Comorbid Conditions

Earlier in this chapter we made the case that it is important to assess for co-occurring conditions in working with depressed patients. A number of different models have been proposed to account for comorbidity among psychiatric disorders, and the reader who is interested in systematic reviews of these models is referred to Krueger and Markon (2006). Although a full review of these models is beyond the scope of this chapter, we discuss several of the most commonly studied models of comorbidity. Specifically, given that the focus of the chapter is case conceptualization in CT for depression, we discuss the application of these models to cognitive factors in depression. However, it should be noted that Beck (1991) clearly asserts that cognitive theory does not claim that depression is caused by negative cognitions, noting instead that depression is caused by a combination of biological, genetic, familial, developmental, personality, and social factors. Whereas cognitive theory is compatible with other models of vulnerability for depression, the theory proposes that these other factors are important in that they activate latent maladaptive schemas, which are the cognitive mechanism by which depression develops. Thus, we focus our discussion on implications of comorbidity models as they may influence the activation of the cognitive mechanisms (i.e., maladaptive schemas) of depression. Diagrams of these three models are provided in Figure 2.1.

The first model of comorbidity is a correlated liabilities model, in which both depression and comorbid conditions have their own liability or vulnerability factors, but the liability or vulnerability factors are correlated (i.e., an increase in risk factors for one condition is associated with an increase in risk factors for the other condition). As applied to the cognitive theory of depression, the correlated liabilities model suggests that depression and co-occurring clinical conditions each have their own cognitive vulnerability. Such a perspective is consistent with one of the basic tenets of cognitive theory, namely, the cognitive content specificity hypothesis. According to this

FIGURE 2.1. Representations of hypothetical associations between latent liability factors (L) and observed symptoms (Sx) for disorders 1 and 2.

perspective, psychological disorders are distinguished by the form and content of their associated dysfunctional cognitions, beliefs, attitudes, and processes: "The key differences among the neuroses are revealed in the content of the aberrant thinking rather than in its form" (Beck, 1976, p. 82). The thought content associated with depression is believed to center on significant losses, particularly with reference to the loss of something considered essential to one's happiness. This can be contrasted with disorders such as mania, which is associated with an exaggerated positive view of self, world, and the future, or anxiety, which is associated with threat or danger. As reviewed elsewhere, there is considerable support for the content specificity hypothesis in terms of depression and anxiety (R. Beck & Perkins, 2001), although there has been less research evaluating specificity between depression and other disorders. Furthermore, although the content specificity hypothesis was originally proposed to account for differences in Axis I disorders, it has more recently been applied to Axis II disorders as well; that is, each personality disorder is hypothesized to have its own set of idiosyncratic beliefs and attitudes, which in turn give rise to the idiosyncratic behavioral patterns associated with that specific personality disorder (Beck, Freeman,

Davis, & Associates, 2003). Support for this perspective comes from research indicating that each personality disorder does indeed have a unique set of dysfunctional beliefs, and that these belief systems tend to be correlated with one another (Beck et al., 2001).

As applied to CT for depression with comorbid conditions, the cognitive content specificity hypothesis predicts that in some situations, a patient presenting with depression and a comorbid condition would have dysfunctional cognitions associated with not only depression but also the content of each of the comorbid conditions. Thus, it would be expected that the cognitive content of a person with comorbid depression and anxiety would include both loss and threat, whereas that of a person with depression and a narcissistic personality disorder would include both loss and views of self as inferior and others as superior, hurtful, and demeaning. The implication of this model is that in such situations, CT with a patient with comorbid conditions may require more targeting of additional beliefs than would be the case for someone with "pure" depression.

It should be noted that the cognitive content specificity hypothesis was advanced to account for the differences between disorders, not to explain the comorbidity that occurs between disorders. However, we believe that this perspective can be expanded to account for comorbidity as well. Specifically, whereas each disorder may indeed have its own unique cognitive content, people who endorse one set of such beliefs are also likely to endorse other sets of beliefs. In other words, the degree or magnitude of endorsement of cognitive vulnerabilities for one disorder is likely to be correlated with the degree or magnitude of endorsement of cognitive vulnerabilities for another disorder. Therefore, comorbidity between depression and another condition in some situations might occur because the specific, underlying cognitive vulnerabilities for the two conditions are themselves correlated, which is what the correlated liabilities model of comorbidity hypothesizes. Support for this perspective comes from research finding correlations between cognitive contents associated with depression and anxiety (R. Beck & Perkins, 2001) and among the cognitive contents of different personality disorders (Beck et al., 2001).

