992), pp. 250-253Published by: Taylor & Francis, Ltd.Stable URL: http://www.jstor.org/stable/1449371 .

Accessed: 14/06/2014 01:49

Your use of the JSTOR archive indicates your acceptance of the Terms & Conditions of Use, available at .http://www.jstor.org/page/info/about/policies/terms.jsp

.JSTOR is a not-for-profit service that helps scholars, researchers, and students discover, use, and build upon a wide range ofcontent in a trusted digital archive. We use information technology and tools to increase productivity and facilitate new formsof scholarship. For more information about JSTOR, please contact [email protected].

.

Taylor & Francis, Ltd. is collaborating with JSTOR to digitize, preserve and extend access to PsychologicalInquiry.

http://www.jstor.org

This content downloaded from 195.34.78.191 on Sat, 14 Jun 2014 01:49:59 AMAll use subject to JSTOR Terms and Conditions

http://www.jstor.org/action/showPublisher?publisherCode=taylorfrancis

http://www.jstor.org/stable/1449371?origin=JSTOR-pdf

http://www.jstor.org/page/info/about/policies/terms.jsp


250 COMMENTARIES

Hammen, C., Marks, T., Mayol, A., & de Mayo, R. (1985). Depressive self-schemas, life stress, and vulnerability to depression. Journal of Abnormal Psychology, 94, 308-319.

Hammen, C., Mayol, A., de Mayo, R., & Marks, T. (1986). Initial symptom levels and the life-event-depression relationship. Journal of Ab- normal Psychology, 95, 114-122.

Peterson, C., & Seligman, M. (1984). Causal explanations as a risk factor for depression: Theory and evidence. Psychological Review, 91, 347- 374.

Robins, C. (1990). Congruence of personality and life events in depression. Journal of Abnormal Psychology, 99, 393-397.

Cognitive Models of Depression From a Psychobiological Perspective

Steven D. Hollon Vanderbilt University

In the target article, Segal and Dobson provide a thoughtful summary of the major points emerging from a recent consensus conference on the status of cognitive models of depression. As with any effort at consensus, I find myself more in agreement with some points than with others. In the comments to follow, I describe my own reactions to the conference and the recommendations that emerged. In particular, I attempt to relate the issues discussed to what I think are strikingly parallel issues arising from the study of biological processes in depression.

Are Cognitions Causal to Depression?

My own sense is that the pervasive optimism that marked the proponents of etiological cognitive theories of depression during the 1970s has given way to a more sober reassess- ment. The essence of a cognitive theory of depression is that thinking plays a causal role in the onset (or at least the main- tenance) of the disorder (Kovacs & Beck, 1978). It has been difficult, however, for researchers to find evidence of such a causal role (Barnett & Gotlib, 1988). Although thinking is typically more negative in people who are depressed, it typically normalizes as depression remits, and there is little good evidence that differences in thinking predict risk among euthymic individuals.

Against this backdrop, why would anyone retain an interest in cognition as a causal process? My sense is that the existing literature consists largely of studies (my own included) that have treated cognitive proclivities as stable traits that are manifest under all conditions. However, as Riskind and Rholes (1984) pointed out, major cognitive theories posit the existence of latent predispositions that are activated (and therefore made manifest) only under certain conditions, typically those involving the occurrence of negative life events (Abramson, Metalsky, & Alloy, 1989; Kovacs & Beck, 1978). Thus, although differences in propensities may exist, they are not likely to be evident unless people are put under stress. Because most of the existing studies have assessed cognition in euthymic individuals in the absence of such stressors, they may not have provided adequate tests of the models they purport to test.

If true, then efforts directed at the detection of cognitive predispositions would need to provide appropriate prompts and cues. Recent efforts along these lines have provided support for the cognitive models (Miranda, Persons, & Byers, 1990; Teasdale & Dent, 1987). These studies are by no means conclusive, because they have typically relied on

the induction of negative affect as the priming event, but the emergence of depressotypic thinking among individuals at risk is quite consistent with the notion of latent predispositions.

Are such models unscientific? They are not. They do spec- ify the conditions under which differences in presumably latent predispositions will become manifest and are therefore subject to disconfirmation. In this sense, they are quite similar to the dysregulation models currently in vogue in biological psychiatry (see Shelton, Hollon, Purdon, & Loosen, 1991). It is now well established that persons at risk for depression will show a propensity for dysregulation in key biological systems following psychological or pharmacological challenge that is not apparent under normal conditions. This holds for neurotransmitter systems (Siever & Davis, 1985), neuroendocrine processes related to stress respon- sitivity (Carroll et al., 1981) and subjective well-being (Loosen, 1986), and the integration of biological rhythms (Ehlers, Frank, & Kupfer, 1988).

