Necessary versus sufficient causes of impaired physiological functioning in generalized anxiety disorder.

Open Access
Fisher, Aaron Jason
Graduate Program:
Doctor of Philosophy
Document Type:
Date of Defense:
May 18, 2011
Committee Members:
  • Michelle Gayle Newman, Dissertation Advisor
  • Michelle Gayle Newman, Committee Chair
  • Kristin Buss, Committee Member
  • William Ray, Committee Member
  • Douglas Granger, Committee Member
  • Generalized anxiety disorder
  • autonomic nervous system
  • cardiac
  • health
  • emotion
An extensive body of literature has established the role of impaired autonomic nervous system (ANS) functioning in individuals with clinically-diagnosed generalized anxiety disorder (GAD; c.f. Hoehn-Saric, McLeod, Funderburk, & Kowalski, 2004). Worry is the cardinal feature and central facet of GAD specifically, as well as a major component of anxiety and mood disorders more broadly (Barlow, 2004). Worry has been shown to disrupt the adaptive responsiveness of physiological systems in anxious individuals as well as controls. Worrisome thinking prior to exposure to a phobic image has been shown to preclude cardiovascular response to the image in anxious individuals (Borkovec & Hu, 1990; Borkovec, Lyonfields, Wiser, & Deihl, 1993) and the induction of worry in non-anxious controls has been shown to cause significant reductions in heart rate variability (HRV) – a proxy for parasympathetic control of heart rate (HR; Hofmann, et al., 2005; Lyonfields, Borkovec, & Thayer, 1995; Thayer, Friedman, & Borkovec, 1996). If worry is both necessary and sufficient for physiological impairment, it would be expected that a non-clinical, high-worry control group would exhibit impairments in physiological functioning equivalent to clinically-diagnosed GAD participants at resting baseline, and that phasic increases in state worry would impair physiological reactivity across healthy controls, high-worry controls, and GAD participants in response to a stressful task. However, although prior research seems to indicate that worry is necessary, it may be that clinical distress, significant impairment, or other aspects of the clinically-diagnosed GAD syndrome – such as the inability to control worry – are required for the development of significant physiological dysfunction. It is precisely this question that the present study aimed to address. The present study compared clinically-diagnosed GAD patients to both healthy controls, and high-worry controls. The lattermost group demonstrated significant elevations in worry that placed them within a clinical range, but did not meet clinical criteria for GAD or any other Axis I disorder as determined by structured interview. Moreover, phasic variability in state worry was tracked across baseline, during the experimental induction of worry versus relaxation, during two laboratory stressors, and finally following a 20-minute recovery period. Measures of HR, HRV, salivary alpha-amylase – an index of adrenergic sympathetic tone, and cortisol were taken across the study. Thus, we examined the relatively effects of state, trait, and clinical worry (GAD) on sympathetic, parasympathetic, and hypothalamic-pituitary-adrenal (HPA) axis systems at resting baseline, in response to a laboratory stressor, and following recovery. Results indicated that clinically-diagnosed GAD accounted for impairments in parasympathetic, sympathetic, cardiovascular, and HPA systems above and beyond state and trait worry. Individuals with GAD exhibited reduced vagal cardiac control at baseline and recovery, poor coordination of sympathoexcitatory-HPA axis stress reactivity, and rigidity in cardiovascular reactivity resulting from experimentally induced worry. In addition, it was demonstrated that impairments in vagal cardiac control following recovery were a function of expressed anger and the degree to which individuals with GAD were able to expressed sadness and/or contentment counteracted the negative effect of anger.