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Cardiac Vagal Tone: Regulator of Inflammation and Clinical Symptoms in Insomnia and Schizophrenia

  • Author(s): Reed, Alexandra Claire
  • Advisor(s): Yee-Bradbury, Cindy M.
  • Bower, Julienne E.
  • et al.
Abstract

Cardiac vagal tone (CVT) reflects the contribution of the parasympathetic nervous system to cardiac regulation and is hypothesized to contribute to the regulation of inflammation and expression of psychopathology. CVT may play an important role in sleep disturbance and insomnia treatment. Through a series of four studies, this dissertation interrogated the associations between CVT, inflammation, and clinical symptoms in sleep disturbed samples and evaluated possible roles for CVT in insomnia intervention. Studies 1 and 2 proposed a specific model: chronic sleep disturbance reduces CVT with downstream effects on inflammation and clinical symptoms. Studies 1 and 2 then evaluated cross-sectional associations between these variables and tested exploratory mediation models in two samples with poor sleep quality: 106 older adults with insomnia and 39 patients with first episode schizophrenia. Overall, results did not support the mediation models in either sample. However, findings revealed novel associations between CVT and cellular inflammatory processes in older adults and extended a negative association between CVT and systemic inflammation to schizophrenia, consistent with the cholinergic anti-inflammatory pathway. Studies 3 and 4 then evaluated possible roles for CVT in a randomized controlled trial which compared active behavioral treatments (Cognitive Behavioral Therapy for Insomnia and Tai Chi Chih) to sleep education in older adults with insomnia. Study 3 revealed that active behavioral interventions led to improvements in insomnia and clinical symptoms without up-regulating CVT, indicating that CVT is unlikely to be a mechanism supporting insomnia recovery. Study 4 then determined whether individual differences in CVT at pre-treatment moderated the effects of active behavioral interventions on key trial outcomes. Results showed that CVT did not moderate treatment effects. Null findings from Studies 3 and 4 underscore the need for further identification and evaluation of candidate mechanisms and moderators to maximize existing behavioral treatments for insomnia. Taken together, present results add to the mixed literature on CVT. Findings simultaneously challenge the assumption that CVT is a reliable correlate of clinical state and extend prior research on the role of the anti-inflammatory pathway in two unique samples with poor sleep quality.

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