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This randomized-controlled trial with 62 participants investigated whether Cognitive Behavioral Therapy for Insomnia (CBTi), the first-line treatment for insomnia disorder, affects cardiovascular and immune system biomarkers. Researchers measured blood pressure, heart rate, heart rate variability, and inflammatory markers including C-reactive protein, tumor necrosis factor-alpha, interleukin-6, and brain-derived neurotrophic factor before and after treatment. The study found no significant changes in any cardiovascular or inflammatory markers following CBTi treatment, suggesting that while CBTi effectively treats insomnia symptoms, it does not produce detectable physiological changes in these specific biomarkers among otherwise healthy individuals with insomnia.
Why it matters
These findings indicate that the benefits of CBTi for insomnia may be primarily psychological and sleep-related rather than producing measurable improvements in cardiovascular or immune function, at least in healthy populations. This helps clinicians set appropriate expectations about treatment outcomes and suggests that additional interventions may be needed to address physical health risks associated with chronic insomnia.
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⚠️ Preprint – Noch nicht peer-reviewed
Dieser Artikel wurde noch nicht von unabhängigen Experten begutachtet. Die Ergebnisse sind vorläufig und sollten mit Vorsicht interpretiert werden.
Evidence suggests that insomnia disorder is associated with pathophysiological alterations that may contribute to long-term physical, mental and inflammatory-related 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 randomized-controlled trial examined the effects of CBTi on cardiovascular and immunological biomarkers. Sixty-two participants with insomnia disorder were randomized to group-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- ), interleukin-6 (IL-6) and brain-derived neurotrophic factor (BDNF). All outcomes were assessed at baseline (T1), post-treatment assessment (T2, following completion of CBTi or WL period), and 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 > .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 physiological responses to CBTi are complex and may reflect dynamic and context-dependent processes (https://www.isrctn.com/ISRCTN13983243).