Emotional disorders can be characterized or classified at different levels of abstraction, and the most appropriate level for focus may depend on the question or circumstances at issue. Consider the case of generalized anxiety disorder and panic disorder. Both are anxiety disorders (at a high level), and for some purposes it may be legitimate to collectively group them as a "single" disorder. Indeed, this was the case (i.e., in the diagnosis of "anxiety neurosis") in classification systems not long ago. The shifts in the diagnostic classification of the two disorders can be interpreted as demonstrating that there are both similarities and differences between these disorders in their underlying causal mechanisms. For example, an underlying core of "inappropriate fear" would seem a common element of anxiety disorders, yet its manifestations vary in different disorders. For example, the core state of fear is persisting and low grade in generalized anxiety disorder, and its manifestations may be muted or curbed by the presence of a largely abstracted and verbal worry process (see chap. 7, this vol.). In contrast, the fear state seems to erupt into a full-blown and uncurbed crescendo in panic disorder. Taken collectively, there is clearly a need to understand both the similarities and dissimilarities in the causes of various emotional disorders.
Relations Between Noncognitive Factors and Cognitive Vulnerability
Additional factors potentially related to vulnerability to emotional disorders—such as personality and demographic variables, developmental experiences, or interpersonal patterns—can be logically placed within the cognitive paradigm. For example, personality characteristics such as negative affectivity or neuroticism can be seen as the consequences of the activation of underlying negative schemata (e.g., Jolly & Kramer, 1994). Factors, such as the availability of social support or of intimate relationships with spouses (or lovers), can be seen as moderating the impact of cognitive vulnerability and stress, because they help to highlight to people that they have positive aspects to their self-identities, world, or future prospects. Hence, having access to social support could perhaps "buffer" vulnerable individuals from the possible detrimental effects of stress by preventing them from succumbing to hopelessness (Dobkin, Panzarella, Fernandez, Alloy, & Cascardi, 2004; Panzarella et al., 2004). For example, in social support, the imparting of more adaptive inferences about the causes, meaning, and consequences of negative life events is particularly helpful. Similarly, factors such as gender or gender-roles can be interpreted within the cognitive paradigm in terms of their relation to dysfunctional rumination patterns that affect a person's focus of attention (e.g., Nolen-Hoeksema, Morrow, & Fredrickson, 1993). Likewise, factors such as physical illness or age could be hypothesized to influence mental or coping resources (e.g., Baumeister & Heatherton, 1996) for counteracting ingrained cognitive biases or neutralizing proximal dysfunctional cognitions when they arise. In these ways, it is often possible to specify test able mental mechanisms or processes by which "noncognitive" variables interact with the cognitive system.
Cognitive models are often based on empirical phenomena or observations that were originally conceptualized in other terms. For example, Lewinsohn's (1974) behavioral theory of depression reinterpreted the psychoanalytic concepts of "loss" and "dependency," respectively, in terms of the ideas of "loss of reinforcement" and "lack of social skills." Current cognitive theories of depression reinterpreted the same phenomena in terms of cognitive processes such as "depressive" inference patterns (see chap. 2, this vol.) or memory structures (see chap. 3, this vol.). Another good example is the "looming vulnerability" model of anxiety (see chap. 7, this vol.). Here, ethological observations of fearful responses to forward moving objects are seen as a "low order" instance of a more general theme and hypothesized effect of inner mental representation of rapidly intensifying danger in humans. As a consequence, cognition includes a broad set of phenomena, and the cognitive clinical paradigm is flexible enough, without much stretching, to include new ideas. Furthermore, by bringing in new observations (e.g., from psychoanalytic, behavioral, ethological, experimental cognitive research), we can broaden our knowledge by making statements of cognitive theory that are not merely explanatory, but also expansive.
Biological Factors and Cognitive Vulnerability-Stress Interactions
In the absence of a relevant cognitive vulnerability, it is also plausible that biologically vulnerable individuals are relatively unlikely to develop an emotional disorder, just like the mere presence of hydrogen molecules is unlikely to coalesce into water (H2O) without oxygen. For example, it is often suggested that seasonal affective disorder (SAD) or premenstrual syndrome (PMS) are largely biological. However, a common clinical impression of individuals with these disorders is that they often have more generalized cognitive vulnerabilities to depression. Unwanted changes in seasonal patterns of light, or of bodily symptoms due to PMS, may serve as "stresses" in cognitive vulnerability-stress interactions.
It is possible that cognitive vulnerabilities and biological diatheses mutually moderate each other's effects on the development of future emotional disorders. For example, genetic diathesis-stress interactions maybe better predictors when individuals have cognitive vulnerabilities. The "stress" produced by psychosocial stressors (i.e., the appraisal of the meaning of the stresses) is dependent on individuals' cognitive vulnerabilities. By the same token, cognitive vulnerability-stress interactions may be more potent predictors of future disorder when individuals have a higher familial genetic risk for the given disorder(s).
Consequently, it could be useful in the future to include assessments of cognitive and biological vulnerability, as well as stress, within the same studies of emotional disorder. For example, a well-known study by Kendler, Neale, Kessler, and Heath (1992) found that anxiety and mood disorders seemed to originate from the same genes, but partly different environments. Had Kendler et al. assessed cognitive vulnerabilities, they might have discovered that anxiety and mood disorders arise from the "same genes, but different cognitive vulnerabilities."
