Background & Aims

Generalized anxiety disorder (GAD) is a common (1–8) condition characterized by persistent, uncontrollable worry (9). Extant literature has linked GAD diagnosis with increased risk of experiencing pain symptoms and pain disorder (10–16). Indeed, more than one-third of primary care patients with GAD identify pain as their primary complaint (4). Similarly, higher GAD prevalence has been documented among individuals with chronic pain compared to the general population (17). Relatively fewer studies have examined the implications of comorbid GAD in individuals with chronic pain, but preliminary results suggest it may be associated with greater pain severity (14,17) relative to chronic pain without GAD. Examinations of the association between GAD and pain interference have yielded mixed results (14,18). The present study examines the relationship between GAD symptom severity and chronic pain outcomes in a nationally representative sample of U.S. adults.

Methods

We used cross-sectional data from the 2019 National Health Interview Survey, a survey of the U.S. civilian, noninstitutionalized population. Participants self-reported their GAD (GAD-7) (19) and depression (Patient Health Questionnaire-8) (20) symptoms. We used a logistic regression in the full sample (N=31,304 adults) to assess the relationship between GAD symptoms and chronic pain status (i.e., pain experienced most days or daily over the past three months). Next, we used a series of logistic regressions in the chronic pain subsample (n=7,184) to examine the relationship between GAD symptoms and the likelihood of self-reporting severe pain, effective pain management, pain interference, and receipt of pain treatment. All analyses adjusted for established demographic and socioeconomic correlates of chronic pain. Data were weighted to adjust for non-responses (21). We used Benjamini-Hochberg false discovery rate (22) correction to control the Type I error rate.

Results

There were 7,184 adults (22.9%) who reported chronic pain. After adjusting for established demographic (age, sex, race, and ethnicity) and socioeconomic (income and education) correlates of pain conditions, GAD symptoms were associated with chronic pain status (b=0.115, SE=.003, t=37.800, p< .001). Depression was excluded from all reported models due to high multicollinearity with GAD (r=.790). Within the subsample who endorsed chronic pain, greater (more severe) GAD symptoms were associated with greater likelihood of endorsing severe pain (b=0.063, SE=.005, t=13.299, p< .001) and pain interference (b=0.096, SE=0.005, t=20.746, p< .001). Greater GAD symptoms were associated with lower likelihood that the individual effectively managed their chronic pain symptoms (b=-0.058, SE=0.005, t=-11.050, p< .001). GAD symptoms were associated with a slightly greater likelihood of receiving pain treatment (b=0.017, SE=0.005, t=3.419, p=.001).

Conclusions

The present study builds on evidence that GAD diagnosis is related to pain symptoms and pain disorders (10–17) by demonstrating an association between a dimensional measure of GAD symptoms and chronic pain status, even when controlling for known predictors of chronic pain. Furthermore, this study found that among individuals with chronic pain, GAD symptoms were positively associated with severe pain, pain interference, and likelihood of receiving treatment for chronic pain and negatively associated with effective pain management, thereby advancing understanding of the implications of GAD within chronic pain conditions. These associations held after adjusting for established correlates of chronic pain (i.e., age, sex, race, ethnicity, income, and education). Despite modest effect sizes, this study highlights the incremental value of GAD symptoms in predicting adverse pain outcomes and underscores the importance of considering GAD symptoms when treating chronic pain.

References

Kroenke K, Spitzer RL, Williams JBW, Monahan PO, Löwe B. Anxiety Disorders in Primary Care: Prevalence, Impairment, Comorbidity, and Detection. Ann Intern Med. 2007 Mar 6;146(5):317.

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Presenting Author

Kerry L. Kinney

Poster Authors

Kerry Kinney

PhD

Vanderbilt University

Lead Author

Ashley Watts

PhD

Vanderbilt University

Lead Author

Katja Beesdo-Baum

Dr. rer. nat.

TUD – Dresden University of Technology

Lead Author

Matthew Morris

Vanderbilt University Medical Center

Lead Author

Topics

  • Mechanisms: Psychosocial and Biopsychosocial