102 COGNITIVE THEORY AND RESEARCH ON ANXIETY
In each of these case illustrations the emergence of an anxiety disorder occurred
within the context of predisposing factors and precipitating circumstances. Frequently
individuals with anxiety disorders report a predisposition toward high anxiety, ner-
vousness or worry, as well as precipitating events that escalate their daily stress. Since
predisposing biological or psychological characteristics and environmental factors are
both involved in the etiology of clinical anxiety, diathesis– stress models are frequently
proposed to account for individual differences in risk for anxiety (Story, Zucker, &
Craske, 2004). In many cases major life events, traumas, or ongoing adversities are
involved in anxiety; in others, the precipitants are not so dramatic, and fall within the
realm of normal life events (e.g., increased work stress, an uncertain medical test, an
embarrassing experience). These differences in clinical presentations have led research-
ers to search for vulnerability and risk factors that might predict whether a person
develops an anxiety disorder.
In this chapter we present the cognitive model of vulnerability to anxiety. We begin
by defining some of the key concepts employed in etiological models of disorder. This is
followed by an overview of the role that heritability, neurophysiology, personality, and
life events may play in the origins of anxiety disorders. We then present the cognitive
vulnerability model of anxiety that was first articulated in Beck et al. (1985). The chap-
ter concludes with a discussion of the empirical support for the last two hypotheses of
the cognitive model, elevated personal vulnerability and enduring threat- related beliefs,
that pertain directly to the issue of etiology.
vulnerability: Definitions anD CarDinal featuresAlthough often used interchangeably, the terms “vulnerability” and “risk” have very
distinct meanings (see Ingram, Miranda, & Segal, 1998; Ingram & Price, 2001). Risk
is a descriptive or statistical term referring to any variable whose association with a
disorder increases its likelihood of occurrence (e.g., gender, poverty, relationship status)
without informing about actual causal mechanisms. Vulnerability, on the other hand,
is a risk factor that has causal status with the disorder in question. Vulnerability can be
defined as an endogenous, stable characteristic that remains latent until activated by a
precipitating event. This activation can lead to the occurrence of the defining symptoms
of a disorder (Ingram & Price, 2001). Knowledge of vulnerability factors has treatment
implications because it will elucidate the actual mechanisms of etiology (Ingram et al.,
1998). However, vulnerability does not directly lead to disorder onset but instead is
mediated by the occurrence of precipitating events.
Vulnerability factors are internal, stable, and latent or unobservable until activated
by a precipitating event (Ingram et al., 1998; Ingram & Price, 2001). This private, unob-
servable nature of vulnerability in asymptomatic individuals has presented special chal-
lenges for researchers in search of reliable and valid methods for detecting vulnerability
(Ingram & Price, 2001). Moreover, vulnerability constructs must have high sensitivity
(i.e., must be present in disordered individuals), a moderate level of specificity (i.e., more
prevalent in the target disorder than in controls), and be distinct from the precipitating
life event (Ingram et al., 1998). In Beck’s cognitive model vulnerability constructs are
neither necessary nor sufficient but rather contributory causes of psychopathology that
may interact or combine with other etiological pathways that are present at the genetic,