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CHAPTER 1

Understanding Psychopathology

THE ROLE OF VULNERABILITY

Rick E. Ingram and Joseph M. Price

We believe there is no more important goal in psychopathology research than understanding the causes of psychopathology. Although there may be multiple pathways to such an understanding, theory and research on vulnerability are indispensable to this quest for causality. In a broad sense, it is difficult to envision an effective effort to understand the causes of disorder that does not include an examination of the processes that give rise to the disorder. Even more broadly, a case can be made that efforts to understand vulnerability to psychopathology underlie virtually all efforts to understand psychopathology itself.

Theory and research related to a number of different psychopathological conditions are examined in the various chapters in this book. Each of these examinations focuses on the specific vulnerability theory and data that are relevant to particular disorders. We start here, however, with a broader examination of the idea of vulnerability that can serve as a foundation for understanding vulnerability in these more specific disorders. In this vein, we start by briefly examining what is arguably the single most important aspect of psychopathology, that is, the concept of causality in psychopathology. We follow with a discussion of the notion of vulnerability itself and then move to issues concerning the relationships among vulnerability, risk, and resilience, and then finally to issues concerning the distinction between childhood and adulthood.

WHAT IS CAUSALITY?

In the most obvious sense, "causality" refers to the processes that create or facilitate the transition from a normal state of psychological functioning into an abnormal psychological state. Although this concept of causality is accurate, it is incomplete; causality does not refer simply to this onset phase but also to other important processes in the course of psychopathology. As such, a more complete examination of causality necessitates some discussion of both onset and maintenance processes.

Onset Causality

Whether a first onset of a disorder or the occurrence of a subsequent episode of a disorder, understanding the processes involved in onset are critical to understanding the causes of psychopathology. From a vulnerability perspective, data on these processes inform researchers about the factors that place individuals at risk for experiencing a disorder. Similarly, data have also provided insights into how these risk processes in the nondisordered person are translated into a psychopathological state in that same person.

Onset can be further understood in the context of distal and proximal vulnerability. Although investigators differ to some extent in drawing the temporallines for these different risk processes, proximal factors are generally regarded as those that become apparent right before the onset of a disorder. Distal factors, however, occur before the disorder but more distant in time from its appearance. For example, a model of a psychopathological state that specified certain psychological or physiological responses to life events would be specifying a more proximal cause, whereas a model that focused on the creation of risk factors in childhood would be focusing on more distal variables.

Maintenance Causality

Some researchers have differentiated between the onset and the maintenance of a disorder and have tacitly suggested that the onset or appearance of psychopathology is synonymous with causality. Correspondingly, maintenance processes are not viewed as causal, and hence relatively little importance is ascribed to these factors (Ingram, Miranda, & Segal, 1998). We argue, however, that causality is not synonymous solely with onset and that the factors that maintain a disorder can be legitimately seen as causal.

We thus suggest that an exclusive focus on onset is too narrow a conception of the construct of causality. Consider the case of depression. A considerable amount of data shows that depression is a persistent disorder, with symptoms lasting months and in some cases years (e.g., dysthymia). Moreover, data also show that untreated depression lasts between 6 months to 1 year or, depending on the severity of the episode, possibly up to 2 years (Goodwin & Jamison, 1990). Unless a model argues that the factors that lead to the onset of a disorder are identical to the factors that maintain the disorder (and few even address this idea), the processes associated with the perpetuation of psychopathology can be considered to have real causal significance. Indeed, a case might be made that such factors are more meaningful than onset factors — that is, the psychological, interpersonal, occupational, academic, and perhaps biological damage associated with a disorder like depression arises not because it occurred but rather because it persists over weeks, months, and perhaps years.

Although we focus on depression in this example, virtually all psychopathological states are problematic not only because they occur but also because they are maintained over time. We can therefore legitimately ask whether the causes of this occurrence over time are any less important than the causes of its initial appearance. Thus, we argue that fully understanding vulnerability requires investigating not only the factors that bring about a disordered state but also those that result in its continuation over time.

HOW DO WE DEFINE VULNERABILITY?

It seems reasonable to assume that a volume on vulnerability to psychopathology should offer, at a minimum, some ideas on how to define the vulnerability construct. Although the vulnerability approach to psychopathology is at least several decades old, little consensus has been reached on what constitutes an adequate definition of "vulnerability" (Ingram et al., 1998). This definitional shortcoming persists even though ideas about vulnerability have generated a significant body of theory and data. Such a corpus of knowledge is possible because we arguably know vulnerability when we see it and because researchers can identify demonstrably vulnerable groups to study. For example, data show that people who have experienced a disorder are at greater likelihood of experiencing another disorder, and hence investigators can assemble such groups to study vulnerability. Yet, these operational definitions leave aside the broader question about what constitutes the vulnerability construct itself.

