ABSTRACT
This book has shown that anxiety sensitivity (AS) appears to play an important role in many forms of psychopathology; it is especially important in identifying people at risk for panic attacks. Given the importance of AS, it comes as no surprise that it is attracting increasingly more attention from theorists, researchers, and clinicians. The construct of AS has become refined and elaborated over time. Herein, details of its structure have been elaborated (chap. 5) and its relationships to related variables have been clarified (chaps. 1, 2, 3, 6, and 7). Thus, AS is not an immutable construct; it is an open concept (cf. Pap, 1958, 1962). That is, it is a work in progress, amenable to refinement, elaboration, and other changes. This concluding chapter considers what are seen as some of the most important issues for further research. Our understanding of AS may be enhanced by addressing the following:
Is AS best regarded as an entirely dimensional construct or are there categorical (taxonic) forms of AS?
If AS is hierarchically structured with lower and higher order factors (dimensions), how many factors are at each level?
How is AS related to other sensitivities (e.g., fear of pain; illness/injury/death sensitivity) as described in Reiss’ sensitivity theory (chap. 3)? Is AS really a fundamental fear (sensitivity) or the product of more basic fears?
How is AS related to or distinct from conceptually similar constructs such as trait anxiety or fear of negative evaluation (FNE)? For example, is AS a product of trait anxiety or is there some other relationship among the two constructs (e.g., AS may be a cause of trait anxiety)? Does the fear of publicly observable anxiety reactions belong to the domain of AS or is it part of FNE? Does it consist of a blend of the two?
Given the recent failures to support the expectancy theory (chap. 2), the question arises as to the nature of the relation between AS and anxiety expectancies. How do these constructs interact to cause or exacerbate anxiety-related phenomena (i.e., fear, anxiety, panic, and related avoidance)?
AS is correlated with many forms of psychopathology and tends to be elevated in clinical samples relative to normal controls. Does this mean that AS—or some dimensions thereof—are nonspecific vulnerability factors? If so, what are the implications for the expectancy theory (chap. 2) and sensitivity theory (chap. 3)?
Although AS tends to be elevated in clinical samples (relative to controls), it also varies in particular ways across various disorders (e.g., it is highest in panic disorder and posttraumatic stress disorder [PTSD] relative to other disorders). What causes the differences across disorders?
What are the environmental (e.g., social learning) and genetic determinants of AS? How important are environmental compared with genetic factors? Does their relative importance differ across the various lower and higher order AS factors?
If AS is “located” in the brain, what are its neurobiological substrates and how do they produce individual differences in AS? Do environmental factors influence these substrates?
How does AS unfold over time? At what point in the life span do individual differences in AS generally emerge? What sorts of cognitive operations are required? Do individual differences remain stable once they emerge or do they change in later life?
What are the major clinical implications of AS?
