Effect of Obstructive Sleep Apnea and CPAP on Telomere Length and Its Associated Mechanisms: A Pilot Study.

The present study aimed to investigate the effect of obstructive sleep apnea (OSA) and its treatment with continuous positive airway pressure (CPAP), the gold standard treatment for OSA on changes of telomere length and its associated mechanisms. In this mechanistic pilot study of a selective patient population (middle-aged men, BMI < 35 kg/m2, moderate-severe OSA), a 6-month randomized, double-blind, and sham-controlled clinical trial was conducted (Clinical Trials: NCT04872816, April 29, 2021 retrospectively registered). Participants were randomized to CPAP or sham-CPAP (randomization schema 2:1) and attended 7 visits, undergoing clinical assessments and blood collection to determine mean leukocyte telomere length (LTL) and assess metabolic and inflammatory markers. Among 127 individuals contacted, 46 met the inclusion criteria (n = 30 in the CPAP group and n = 16 in the sham-CPAP group). At baseline, individuals in both groups were homogeneous with respect to LTL (p = 0.106). Adherence during the intervention was measured in hours per night, recorded as 5.29 ± 1.09 hours/night for the sham-CPAP group and 5.71 ± 0.19 hours/night for the CPAP group, representing the last 30 days prior to the final visit. Three measurements of LTL were taken at baseline, 3 months, and 6 months. After 6 months of intervention, a statistically significant effect of treatment was observed (p = 0.001) on LTL, with the sham-CPAP group showing a greater reduction (1.0117 ± 0.1552, 0.9457 ± 0.0747, 0.8482 ± 0.2163) compared with the CPAP group (1.0960 ± 0.1122, 1.0521 ± 0.1094, 1.0675 ± 0.1225). Furthermore, a negative correlation between delta LTL and delta TNF-α at Visit 7 and Visit 1 was found (ρ = -0.216, p = 0.003), primarily attributed to the sham-CPAP intervention (ρ = -0.383, p = 0.009) compared with CPAP use (ρ = 0.021, p = 0.800). We conclude that CPAP, compared with sham-CPAP placebo, was associated with stabilization in LTL, potentially through modulation of TNF-α.