The types of causal relations postulated by a cognitive model are central to selecting an appropriate research design. In addition to the distinction between distal and proximal causes, the appropriate design is also influenced by whether the hypothesized causal role is necessary, sufficient, or contributory. In terms of the latter roles, a necessary cause is an etiological factor that is an essential condition (either in the present or the past) for the disorder to occur. In the absence of the etiological factor, the disorder cannot occur, although the factor by itself does not require the disorder to occur (i.e., the factor is necessary but not sufficient). A sufficient cause is an etiological factor that guarantees the occurrence of the disorder, although the factor may not be necessary for the disorder (e.g., the factor is sufficient but not necessary). A contributory cause increases the statistical likelihood that the disorder will occur by playing a supporting causal role, but is neither necessary nor sufficient for the occurrence of the disorder (Abramson et al., 1989). As previously noted, the distinction between specific and nonspecific causal factors is also important, and has been a major impetus for the emphasis that many recent cognitive models have given to disorder-specific cognitions.
Another chief element of the causal relations in cognitive models has to do with the cognitive vulnerability-stress combination (e.g., Abramson, Alloy, & Hogan, 1997; Alloy et al., 1999; Monroe & Simons, 1991). On the one hand, some cognitive models may hypothesize that the cognitive vulnerability and stress combine in an additive fashion as a straightforward summation. On the other hand, in other models there is true statistical interaction. Here, the cognitive vulnerability and stress are assumed to combine in a true interactive synergism that predicts outcomes beyond the separate additive effects of the vulnerability and stress. For instance, a combination of a high level of cognitive vulnerability and high stress is more likely to lead to an episode of the emotional disorder in question than either factor (or their additive combination) alone. The specific manner in which these factors are postulated to combine determines the appropriate statistical analyses that are needed, as well as the levels of the cognitive vulnerability-stress combination that must be sampled (or experimentally manipulated) to test the model (see Alloy et al., 1999).
Still another element relevant to the hypothesized causal relations lies in the distinction between moderating and mediating factors (Baron & Kenny, 1986; Holmbeck, 1997). A moderator is a third variable that codetermines outcomes by affecting the relation between the independent variable (e.g., the cognitive vulnerability or stress or both) and the dependent variable (disorder). In essence, a moderator statistically interacts with the vulnerability or stress (or both) and affects the direction or strength of the relation between the vulnerability-stress combination and disorder. For example, suppose that gender is a moderator. This would mean that the direction and/or strength of the cognitive vulnerability-stress combination would depend on whether participants were male or female. It is also possible that there are even moderator variables that can lead certain cognitive vulnerability factors, under rather limited conditions, to play a protective rather than a vulnerability role.
In contrast, a mediator is a third variable assumed to account for the relation between an independent variable (e.g., the distal cognitive vulnerability and proximal stress, or their combination) and the dependent variable (e.g., the disorder). The mediator can be seen as the transitional process or intermediary mental mechanism by which the cognitive vulnerability-stress combination becomes converted into an episode of disorder. For example, as shown in Fig. 1.1, biases in mental processes of memory or attention could be seen as a third variable that mediates the relation between a cognitive vulnerability and the onset of disorder. In essence, moderators specify the conditions under which a vulnerability-stress combination will lead to a disorder. In contrast, mediators specify how or why the vulnerability-stress combination leads to disorder.
The two previous roles become more complicated when third variables simultaneously act as both moderators and mediators (i.e., moderating mediators). To illustrate, a disorder-specific processing bias is hypothesized to play a mediator role in the causal chains by which certain cognitively vulnerable individuals (e.g., with a depressive inferential style) develop an emotional disorder (see Fig. 1.1). At the same time, the disorder-specific processing bias is a third variable that can be hypothesized to play a moderator role in that other cognitively vulnerable individuals who lack the disorder-specific processing bias do not show an equal probability of developing the disorder. In this more complex case, a third variable (e.g., a disorder-specific processing bias) serves to both moderate and mediate the impact of a cognitive vulnerability on the development of a disorder (see Baron & Kenny, 1986, on moderated mediators).