Of course, simple definitions of "vulnerability" abound, and for the public at large such terms are quite appropriate. For example, those who are vulnerable are liable to, or susceptible to, psychopathology. From a scientific standpoint, however, exchanging one poorly defined term for another is an unsatisfactory means of appreciating the nature and complexity of the vulnerability construct. Although truly comprehensive definitions of vulnerability are rare, one can derive a conceptual understanding of this construct by examining its core features, that is, those features that have been examined in theory and research and that can therefore offer important clues about its nature (Ingram et al., 1998).

Core Features of Vulnerability

Examination of the literature suggests that several themes appear repeatedly in discussions of vulnerability, which focus on vulnerability as a stable trait, the endogenous and latent nature of vulnerability, and the role of stress in actualizing vulnerability. We now turn to a brief examination of each theme.

Vulnerability as a Stable Trait

Researchers frequently discuss vulnerability as an enduring trait. Zubin and Spring (1977) pioneered many of the ideas about vulnerability in their work on understanding causal processes in schizophrenia. Zubin and Spring were also the most specific about what they regarded as the trait-like nature of vulnerability: "We regard [vulnerability] as a relatively permanent, enduring trait" (p. 109); "the one feature that all schizophrenics have ... is the everpresence of their vulnerability" (p. 122). They leave little doubt that "vulnerability" refers to processes that endure over time.

Other investigators have tended to be not quite as specific, but the trait-like nature of vulnerability is nevertheless implicit in many of their discussions of vulnerability. Such assumptions of permanence are likely rooted in the genetic level of analysis employed by researchers who pioneered this concept. For example, many schizophrenia researchers emphasize the genetic endowment of individuals who are at risk for this disorder. Meehl's (1962) pioneering concept of schizotaxia represents an inherited neural deficit, whereas other influential researchers such as Zubin and Spring (1977) and Nicholson and Neufeld (1992) are quite explicit that genetic factors determine the relative level of vulnerability (at least for schizophrenia).

Permanence, however, need not be rooted in genetic factors. An example from the schizophrenia literature is again illustrative. Researchers have suggested that prenatal stress or trauma may lead to vulnerability to schizophrenia (Brennan & Walker, Chapter 14, this volume). For example, both maternal influenza and significant famine have been linked to a rise in the rate of schizophrenia. In regard to the latter example, a two-fold increase in schizophrenia was subsequently reported following a massive famine in China between 1959 and 1961 (St. Clair et al., 2005). Postnatal factors, such as exposure to environmental toxins, have also been implicated (Brown, 2007), which may interact with genetic liabilities to render the vulnerability even more permanent.

Such conceptualizations tend to posit that no decrease in absolute vulnerability levels is possible. This is not to suggest, however, that functional vulnerability levels cannot be attenuated by several factors, such as those that affect neurochemistry. For instance, medications such as lithium carbonate, which alters the likelihood of developing the symptoms of a bipolar episode by presumably controlling the neurochemistry of the underlying vulnerability, may prove helpful. Similar diminishment of functional vulnerability may be seen in the actions of psychopharmacological treatments for depression with medications such as the various generations of tricyclic agents and the more recent selective serotonin reuptake inhibitors (Potter, Padich, Rudorfer, & Krishnan, 2006; Shelton & Lester, 2006). Even though functional vulnerability may be altered and individuals are less likely to develop the disorder, the vulnerability persists; for example, in many cases the probability of experiencing a psychiatric episode is increased if the medication is discontinued. Thus, even though the vulnerability may be controlled, the vulnerability trait itself remains.

The trait-like nature of vulnerability is perhaps most clearly seen in contrasting it to the episodic nature of psychological disorders. For instance, Zubin and Spring (1977) clearly distinguish between an enduring vulnerability trait and episodes of schizophrenia that "are waxing and waning states" (p. 109). Hollon, Evans, and DeRubeis (1990) and Hollon and Cobb (1993) also distinguish between (1) stable vulnerability traits that predispose individuals to the disorder but do not constitute the disorder and (2) state variables that represent the occurrence of the symptoms that reflect the onset of the disorder. Thus, while predisposing factors are enduring traits, virtually all investigators characterize the disorder itself as a state. Disordered states can therefore emerge and decline as episodes cycle between occurrence and remission, but the traits that give rise to vulnerability for the disordered state are typically thought to remain constant.

