Carroll Judith E, Esquivel Stephanie, Goldberg Alyssa, Seeman Teresa E, Effros Rita B, Dock Jeffrey, Olmstead Richard, Breen Elizabeth C, Irwin Michael R
University of California, Los Angeles, Cousins Center for Psychoneuroimmunology, Semel Institute for Neuroscience and Human Behavior, Los Angeles, CA.
Children's National Medical Center, Department of Pediatrics, Washington, DC.
Sleep. 2016 Mar 1;39(3):559-64. doi: 10.5665/sleep.5526.
Insomnia, particularly in later life, may raise the risk for chronic diseases of aging and mortality through its effect on cellular aging. The current study examines the effects of insomnia on telomere length, a measure of cellular aging, and tests whether insomnia interacts with chronological age to increase cellular aging.
A total of 126 males and females (60-88 y) were assessed for insomnia using the Diagnostic and Statistical Manual IV criterion for primary insomnia and the International Classification of Sleep Disorders, Second Edition for general insomnia (45 insomnia cases; 81 controls). Telomere length in peripheral blood mononuclear cells (PBMC) was determined using real-time quantitative polymerase chain reaction (qPCR) methodology.
In the analysis of covariance model adjusting for body mass index and sex, age (60-69 y versus 70-88 y) and insomnia diagnosis interacted to predict shorter PBMC telomere length (P = 0.04). In the oldest age group (70-88 y), PBMC telomere length was significantly shorter in those with insomnia, mean (standard deviation) M(SD) = 0.59(0.2) compared to controls with no insomnia M(SD) = 0.78(0.4), P = 0.04. In the adults aged 60-69 y, PBMC telomere length was not different between insomnia cases and controls, P = 0.44.
Insomnia is associated with shorter PBMC telomere length in adults aged 70-88 y, but not in those younger than 70 y, suggesting that clinically severe sleep disturbances may increase cellular aging, especially in the later years of life. These findings highlight insomnia as a vulnerability factor in later life, with implications for risk for diseases of aging.
失眠,尤其是在晚年,可能通过其对细胞衰老的影响增加衰老慢性病和死亡风险。本研究探讨失眠对端粒长度(一种细胞衰老的指标)的影响,并测试失眠是否与实际年龄相互作用以增加细胞衰老。
使用《精神疾病诊断与统计手册》第四版中原发性失眠的标准以及《国际睡眠障碍分类》第二版中一般失眠的标准,对总共126名男性和女性(60 - 88岁)进行失眠评估(45例失眠患者;81例对照)。采用实时定量聚合酶链反应(qPCR)方法测定外周血单个核细胞(PBMC)中的端粒长度。
在调整体重指数和性别的协方差分析模型中,年龄(60 - 69岁与70 - 88岁)和失眠诊断相互作用,可预测PBMC端粒长度较短(P = 0.04)。在最年长的年龄组(70 - 88岁)中,失眠患者的PBMC端粒长度明显较短,平均值(标准差)M(SD)=0.59(0.2),而无失眠的对照组M(SD)=0.78(0.4),P = 0.04。在60 - 69岁的成年人中,失眠患者和对照组的PBMC端粒长度没有差异,P = 0.44。
失眠与70 - 88岁成年人较短的PBMC端粒长度相关,但与70岁以下成年人无关,这表明临床上严重的睡眠障碍可能会增加细胞衰老,尤其是在生命的后期。这些发现突出了失眠是晚年的一个易患因素,对衰老相关疾病的风险有影响。