A preceding section briefly alluded to the idea that the degree to which a cognitive vulnerability is in play can be important in cognitive models. Indeed, several models have emphasized that cognitive vulnerabilities can vary dramatically in the degree to which they are engaged and "put into play" in processing at different times (e.g., Ingram, Miranda, & Segal, 1998). During periods when such vulnerabilities are in an inactive or latent state, a cognitive priming task such as a relevant mood-induction or activating provocation task (Riskind & Rholes, 1984) could be required to detect them. Thus, there is an analogy between a cardiac stress test (which is used to reveal a hidden coronary dysfunction) and a cognitive priming task (which is used to reveal a hidden cognitive vulnerability). This being so, it may sometimes be necessary to bring out a latent vulnerability with the aid of an appropriate priming test (for evidence, see chap. 3, this vol.).
Together with a priming task, it may sometimes help in detecting cognitive vulnerabilities to reduce thought suppression. For example, some research shows that an imposed cognitive load (e.g., being asked to retain a sequence of numbers in mind) can help reveal dysfunctional beliefs that are suppressed (Wenzlaff, 1993). Research also suggests that whereas under no load conditions, individuals are apparently able to correct for un derlying biases, under cognitive load conditions, they may evidence biases to make negative judgments about other people (Weary, Tobin, & Reich, 2001).
Future research is clearly needed to determine the extent to which the notion of cognitive priming, perhaps in conjunction with an imposed cognitive load, is valuable when attempting to detect different cognitive vulnerabilities (see Alloy et al., 1999). In this regard, certain kinds of cognitive vulnerabilities (e.g., the depressive inferential style, see chap. 2, this vol.) could be chronically accessible (i.e., "pre-potent") because of their frequent use in daily thinking, and hence not require a priming procedure to be observed. The extent to which the detection of different kinds of cognitive vulnerabilities require specific priming for their detection needs further work.
Logical Criteria Necessary for Support of a Putative Cognitive Vulnerability
The main logical criteria that must be satisfied to establish strong empirical support for a hypothesized cognitive vulnerability have not been identified. There are four such criteria. First, the temporal precedence and stability of the vulnerability independent of the symptoms of the disorder must be established (e.g., Alloy et al., 1999; Ingram et al., 1998). That is, the putative vulnerability must temporally precede the initial onset of the disorder, or, in the case of a vulnerability factor for the course of a disorder, it must precede episodes or symptom exacerbations of the disorder (i.e., it has predictive validity). Second, it must exhibit some degree of stability independent of the symptoms of the disorder. That is, the vulnerability must be shown to be more than just a transient state manifestation or consequence of the changing symptoms of the disorder.
Third, and of equal importance, alternative explanations of results must be eliminated as plausible options. This aim is achieved in part by establishing that the predicted relationships are not due to potential third variables or confounds (J. Cohen & P. Cohen, 1983; Cook & Campbell, 1979). In this regard, further confidence in the validity of the putative vulnerability is also achieved by providing supplementary evidence that the vulnerability factor plays a causal role in the development of symptoms or onset of disorder (i.e., obtaining evidence for its construct validity). That is, confidence in the putative vulnerability is increased by evidence that it is attended by a set of causal mechanisms and causal chains hypothesized by the model (e.g., seen in the figure). Along these lines, important evidence on these issues is supplied by a network of findings showing predicted differences in personality characteristics, information processing, coping patterns, and so forth of individuals who are high or low in cogni tive vulnerability (see chap. 2, this vol., for an excellent example). For example, results that can be interpreted as demonstrating the developmental antecedents or mediating processing deficits that are the specific predicted outcomes for the cognitive theory (but not a "rival" third factor) can support the construct validity of the putative cognitive vulnerability.
A fourth, and final, criterion for causal status should also be mentioned. If a theory of interest claims that the vulnerability factor is specific or near-exclusively applicable to a certain disorder, then it must further be shown that the factor is largely applicable to the disorder of interest and not to other disorders (i.e., it has discriminant validity). Hence, evidence that the putative vulnerability to a disorder has temporal precedence and stability, while supporting a causal role, does not provide a sufficient basis to establish that the vulnerability factor has specificity. The upshot is that to establish that cognitive factors are specific causes, it is also imperative to directly test the specificity of the predicted outcomes.
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