Targeting Anxiety Sensitivity in Prevention Treatments: A Meta-Analysis

Anxiety sensitivity refers to fears of anxiety-related sensations (e.g., your chest feeling tight) because of catastrophic beliefs about what those sensations mean (Reiss et al., 1986). Although anxiety sensitivity was originally studied in relation to panic- and anxiety-related disorders, it subsequently has been conceptualized as a transdiagnostic measure of distress intolerance and a risk factor for important health behaviors (Otto et al., 2016). Indeed, anxiety sensitivity relates to a wide range of psychopathology and negative health behaviors and is associated with the top three preventable causes of disease and death in the United States: (1) tobacco use, (2) poor diet and physical inactivity (obesity), and (3) alcohol overuse (see Otto et al., 2018). Because of such widespread relationships, anxiety sensitivity is an important mechanismto investigate.

Promoting mechanisms-focused science to transform how clinical scientists address the substantial effect of behaviors on a wide range of health and disease outcomes is a central goal for the NIH Science of Behavior Change Common Fund (Nielsen et al., 2018). These mechanisms are malleable treatment targets that play a role in initiating or maintaining behavior change; anxiety sensitivity is one such target.

Importantly, anxiety sensitivity is a malleable risk factor that can be addressed with a range of short-term interventions, making it a potentially important treatment target for both intervention and prevention efforts. We attend to this latter goal in our article, in relation to an experimental medicine approach to treatment development, which involves the following four steps: (1) identifying an intervention target, (2) developing/utilizing measures to permit verification of the target, (3) engaging the target through intervention, and (4) testing the degree to which target engagement produces the desired behavior change (Nielsen et al., 2018). Our meta-analysis of the anxiety sensitivity treatment literature attended to stages 3 and 4 of this clinical-science developmental model.

We included studies that tested the efficacy of interventions specifically designed to reduce anxiety sensitivity in adults through a randomized-controlled trial design. Importantly, included studies had to have selected their sample based on having a risk factor for psychopathology – for example, having elevated anxiety sensitivity. The interventions additionally needed to be brief: six sessions or less. We were interested in answering two main questions: (1) do these interventions reduce anxiety sensitivity, and (2) do these interventions reduce relevant clinical outcomes – including sleep-related, alcohol-related, depressive-related, trauma-related, obsessive-compulsive-related, and anxiety-related outcomes?

We found a total of 28 studies that met our inclusion criteria: 21 of those were main outcome studies and 7 of those were secondary analysis studies based on one of the 21 main outcomes studies. We found that anxiety sensitivity focused interventions, compared to the control conditions, significantly reduced anxiety sensitivity from the start to end of treatment (d = 0.54; a moderate effect size), and from the start of treatment to short-term follow-up assessment timepoints (d = 0.78; a large effect size), but not from the start of treatment to long-term follow-up assessment timepoints (d = 0.29). It’s important to note that heterogeneity – or the included studies having large variations in outcomes – was high for these latter two effects and thus should be interpreted with caution.

In terms of the second question (clinical outcomes), we found a significant decrease in clinical outcomes for anxiety sensitivity focused interventions compared to control conditions from the start to end of treatment (d = 0.41; a moderate effect size), from the start of treatment to short-term follow-up assessment timepoints (d = 0.27; a small-to-moderate effect size), and from the start of treatment to long-term follow-up assessment timepoints (d = 0.20; a small-to-moderate effect size).

In sum, our meta-analytic findings showed that brief (average of 80 total minutes) anxiety sensitivity interventions successfully reduce anxiety sensitivity, and, due to their effects on associated psychopathology and health behaviors, may be an important target for prevention efforts.

Target Article

Fitzgerald, H. E., Hoyt, D. L., Kredlow, M. A., Smits J. A. J., Schmidt, N. B., Edmondson, D., & Otto, M. W. (in press). Anxiety sensitivity as a malleable mechanistic target for prevention interventions: A meta-analysis of the efficacy of brief treatment interventions. Clinical Psychology: Science and Practice.

Discussion Questions

  • What further research would help us to understand the implications of treating Anxiety Sensitivity in prevention interventions?
  • What are the benefits of prevention efforts in reducing later mental health burden?
  • What barriers might exist for implementing Anxiety Sensitivity prevention interventions?

About the Authors

Hayley E. Fitzgerald, M.A., is a clinical psychology PhD student at Boston University in Michael Otto’s Translational Research Program. She is interested in the mechanisms underlying the development, maintenance, and treatment of anxiety and fear-based disorders. In addition to her research, Ms. Fitzgerald has worked clinically with individuals at the Center for Anxiety and Related Disorders, McLean Hospital, and the Boston VA.

Danielle L. Hoyt, M.A., is pursuing her clinical psychology PhD at Rutgers, the State University of New Jersey. She works in Dr. Teresa Leyro’s Affective and Biological Underpinnings of Substance use and Anxiety (ABUSA) lab, and in Dr. Leyro and Dr. Samantha Farris’ Addiction-Health Behavior Center. Her primary research interests lie at the intersection of substance use, anxiety-, and mood-related disorders, with particular emphasis on the underlying transdiagnostic risk factors as well as effective treatment dissemination.

Michael W. Otto, Ph.D., Michael W. Otto, Ph.D. is Professor of Psychological and Brain Sciences and Senior Fellow at the Institute for Health System Innovation and Policy at Boston University. Dr. Otto has had a major career focus on developing and validating new psychosocial treatments for mood, anxiety, and substance use disorders, as well as work in health promotion ranging from medication adherence to exercise behaviors. An enduring theme across these disorders is the role of exposure-based emotional tolerance/acceptance strategies in improving mental health, and the role of cognitive and affective risk factors in derailing adaptive behavior and goal attainment.

References Cited

Nielsen, L., Riddle, M., King, J. W., and the NIH Science of Behavior Change Implementation Team: Atklin, W. M., Chen, W., … Weber, W. (2018). The NIH Science of Behavior Change Program: Transforming the science through a focus on mechanisms of change. Behaviour Research and Therapy, 101, 3-11.

Otto, M. W., Eastman, A., Lo, S., Hearon, B. A., Bickel, W. K., Zvolensky, M., Smits, J. A. J., & Doan, S. N. (2016). Anxiety sensitivity and working memory capacity: Risk factors and targets for health behavior promotion. Clinical Psychology Review, 49, 67-78.

Otto, M.W., Smits, J. A. J., Fitzgerald, H.E., Powers, M.B., & Baird, S.O. (2018). Anxiety sensitivity and your clinical practice. In J. A. J. Smits, M. W. Otto, M. B. Powers & S. O. Baird (Eds.) Anxiety sensitivity: A clinical guide to assessment and treatment. San Diego, CA: Academic Press.

Reiss, S., Peterson, R., Gursky, D., & McNally, R. J. (1986). Anxiety sensitivity, anxiety frequency and the prediction of fearfulness. Behaviour Research and Therapy, 24(1), 1-8.