It is not that cognitive theorists have adopted more complex causal models in the face of empirical disconfirmation; the specification of a latent-predisposition model dates to the early 1960s and anticipated the specification of similar models in the biological domain by nearly two decades (Beck, 1963). What appears to have happened is that a model that was always more complex in theory has been operationalized routinely in an overly simplistic fashion. Whether the latent- predisposition model will prove to be as robust with respect to cognitive predispositions as it appears to be with respect to biological dysregulation remains to be determined, but it is clear that tests of such theories must invoke some type of challenge or prime if they are to be considered adequate empirical trials.

Causal Chains and Consequentiality

I am more certain that negative cognitions are consequences of depression than I am that they are its causes, although there is no reason why they cannot be both (Hollon, DeRubeis, & Evans, 1987). In an earlier study, we found that bipolar patients evidenced a pattern of cognitive abnormality comparable to that seen in unipolar patients and that in both sets of patients those tendencies normalized with remission (Hollon, Kendall, & Lumry, 1986). We have recently begun working with patients with depression secondary to Cush- ing's disease, a hormonal disorder typically caused by a tumor in the pituitary that results in cortisol hypersecretion.



COMMENTARIES 251

These patients show most of the aspects of negative cognition typically found in patients with primary depressions. Although it is possible that cognitive factors play a causal role in the onset of both bipolar disorder and depression secondary to Cushing's disease, that seems unlikely. It seems more likely that the indications of cognitive abnormality in such patients reflect the operation of a causal path from depression (or its causes) to cognition. (I am indebted to my colleague, Peter Loosen, for introducing me to this population and for overseeing the project in which these observa- tions were made.)

At the same time, it is quite possible that different aspects of cognition will play different roles in the causal process. In an earlier article with Judy Garber, we suggested that attributional style stood further "upstream" in the causal chain than did negative expectations (Hollon & Garber, 1980). A more elegant version of this model was put forward independently by Abramson et al. (1989) in their hopelessness theory of depression. In either model, some aspects of cognition are said to be more distal, occurring earlier in the causal chain and more remote from the actual experience of symptoms, whereas others are said to be more proximal, occurring later in the causal chain and mediating the impact of the distal causes on the consequent symptoms. The same logic can be applied to the biologic processes that have been linked to depression (see, e.g., Weiss & Simpson, 1985, on the pathophysiology of noradrenergic overactivation following exposure to uncontrollable stress). Those cognitive (or biological) processes that are most distal are precisely those processes least likely to be universally aberrant in all depressions, whereas those processes that are most proximal are most likely to approach universality in their expression (pure epiphenomena are, of course, likely to be more common still). In this regard, early findings from the project with the Cushing's patients previously described suggest that attributional style (as measured by the Attributional Style Question- naire, or ASQ; Seligman, Abramson, Semmel, & von Baeyer, 1979) is less likely to be aberrant in those patients when depressed than are measures of expectations and "stream-of-consciousness" ruminations.

Temporality in Depression

In a phenomenon so clearly temporal in nature as depression, the timing of assessments relative to the course of the underlying disorder becomes crucial. Depression tends to be self-limiting-that is, it tends to resolve spontaneously, even in the absence of treatment. It also tends to recur. Anywhere from 50% to 85% of all individuals who have one episode of depression will have two or more (Consensus Development Panel, 1985), and the modal depressed patient will have at least three. What this suggests is that risk for a given episode is not randomly distributed across the larger population; some people are at greater risk for recurrent depression than would be predicted by chance alone (it remains possible that risk for initial episodes is randomly distributed, with risk for subsequent episodes increasing as a direct consequence of that initial exposure).

The typical episode of depression lasts about 3 to 9 months in outpatients and 6 to 12 months in inpatients (Beck, 1967; Keller, Shapiro, Lavori, & Wolfe, 1982). Although pharmacological interventions reduce the expression of symptoms, they appear to do little to reduce subsequent risk (Prien &

Kupfer, 1986). Patients treated to remission pharmacologically appear to be at two to three times the risk of symptom return if discontinued from medications before the end of the expected life of the episode than if withdrawn after that point (Hollon, Evans, & DeRubeis, 1990). What this suggests is that the episode has a life of its own that is not defined solely by the expression of manifest symptoms. Thus, it is quite possible for a recently remitted patient to be totally symptom free while continued on medications and still be "in episode" with regard to the underlying pathophysiology or psycho- pathology.

