A central premise of some cognitive approaches to depression is that vulnerable individuals possess cognitive risk factors that are largely inactive until individuals encounter adversity in a domain that is central to their sense of self-worth. For example, in Beck's model, stress in the person's environment is postulated to activate the negative self-schema, particularly stress matching the individuals' core doubts and concerns about self-worth (Segal, Shaw, Vella, & Katz, 1992). Even though a number of studies have assessed cognitive functioning during a depressive episode, because this cognitive functioning could be a consequence of depression, these studies are usually uninformative about cognitive processes that are thought to be linked to the onset of a depressive episode (Barnett & Gotlib, 1988). Additionally, research examining cognitive functioning in currently nondepressed but vulnerable individuals has generally failed to show that they think in depressotypic ways, but this too is also uninformative because it fails to take into account the diathesis-stress nature of most cognitive theories (Ingram et al., 1998).
In contrast, "priming" studies explicitly focus on diathesis-stress perspectives that are central to many cognitive theories of depression (Hol-lon, 1992), and thus assess the outcomes associated with the activation of negative self-referent cognitive structures in response to stresslike encounters. These studies typically rely on inducing a negative mood state in nondepressed but vulnerable individuals, with the hope of modeling in the laboratory the effect that stress has on most people—that is, the production of negative mood. In theory, this brief negative mood state should activate the kind of cognitions that serve as vulnerability factors for the more severe mood state that is a depressive episode. More generally, these studies seek to model the processes whereby the normal sad mood states that are occasionally experienced by everyone energize the mechanisms the lead to a downward spiral into depression for some people (i.e., those who are vulnerable). In more specific terms, vulnerability is conceptualized as the availability of relatively well-developed and well-elaborated cognitive structures that are linked to negative affective structures (Ingram, 1984; Ingram et al., 1998). Once brought about by any variety of life events, the structures responsible for the experience of sadness provide access to the extensive and elaborate processing of depressive information. This process serves to generate a downward extension of normal depressed mood into the more significant and debilitating experience of depression by those who possess these networks. Thus, once this intricate system of dysfunctional themes is activated by the type of negative mood that is thought to follow the experience of stress, a pattern of negative self-referent information processing is precipitated that escalates into depression for vulnerable people (Segal & Shaw, 1986). Priming studies are intended to model this process.
Some priming failures have been reported in the literature. For example, Brosse, Craighead, and Craighead (1999) found that increased endorsement of dysfunctional attitudes following a negative mood induction was unrelated to depression history. Dykman (1997) also documented that shifts in dysfunctional attitudes following a mood induction were unrelated to depression history. Similarly, Solomon, Haaga, Kirk, and Friedman (1998) failed to find differences in irrational beliefs between never depressed and recovered depressed persons following priming by negative sociotropic and autonomous event scenarios.
Despite some failures, there is enough evidence of priming effects to support a consensus that vulnerable individuals do possess dormant but reactive cognitive schemas of the type that should be linked to cognitive vulnerability to depression (Gotlib & Krasnoperova, 1998; Ingram et al., 1998; Scher, Segal, & Ingram, in press; Segal & Ingram, 1994). For instance, using a variety of cognitive measures that reflect dysfunctional cognition, studies by Teasdale and Dent (1987), Dent and Teasdale (1988), Miranda, Persons, and Byers (1990), Miranda, Gross, Persons, and Hahn (1998), Hedlund and Rude (1995), Ingram, Bernet, and McLaughlin (1994), Ingram and Ritter (2000), Taylor and Ingram (1999), and Segal, Gemar, and Williams (1999) all supported the activation of what appear to be cognitive diatheses. Some research has described evidence of cognitive diatheses in children as young as 8 years old (i.e., Taylor & Ingram, 1999).
The previous studies supported the activation of dysfunctional self-schemas, but Segal et al. (1999) in particular provided evidence that these schemas not only can be activated, but that they appear to be associated with vulnerability to the experience of depression. In this study, depressed patients who had recovered after being treated with either cognitive behavioral therapy (CBT) or pharamacotherapy (PT) completed ratings of dysfunctional attitudes before and after a priming procedure (i.e., a negative mood induction). Following priming, PT patients showed a significant increase in dysfunctional cognitions, a finding that is consistent with other priming data (see Segal & Ingram, 1994). CBT patients, on the other hand, showed no change in DAS scores. Several years after initial testing, a follow-up study reassessed patients and found that their cogni tive reactions to the mood induction predicted relapse, even after controlling for the effects of previous depression history. Thus, these data suggest a link between cognitive reactivity and risk for later depressive relapse, a key element of schema theories of depression.
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