The second comorbidity model is an alternate forms model, in which depression and comorbid conditions are alternate manifestations of a single liability or vulnerability factor. According to this model, comorbid conditions share a single vulnerability factor. A common example of an alternate forms model that is advanced to account for the comorbidity between depression and anxiety is the recently updated tripartite model—the revised integrative hierarchical perspective (Mineka, Watson, & Clark, 1998). This model hypothesizes that depression and anxiety share a common higher-

order vulnerability of trait negative affectivity and the related personality trait of neuroticism. Results from population-based samples suggest that the personality trait of neuroticism may indeed help to account for the cooccurrence of depressive and anxiety disorders (e.g., Weinstock & Whisman, 2006).

As applied to the cognitive model of depression, there may be cognitive vulnerability factors that give rise both to depression and to comorbid conditions. As previously discussed, Beck (1983) identified two cognitive-personality dimensions—sociotropy and autonomy—that are believed to be important in understanding depression onset, symptomatology, and treatment response. The introduction of these two dimensions represents a shift in the evolution of cognitive vulnerabilities for depression, because cognitive theory for depression before this time focused more on specific, idiosyncratic negative schemas (Clark et al., 1999). Although they were initially proposed as vulnerabilities to depression, research has shown that sociotropy and autonomy are also associated with other Axis I disorders, including anxiety (e.g., Alford & Gerrity, 1995) and bulimia (e.g., Hayaki, Friedman, Whisman, Delinsky, & Brownell, 2003); with personality disorders (e.g., Ouimette, Klein, Anderson, Riso, & Lizardi, 1994); and with other clinical conditions that co-occur with depression, such as problematic interpersonal relationships (e.g., Lynch, Robins, & Morse, 2001). Thus, emerging evidence that sociotropy and autonomy may represent broad-based cognitive vulnerabilities that give rise to depression and other clinical conditions would be consistent with the alternate forms model of comorbidity.

As applied to CT for depression with comorbid conditions, the alternate forms model of comorbidity suggests that in some situations, comorbid conditions and depression have a common, underlying cognitive vulnerability. For example, a highly sociotropic patient, who believes that he or she is unlovable, might worry about forming and maintaining relationships, avoid situations in which interpersonal rejection is possible, and experience distress when an interpersonal relationship ends. In this example, comorbid generalized anxiety disorder, social phobia, and depression could all be alternate manifestations of the same underlying cognitive vulnerability of sociotropy and the core belief of being unlovable. The implication of this model is that treating the common underlying cognitive mechanism should help reduce both depression and the comorbid condition(s).

In a final comorbidity model, the causation model, one condition has a direct influence on the development of another condition, or the two can directly influence each other in a reciprocal fashion. In discussing causation models, it is important to consider the temporal ordering of onset of depres sion relative to other conditions. In a large, representative community survey, Kessler et al. (1996) found that lifetime cases of depression were most often secondary to other Axis I disorders, with anxiety disorders being the most common primary disorders associated with secondary depression. Interestingly, they also found that secondary depression was more severe and persistent than primary or pure depression. Although temporal precedence does not in itself imply causation, these findings are important in suggesting that depression may in many cases be secondary to other Axis I psychiatric disorders. Similarly, other clinical conditions have also been shown to precede and, therefore, potentially to be related causally to depression. For example, depression is secondary to many medical conditions (Stevens et al., 1995), and there is evidence that adverse social relationships, such as marital discord, are predictive of depression onset (e.g., Whisman & Bruce, 1999).

As applied to cognitive theory of depression, relatively few causation models have been advanced to account for the comorbidity between depression and other conditions. One notable exception is a model proposed by Alloy, Kelly, Mineka, and Clements (1990) to account for the comorbidity between depression and anxiety. According to this model, depressive and anxiety disorders share a cognitive vulnerability of expectation of uncontrollability (i.e., an expectation of helplessness), but depression occurs only when helplessness turns into hopelessness. Specifically, this model suggests that people who expect to be helpless in controlling important future outcomes, but are unsure of their helplessness, exhibit anxiety. If they then become convinced of their helplessness, but are still uncertain about the future likelihood of negative events, they experience mixed anxiety and depression. Finally, if the perceived probability of future negative events becomes certain, then helplessness becomes hopelessness, and they exhibit depression.

As applied to CT for depression with comorbid conditions, the causation model of comorbidity suggests that in some situations, comorbid conditions may be a cause of depression (i.e., primary), whereas in other situations they could be a consequence of depression (i.e., secondary). As such, this model suggests that treating the primary condition may enhance the impact of treatment for the secondary condition. For example, if interpersonal problems (e.g., relationship or marital problems) are conceptualized as occurring before the onset of depression, addressing these problems (e.g., with couple or family therapy) may make it easier to address other factors in CT for depression.

There are other comorbidity models in addition to these three models. For example, it may be that comorbidity is a separate disorder (or a subtype of one of the disorders), with a liability or vulnerability that is independent of either disorder. Because these models do not easily map onto the cognitive theory of depression, they are not discussed here.

In summary, there are at least three ways of conceptualizing comorbidi-ty that may occur between depression and other conditions. Each model has its own implications for how CT may be conducted to deal most effectively with depression and co-occurring conditions.

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