What this means is that longitudinal designs that seek to draw causal inferences on the basis of temporal stability must be more careful than has previously been recognized to spec- ify whether patients are remitted (i.e., no longer symptomatic, but still "in episode") or recovered (i.e., no longer in episode). It is likely that the mechanisms driving the onset and offset of a given episode are distinct from the factors conferring vulnerability for the disorder. Otherwise, all people at risk would be continuously depressed. Therefore, we must strive for even greater precision in our differentia- tion between the two. It is quite possible that the mechanisms driving the specific episode will have normalized if they are assessed after the episode has run its course. In such an instance, inferring noncausality from nonstability would be inappropriate.

In our own work, we have found that patients treated with cognitive therapy have a reduced risk for subsequent relapse relative to patients brought to remission pharmacologically (Evans et al., in press). Further, in that trial, cognitive therapy was associated with greater change in attributional styles than was tricyclic pharmacotherapy, despite the fact that the latter produced comparable change in depression (DeRubeis et al., 1990). Finally, change in attributional style appeared to mediate cognitive therapy's preventive effect: Those patients with the least depressotypic causal attributions following treatment were the least likely to relapse following treatment termination, even after controlling for residual symptomatology (Hollon et al., 1990). Measures of other cognitive constructs typically showed nonspecific change as a function of treatment condition and failed to predict relapse following treatment termination after controlling for residual depression, although expectancy measures did exhibit greater covariation with symptom change in cognitive therapy than in pharmacotherapy (DeRubeis et al., 1990).

These data suggest that attributional style is a particularly promising candidate as a distal cause; it can best be described as a predisposing cause that is neither necessary nor suffi- cient, but contributory to at least the recurrence of depression. To my knowledge, this is the first time that this variable has been included in a controlled comparison between cognitive therapy versus pharmacotherapy. It is intriguing that the data conform so nicely to predictions made over a decade ago (Hollon & Garber, 1980). It is also of interest that other measures of cognition evidenced neither specific change nor prediction of subsequent relapse once residual symptomatology was partialed out. This is consistent with what has been found in other controlled trials (Blackburn & Bishop, 1983; Imber et al., 1990; Simons, Garfield, & Mur- phy, 1984).

Nonetheless, it would be premature to conclude that attributional style plays a causal role in the onset (or recurrence) of depression not played by other aspects of cognition.



252 COMMENTARIES

Although some of the strongest support for a causal role for cognition comes from studies that have used the ASQ (it was more likely to predict subsequent depression than other cognitive measures in the longitudinal literature reviewed by Barnett & Gotlib, 1988), I am not convinced that it is the construct, as opposed to the measurement operation, that is responsible. The ASQ is the only one of the self-report ques- tionnaires assessing cognition that provides its own prompts. Even if these findings do prove replicable, I think it is possible that attributional styles are merely part of a larger sche- matic process (Segal, 1988) and that their apparently greater association to phenomena of theoretical interest is a consequence of the method by which they are assessed.

Can Cognitive and Biological Causes Be Differentiated?

In a recent chapter, Beck argued that it is limiting and ultimately self-defeating to attempt to differentiate between psychological versus biological depressions. Rather, he argued that "the psychological and biochemical phenomena are simply different sides of the same coin" and that it is "reductionistic to presume that the biochemical disorder causes the psychological disorder (or vice versa)" (Beck, 1983, p. 265).

Although I am sympathetic with the core of his argument (that all psychological processes occur in the context of an underlying biological process), I disagree with the conclusions that he draws. It seems perfectly reasonable to discrim- inate between the individual with a normally functioning nervous system who has learned (as a consequence of life events) to interpret relatively benign events in a negative fashion (which I consider "psychological") versus the individual with a propensity for biological dysregulation under conditions that would not be considered stressful by the aver- age person (which I consider "biological"). The fact that information processing in the first instance is mediated by an underlying biological substrate in no way obviates the locus of the pathology; in those cases, the biological system is responding in precisely the way it should and in precisely the way it would in virtually every other member of the species confronted with the same sequence of events. Similarly, the fact that efforts at coping become less effectual and thinking more aberrant following the growth of a pituitary tumor in no way obscures the essential biologic nature of initial dysfunc- tion. In the former instance, psychological processes play the major role in precipitating the depression, whereas in the latter, it is the initial biological abnormality that causally predominates.

In either case, I would expect the subsequent involvement of both psychological and biological processes, both in the form of common proximal mechanisms and nonspecific symptomatic consequences. In this sense, I agree that depression is best conceptualized as a psychobiological disorder, but I think it is quite likely that the distal causal factors can be either predominantly psychological or predominantly biological in any given individual (or episode). This leads me not only to presume that it is meaningful to attempt to dis- criminate between various classes of causes, but to also predict that efforts at prevention will require greater specificity between psychological versus biological domains than will efforts at intervention.

