Mathilde Reyt, Denise C Jarrin, Aurore A Perrault, Florence Borgetto, Dylan Smith, Kirsten Gong, Lukia Tarelli, Josée Savard, Thien Thanh Dang-Vu, Jean-Philippe Gouin
Insomnia disorder is associated with pathophysiological alterations that may contribute to long-term mental and physical health risks. Cognitive behavioral therapy for insomnia (CBTi) is the first-line treatment for insomnia disorder, yet its effects on physiological outcomes remain unclear. This secondary analysis of a randomized-controlled trial examined the effects of CBTi on cardiovascular and immunological biomarkers. Sixty-two participants with insomnia disorder were randomized to CBTi (N = 33, 75.8% female, Mage = 48.8 ± 17.1 years) or Waitlist (WL) control (N = 29, 75.9% female, Mage = 52.2 ± 15.6 years). Cardiovascular parameters included systolic blood pressure (SBP), diastolic blood pressure (DBP), heart rate (HR), and nocturnal heart rate variability (HRV). Inflammatory markers from blood samples included C-reactive protein (CRP), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and brain-derived neurotrophic factor (BDNF). All outcomes were assessed at baseline (T1), at 3 months following completion of CBTi or WL period (T2), and at 6 months for the WL group (T3, after CBTi for the WL participants). No significant Group-by-time effects were observed for SBP, DBP, HR, HRV and any inflammatory markers (ps > 0.05) from T1 to T2. When pooling treatment effects following CBTi exposure across both groups (T1 to T2 in CBTi group and T1 to T3 in WL group), no significant biomarker changes were observed. Overall, results indicate that CBTi did not produce detectable changes in cardiovascular or inflammatory markers among healthy individuals with insomnia disorder. These findings suggest a dissociation between improved subjective insomnia symptoms and the lack of change in cardiovascular and immune biomarkers following CBTi in healthy participants (https://www.isrctn.com/ISRCTN13983243).