Vulnerability to Anxiety 103
biological, and developmental levels (see Abramson, Alloy, & Metalsky, 1988; D. A.
Clark et al., 1999).
The cognitive model of anxiety presented in Chapter 2 (see Figure 2.1) describes
the proximal cognitive structures and processes involved in the persistence of anxiety,
whereas this chapter focuses on distal cognitive variables that are predispositions for
anxiety. These distal cognitive vulnerability factors are moderators (i.e., they affect the
direction and/or strength of association between stress and symptom onset), whereas
more proximal cognitive variables are mediators (i.e., they account for the relationship
between vulnerability, stress, and disorder onset) (see Baron & Kenny, 1986; Riskind &
Alloy, 2006). In the cognitive model multiple distal vulnerabilities are present at the bio-
logical, cognitive, and developmental levels so that some individuals may have multiple
vulnerabilities. These compound vulnerabilities might be associated with even higher
risk for disorder onset, a more severe symptom presentation, or comorbid emotional
conditions (Riskind & Alloy, 2006).
biologiCal DeterminantsIndividual differences in genetics, neurophysiology, and temperament will interact with
a predisposing cognitive vulnerability to heighten or reduce one’s anxiety- proneness in
response to life adversity or threat. Barlow (2002) convincingly argued for a generalized
biological vulnerability to anxiety disorders, in which heritability, a nonspecific vulner-
ability factor, accounts for 30–40% of variability across all anxiety disorders. This
genetic vulnerability is most likely expressed through elevations in broad personality
traits or temperaments like neuroticism, trait anxiety, or negative affectivity. Chronic
arousal, prepotent neuroanatomical structures (e.g., amygdala, locus coeruleus, BNST,
right prefrontal cortex), and neurotransmitter abnormalities in serotonin, GABA, and
CRH are other biological vulnerabilities to anxiety that have etiological significance, in
part by interacting in a synergistic fashion with cognitive vulnerability (see Chapter 1
for further discussion).
personality vulnerabilityNeuroticism and Negative Affectivity
Eysenck and Eysenck (1975) described neuroticism (N) as a predisposition toward emo-
tionality in which the highly neurotic individual is overly emotional, anxious, wor-
risome, moody, and has a tendency to overreact strongly to a range of stimuli. High
N and low E (extraversion) individuals—or introverted individuals—were considered
more likely to develop anxiety because they have an overreactive limbic system that
causes them to more easily acquire conditioned emotional responses to arousing stimuli.
Although there is strong empirical support for high N in the pathogenesis of anxiety
(e.g., see review by Watson & Clark, 1984), empirical evidence for other characteristics
of N, such as its neurophysiological basis, have not been as well supported (Eysenck,
1992).
Watson and Clark (1984) proposed a mood– dispositional dimension called nega-
tive affectivity (NA). NA reflects a “pervasive individual difference in negative emo-