Conclusions

Although a cognitive theory of depression has received little support from the majority of the studies conducted over the last decade, the majority of these trials have tested overly simplistic versions of the model and have failed to assess what are presumed to be latent predispositions in an adequate fashion. Recent studies that have assessed purported cognitive diatheses under conditions of stress or that have primed individuals presumed to differ in risk appear to provide greater support for the model, as do studies of known or differen- tially treated groups that differentiate distal from proximal causes and attend carefully to the temporal parameters of remission and recovery. In this respect, support for a cognitive model of depression is not unlike that for the dysregulation models currently influential in the biological domain; support for the model is more likely to be obtained when attention is paid not only to what is assessed, but also to the conditions and timing of the assessment.

Note

Steven D. Hollon, Department of Psychology, 306 Wilson Hall, Vanderbilt University, Nashville, TN 37240.

References

Abramson, L. Y., Metalsky, G. I., & Alloy, L. B. (1989). Hopelessness depression: A theory-based subtype of depression. Psychological Re- view, 96, 358-372.

Barnett, P., & Gotlib, I. H. (1988). Psychosocial functioning and depression: Distinguishing among antecedents, concomitants, and consequences. Psychological Bulletin, 104, 97-126.

Beck, 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: Harper.

Beck, A. T. (1983). Cognitive therapy of depression: New perspectives. In P. J. Clayton & J. E. Barrett (Eds.), Treatment of depression: Old controversies and new approaches (pp. 265-284). New York: Raven.

Blackburn, I. M., & Bishop, S. (1983). Changes in cognition with pharmacotherapy and cognitive therapy. British Journal of Psychiatry, 142, 469-476.

Carroll, B. J., Feinberg, M., Greden, J. F., Tarika, J., Albala, A. A., Haskett, R. F., James, N. McI., Kronfol, Z., Lohr, N., Steiner, M., deVigne, J. P., & Young, E. (1981). A specific laboratory test for the diagnosis of melancholia. Archives of General Psychiatry, 38, 15-22.

Consensus Development Panel. (1985). NIMH/NIH Consensus Develop- ment Conference Statement on Mood Disorders: Pharmacological prevention of recurrences. American Journal of Psychiatry, 142, 469- 476.

DeRubeis, R. J., Evans, M. D., Hollon, S. D., Garvey, M. J., Grove, W. M., & Tuason, V. B. (1990). How does cognitive therapy work? Cognitive change and symptom change in cognitive therapy and pharmacotherapy for depression. Journal of Consulting and Clinical Psy- chology, 58, 862-869.

Ehlers, C. L., Frank, E., & Kupfer, D. J. (1988). Social zeitgebers and biological rhythms: A unified approach to understanding the etiology of depression. Archives of General Psychiatry, 45, 948-952.

Evans, M. D., Hollon, S. D., DeRubeis, R. J., Piasecki, J., Grove, W. M., Garvey, M. J., & Tuason, V. B. (in press). Differential relapse following cognitive therapy and pharmacotherapy for depression. Archives of General Psychiatry.

Hollon, S. D., DeRubeis, R. J., & Evans, M. D. (1987). Causal mediation of change in the treatment of depression: Discriminating between non- specificity and noncausality. Psychological Bulletin, 102, 139-149.

Hollon, S. D., Evans, M. D., & DeRubeis, R. J. (1990). Cognitive mediation of relapse prevention following treatment for depression: Implica- tions of differential risk. In R. E. Ingram (Ed.), Contemporary psychological approaches to depression (pp. 117-136). New York: Guilford.



COMMENTARIES 253

Hollon, S. D., & Garber, J. (1980). A cognitive-expectancy theory of therapy for helplessness and depression. In J. Garber & M. E. P. Seligman (Eds.), Human helplessness: Theory and applications (pp. 173-195). New York: Academic.

Hollon, S. D., Kendall, P. C., & Lumry, A. (1986). Specificity of depressotypic cognitions in clinical depression. Journal of Abnormal Psychology, 95, 52-59.

Imber, S. D., Pilkonis, P. A., Sotsky, S. M., Elkin, I., Watkins, J. T., Collins, J. F., Shea, M. T., Leber, W. R., & Glass, D. R. (1990). Mode-specific effects among three treatments for depression. Journal of Consulting and Clinical Psychology, 58, 352- 359.

Keller, M. B., Shapiro, R. W., Lavori, P. W., & Wolfe, N. (1982). Recov- ery in major depressive disorder: Analysis with the life table and regres- sion models. Archives of General Psychiatry, 39, 905-910.

