From the Department of Epidemiology (Kusters, Seeman), Fielding School of Public Health, UCLA; Davis School of Gerontology (Klopack, Crimmins), and Leonard Davis School of Gerontology, USC; Department of Geriatrics (Seeman), and Cousins Center for Psychoneuroimmunology (Cole, Carroll), Jane & Terry Semel Institute for Neuroscience & Human Behavior, Department of Psychiatry, David Geffen School of Medicine, UCLA, Los Angeles, California.
Psychosom Med. 2024 Jun 1;86(5):453-462. doi: 10.1097/PSY.0000000000001243. Epub 2023 Aug 21.
Short sleep and insomnia are each associated with a greater risk of age-related disease, which suggests that insufficient sleep may accelerate biological aging. We examine whether short sleep and insomnia alone or together relates to epigenetic age among older adults.
A total of 3795 men (46.3%) and women aged 56 to 100 years from the Health and Retirement Study were included. Insomnia was defined as reporting at least one insomnia symptom (difficulty falling asleep, waking up at night, or waking up too early in the morning) and feeling unrested when waking up most of the time. Those reporting <6 hours of bedtime were categorized as short sleepers. Three second- or third-generation epigenetic age acceleration clocks were derived from the 2016 Health and Retirement Study Venous Blood Study. The linear regression analysis was adjusted for age, sex, race/ethnicity, education, and obesity status.
Insomnia and short sleep were associated with acceleration of GrimAge of 0.49 (95% confidence interval [CI] = 0.03-0.94 years; p = .04) and 1.29 (95% CI = 0.52-2.07 years; p = .002) years, respectively, as well as a faster pace of aging (DunedinPACE; 0.018 [95% CI = 0.004-0.033; p = .02] and 0.022 [95% CI = -0.004 to 0.048; p = .11]). Compared with healthy sleepers, individuals with the combination of short sleep and insomnia had an accelerated GrimAge (0.97 years; 95% CI = 0.07-1.87 years, p = .04) and a greater DunedinPACE (0.032; 95% CI = 0.003-0.060, p = .04).
Our findings indicate that short sleep, insomnia, and the combination of the two are linked to epigenetic age acceleration, suggesting that these individuals have an older biological age that may contribute to risk of comorbidity and mortality.
睡眠不足和失眠均与年龄相关疾病的风险增加相关，这表明睡眠不足可能会加速生理衰老。我们研究了老年人中单纯的睡眠不足和失眠、以及二者同时存在是否与表观遗传年龄有关。
本研究共纳入来自健康与退休研究（Health and Retirement Study）的 3795 名年龄在 56 至 100 岁的男性（46.3%）和女性。失眠的定义为至少有一种失眠症状（入睡困难、夜间醒来或清晨醒来过早），并且大多数时候醒来时感到休息不足。报告睡眠时间<6 小时的人被归类为睡眠不足者。从 2016 年健康与退休研究静脉血研究中提取了三个第二代或第三代表观遗传年龄加速时钟。线性回归分析调整了年龄、性别、种族/民族、教育程度和肥胖状况。
失眠和睡眠不足分别与 GrimAge 加速 0.49 岁（95%置信区间 [CI] = 0.03-0.94 岁；p =.04）和 1.29 岁（95% CI = 0.52-2.07 岁；p =.002）有关，以及衰老速度加快（DunedinPACE；0.018 [95% CI = 0.004-0.033；p =.02] 和 0.022 [95% CI = -0.004 至 0.048；p =.11]）。与健康的睡眠者相比，同时存在睡眠不足和失眠的个体，其 GrimAge 加速（0.97 岁；95% CI = 0.07-1.87 岁，p =.04）和 DunedinPACE 更大（0.032；95% CI = 0.003-0.060，p =.04）。
我们的研究结果表明，睡眠不足、失眠以及两者的组合与表观遗传年龄加速有关，这表明这些个体的生物学年龄更老，可能导致共病和死亡率增加。