Effects of Multiple Cognitive Vulnerabilities on Total Risk, Severity, and Comorbidity
Another pair of questions that remains open is whether there are any additional effects due to multiple cognitive vulnerabilities on both the risk or severity of episodes of given disorders or their symptoms and the risk of comorbidity of disorders? In the first case, research has suggested that as psychosocial risk factors (e.g., family dysfunction, child abuse) accumulate, they impose an increasingly greater cumulative "risk burden" on individuals, such that they are more liable to develop psychological problems or disorder. Perhaps there is a comparable cumulative risk burden for multiple cognitive vulnerabilities. For example, do depression-prone individuals have a higher risk for developing depression because they have a compound vulnerability (i.e., both dysfunctional attitudes and depressive inferential styles), than if they were to have just one of the cognitive vulnerabilities alone, or even than their summation of effects (e.g., see Riskind, Rholes, Brannon, & Burdick, 1989; Robinson & Alloy, 2003)? Alternatively, is the effect of having two separate cognitive vulnerabilities no greater than the simple effect of having only one alone (i.e., there is a threshold, beyond which there is no additional effect)? In this connection, it seems clear that we can sometimes predict disorder by rather complex interactive combinations of cognitive factors (e.g., see chap. 13, this vol.).
In the second case, from the perspective of cognitive theories, how does the comorbidity of emotional disorders develop (Alloy, Kelly, Mineka, & Clements, 1990)? For example, across clinical and nonclinical studies, it is well known that anxiety and depression appear in a comorbid form (e.g., Gotlib, 1984; Zinbarg & Barlow, 1996). In addition, it is known that symptoms of anxiety and depression are often more severe when they co-occur than when they occur separately (see Riskind et al., 1991). If it can be assumed that cognitive vulnerability factors can vary with relative independence of each other across individuals, then it can be inferred that a subset of individuals with compound vulnerabilities may be identified (i.e., they combine cognitive vulnerabilities to different disorders) that are far likelier to develop comorbid emotional disorders. Preliminary support for this general proposition is offered by a recent study (not reported here) that assessed both depressive explanatory style and looming maladaptive style, and examined their main effects and interactions (Riskind & Williams, 2000). As expected, individuals who had the compound vulnerability exhibited more severe symptoms of anxiety and depression than would be expected from the simple summation of their separate effects. Thus, the study of cognitive vulnerability factors holds out promise for understanding the psychological antecedents of comorbid emotional disorders.
Disorder-Specific Developmental Pathways?
The conceptual framework in Fig. 1.1 assumes that people's antecedent childhood experiences can help to mold the nature of the cognitive vulnerabilities they later develop. Indeed, there is evidence that early life experiences and developmental events can lead to cognitive vulnerabilities (e.g., see chap. 2, this vol.; Gibb, Alloy, Abramson, & Marx, 2003; Ingram, 2003; Ingram, Bailey, & Siegle, 2004; Riskind et al., 2004; Rogers, Reinecke, & Setzer, 2004; Safford, Alloy, Crossfield, Morocco, & Wang, 2004; Williams & Riskind, 2004). Examples include faulty attachment relationships, parental psychopathology, emotional or physical abuse, negative life stress, physical illnesses, parental modeling, and parental interpretations to children of the meaning of children's experienced events (e.g., see chap. 2, this vol.). But, a crucial question remains: Why do similar developmental events seem to lead to presumably different cognitive vulnerabilities (e.g., to depression vs. anxiety)?
It seems quite probable that some developmental factors (e.g., childhood events) are likely to be common rather than specific factors in emotional disorders (echoing the point about common versus specific cognitive vulnerabilities themselves). If developmental variables were to constitute such common factors, they would be expected to play a general, but nonspecific, role in the pathogenesis of many disorders.
Moreover, certain sets of developmental factors (e.g., faulty attachments, or peer rejection), on the one hand, and of parental feedback, on the other, may sometimes interact to codetermine the developmental outcomes. If parental (or other adult) feedback is an especially powerful determinant of children's interpretations of events, then it would follow that such feedback has a formidable role in determining the outcome of a developmental event for specific vulnerabilities. For example, the odds that children develop a depressive cognitive vulnerability (e.g., from faulty attachment experiences) could be far higher when their interpretations of the experiences are coupled with depressogenic parental feedback (e.g., "you are worthless and hopeless"). In contrast, the odds that they develop a specific anxiety-related cognitive vulnerability may be far higher when their special meaning is guided by the occurrence of anxiety-producing parental interpretations of the same events (e.g., "displeasing others will cause rejection").
Additionally, and not necessarily incompatible with the aforementioned, it is possible that the variability in the particular factual details of childhood experiences may also help account for differences in the vulnerabilities that are developed. For example, children could be more prone to develop depression-related cognitive patterns if they have been subjected to unremitting or relatively constant parental abuse or criticism. In contrast, they might be more prone to develop anxiety-related patterns if they have been subjected to more variable parental negative events, and/ or if some positive protective factors are present. Therefore, more work on these developmental questions is clearly warranted.
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