Kovacs, M., & Beck, A. T. (1978). Maladaptive cognitive structures in depression. American Journal of Psychiatry, 135, 525-533.

Loosen, P. T. (1986). Hormones of the hypothalamic-pituitary thyroid axis: A psychoneuroendocrine perspective. Pharmacopsychiatry, 19, 401-415.

Miranda, J., Persons, J. B., & Byers, C. N. (1990). Endorsement of dys- functional beliefs depends on current mood state. Journal of Abnormal Psychology, 97, 251-264.

Prien, R. F., & Kupfer, D. J. (1986). Continuation drug therapy for major

depressive episodes: How long should it be maintained? American Journal of Psychiatry, 143, 18-23.

Riskind, J. H., & Rholes, W. S. (1984). Cognitive accessibility and the capacity of cognitions to predict future depression: A theoretical note. Cognitive Therapy and Research, 8, 1-12.

Segal, Z. V. (1988). Appraisal of the self-schema construct in cognitive models of depression. Psychological Bulletin, 103, 147-162.

Seligman, M. E. P., Abramson, L. Y., Semmel, A., & von Baeyer, C. (1979). Depressive attributional style. Journal of Abnormal Psy- chology, 88, 242-247.

Shelton,R.C.,Hollon,S.D.,Purdon,S.E.,&Loosen,P.T. (1991). Bio- logical and psychological aspects of depression. Behavior Therapy, 22, 201-228.

Siever, L. J., & Davis, K. L. (1985). Overview: Toward a dysregulation hypothesis of depression. American Journal of Psychiatry, 142, 1017- 1031.

Simons, A. D., Garfield, S. L., & Murphy, G. E. (1984). The process of change in cognitive therapy and pharmacotherapy for depression. Ar- chives of General Psychiatry, 41, 45-51.

Teasdale, J. D., & Dent, J. (1987). Cognitive vulnerability to depression: An investigation of two hypotheses. British Journal of Clinical Psychi- atry, 26, 113-126.

Weiss, J. M., & Simpson, P. G. (1985). Neurochemical basis of stress- induced depression. Psychopharmacology Bulletin, 21, 447-457.

Consensus and Apple Pie: Comments on a Cognitive Depression Conference

Nicholas A. Kuiper University of Western Ontario

L. Joan Olinger University Hospital London, Canada

As stated by Segal and Dobson, the major goals of the recent Consensus Development Conference on Cognitive Models Depression were to detail "the achievements and enduring challenges facing cognitive models of depression" and "identify productive directions of growth for the field in the 1990s." Their conference report provides recommendations covering four general content areas: (a) cognitive models of depression, (b) cognitive assessment issues, (c) cognitive vulnerability research, and (d) the integration of cognitive models with other theoretical approaches to depression.

Ideally, a conference such as this should provide a unique opportunity to discuss and exchange ideas that may prove beneficial to the field. Scientific progress in any area of inquiry proceeds via several different channels, including peer-reviewed journals, chapters, and books. Conferences, with their emphasis on the dynamics of discussion and di- alogue, provide an important adjunct to these other scientific outlets. In particular, conferences can facilitate the emergence of creative insights and recommendations that may be less readily achieved via the other channels.

In light of this, we can ask: How have the proceedings of this conference laid the groundwork for significantly advanc- ing our knowledge and understanding of cognitive factors associated with depression? Or, stated slightly differently: What are the unique insights and contributions brought about by this conference that will facilitate our exploration and

understanding of cognitive components of depression in the 1990s?

Unfortunately, after reading the report, our response to these queries was not extremely positive. At a general level, we were disappointed with the overall caliber of the recommendations. To be sure, they outline some potentially intriguing avenues of exploration, including the notion of priming as a means to achieve more refined tests of cognitive vulnerability models and the recommendation that cognitive research and theory on depression should focus more specifi- cally on individual components of this disorder. Overall, however, we felt that the major thrust of the recommendations was lost in being too general and shallow. Compound- ing this, several recommendations seemed more appropriate to providing retrospective directions of growth for the field in the 1980s, rather than prospective directions for the 1990s.

We elaborate on these concerns in the remainder of this commentary and also highlight some further potential avenues of exploration associated with several of the recommendations. Finally, we conclude with some cautionary notes on the appropriate role of a consensus conference in science.

Consensus and Apple Pie

In reading Segal and Dobson's report, we found many of the presented recommendations too general and superflcial for in-depth critical reaction. Although this level of gener-



cognitive models of depression from a psychobiological perspective

Documents