Although vulnerability is assumed by many theorists, particularly those working within a genetic framework, to be permanent and enduring, this need not be the case. This is especially true when the level of vulnerability analysis is psychological rather than genetic or prenatal in nature. As we have noted, assumptions of genetic vulnerability offer little possibility for the modification of vulnerability characteristics. Many psychological approaches, however, rely on assumptions of dysfunctional learning as the genesis of vulnerability. Given these assumptions, not only functional but actual vulnerability levels may fluctuate as a function of new learning experiences that influence the particular vulnerability factor. For instance, Hollon, Stewart, and Strunk (2006) have summarized data showing that, compared to pharmacotherapy for depression, cognitive therapy is more effective in preventing relapse and recurrence, presumably because the underlying vulnerability has been at least partially altered. In this vein, Hollon et al. (1990) and Hollon and Cobb (1993) argue that the effects of pharmacological treatments may be largely symptom-suppressive but that psychological interventions such as cognitive therapy are designed to alter dysfunctional cognitive structures and, to the extent that genuine vulnerability is rooted in such structures, may lessen susceptibility to psychopathology. Fewer recurrences of the disorder over time may reflect decreased vulnerability. It is certainly possible that factors other than vulnerability reduction may be at the heart of cognitive therapy's prophylactic effects, but this example does illustrate how, theoretically at least, actual vulnerability levels might be altered.

Of course, from the viewpoint of a psychological level of analysis, vulnerability may decrease with certain corrective experiences, or, alternatively, it may increase over time. This latter possibility would be the case if continued exposure to aversive experiences and stressful life events served the function of enhancing the factors that contribute to vulnerability. Some perspectives have suggested that frequent experiences with the disorder itself may increase vulnerability for future onsets. For example, in describing the idea of kindling, Post (1992, 2007) has proposed such a process in the area of affective disorders. Post suggests that each episode of an affective disorder leaves a residual neurobiological trace that leads to the development of pathways by which increasingly minimal stress becomes sufficient to activate the mechanisms that result in a disorder. Such a process thus leads to increased vulnerability.

The possibility that psychological vulnerability levels can be altered (up or down) suggests a subtle but potentially important distinction between stability and permanence. Stability and permanence are likely to be viewed as synonymous. However, even though the concept of stability clearly suggests a resistance to change, it does not presume that change is never possible. Under the right circumstances, changes in an otherwise stable variable may very well occur. Indeed, the entire concept of psychotherapy is based on precisely this premise. Without intervention or the introduction of other significant life experiences, however, little change in stable psychological variables should occur. On the other hand, variables that are considered to be enduring, particularly biological processes emanating from genetic or prenatal processes, imply a permanence or immutability that is not only resistant to change under ordinary circumstances but is assumed to offer virtually no possibility of change.

Vulnerability as Endogenous and Latent

Another core feature that is possible to glean from vulnerability research is that vulnerability represents an endogenous variable. This is perhaps most clearly seen in genetic conceptualizations of vulnerability, but it is equally relevant for psychological conceptualizations. That is, whether stemming from inborn characteristics or acquired through learning processes, the vulnerability resides within the person. This aspect can be contrasted to other levels of analysis that might, for example, focus on environmental or external sources of stress that initiate a disorder, or perhaps a focus on interpersonal styles that may lead to aversive interactions (see Joiner & Coyne, 1999). We discuss this distinction more fully in the section differentiating vulnerability from risk. For now it is important to note that, although these "external" variables are clearly important, the locus of vulnerability processes is within the person.

In line with the idea that vulnerability is an endogenous process, and that vulnerability remains stable even though observable states of psychopathology arise and then (in many cases) diminish, some investigators have suggested that vulnerability is not easily observable and can thus best be conceptualized as a latent process. From a research perspective, this feature can perhaps be seen most clearly in the empirical search for observable markers of vulnerability; numerous investigators have sought to find reliable empirical indicators of the presence of the vulnerability. There are a variety of research strategies for identifying markers, but in each case they operate with the assumptions that (1) vulnerability processes are present in individuals who have few or no outward signs of the disorder, (2) these processes are causally linked to the appearance of symptoms, and (3) they are not readily observable and are therefore difficult to assess. This sense of latency is particularly the case in investigations that rely on some kind of stressful or challenging event that makes detection of the vulnerability factor possible (see Shelton, Hollon, Purdon, & Loosen, 1991, for a discussion of the challenge paradigm as it pertains to the conceptualization of vulnerability and dysregulation). The search for vulnerability indicators is thus the search for predictors of the disorder in the absence of symptoms of the disorder, an empirical strategy reflecting a conceptual judgment that vulnerability is present and stable but not easily observable—that is, latent.

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Excerpted from "Vulnerability to Psychopathology"
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