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<p>Obstructive sleep apnea (OSA) is characterized by repeated episodes of upper airway obstruction during sleep and leads to oxidative stress, systemic inflammation, and potentially accelerated telomere shortening. Studies comparing telomere length (TL) in individuals with and without OSA have obtained inconsistent results. This study compared TL across individuals without and with OSA of varying severity. We recruited 103 participants from a sleep clinic, all of whom underwent in-laboratory polysomnography and TL measurement. To assess TL, quantitative PCR was conducted for genomic DNA extracted from peripheral blood samples. Four participants were excluded because of sleep durations of &lt; 4&#xa0;h during polysomnography. The final analysis included 99 individuals (46 men and 53 women). Among these individuals, 13 did not have OSA; 28, 24, and 34 had mild OSA, moderate OSA, and severe OSA, respectively. Telomeres were significantly longer in individuals without OSA than in individuals with mild, moderate, and severe OSA (8.4 ± 5.1&#xa0;kb, 5.7 ± 3.1&#xa0;kb, 5.7 ± 2.2&#xa0;kb, and 4.8 ± 2.6&#xa0;kb, respectively; <i>P</i> = 0.009). Among individuals aged &lt; 50 years, no significant difference was observed in TL between the non-OSA and OSA groups. However, among individuals aged ≥ 50 years, individuals without OSA had significantly longer telomeres than did individuals with moderate to severe OSA. Our findings indicate that telomere shortening was significantly more pronounced in patients with increasing OSA severity than in individuals without OSA. Nocturnal hypoxia–induced inflammation in patients with OSA may contribute to telomere shortening.</p>

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Telomere shortening in middle-aged and elderly individuals with varying severities of obstructive sleep apnea

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年8月19日

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  • Yao-Pang Chung,
  • Wei-Sheng Chung

摘要

Obstructive sleep apnea (OSA) is characterized by repeated episodes of upper airway obstruction during sleep and leads to oxidative stress, systemic inflammation, and potentially accelerated telomere shortening. Studies comparing telomere length (TL) in individuals with and without OSA have obtained inconsistent results. This study compared TL across individuals without and with OSA of varying severity. We recruited 103 participants from a sleep clinic, all of whom underwent in-laboratory polysomnography and TL measurement. To assess TL, quantitative PCR was conducted for genomic DNA extracted from peripheral blood samples. Four participants were excluded because of sleep durations of < 4 h during polysomnography. The final analysis included 99 individuals (46 men and 53 women). Among these individuals, 13 did not have OSA; 28, 24, and 34 had mild OSA, moderate OSA, and severe OSA, respectively. Telomeres were significantly longer in individuals without OSA than in individuals with mild, moderate, and severe OSA (8.4 ± 5.1 kb, 5.7 ± 3.1 kb, 5.7 ± 2.2 kb, and 4.8 ± 2.6 kb, respectively; P = 0.009). Among individuals aged < 50 years, no significant difference was observed in TL between the non-OSA and OSA groups. However, among individuals aged ≥ 50 years, individuals without OSA had significantly longer telomeres than did individuals with moderate to severe OSA. Our findings indicate that telomere shortening was significantly more pronounced in patients with increasing OSA severity than in individuals without OSA. Nocturnal hypoxia–induced inflammation in patients with OSA may contribute to telomere shortening.