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睡眠反应性与失眠:遗传与环境的影响。

Sleep reactivity and insomnia: genetic and environmental influences.

机构信息

Henry Ford Hospital, Sleep Disorders and Research Center, Detroit, Michigan 48202, USA.

出版信息

Sleep. 2011 Sep 1;34(9):1179-88. doi: 10.5665/SLEEP.1234.

DOI:10.5665/SLEEP.1234
PMID:21886355
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3157659/
Abstract

STUDY OBJECTIVES

Determine the genetic and environmental contributions to sleep reactivity and insomnia.

DESIGN

Population-based twin cohort.

PARTICIPANTS

1782 individual twins (988 monozygotic or MZ; 1,086 dizygotic or DZ), including 744 complete twin pairs (377 MZ and 367 DZ). Mean age was 22.5 ± 2.8 years; gender distribution was 59% women.

MEASUREMENTS

Sleep reactivity was measured using the Ford Insomnia Response to Stress Test (FIRST). The criterion for insomnia was having difficulty falling asleep, staying asleep, or nonrefreshing sleep "usually or always" for ≥ 1 month, with at least "somewhat" interference with daily functioning.

RESULTS

The prevalence of insomnia was 21%. Heritability estimates for sleep reactivity were 29% for females and 43% for males. The environmental variance for sleep reactivity was greater for females and entirely due to nonshared effects. Insomnia was 43% to 55% heritable for males and females, respectively; the sex difference was not significant. The genetic variances in insomnia and FIRST scores were correlated (r = 0.54 in females, r = 0.64 in males), as were the environmental variances (r = 0.32 in females, r = 0.37 in males). In terms of individual insomnia symptoms, difficulty staying asleep (25% to 35%) and nonrefreshing sleep (34% to 35%) showed relatively more genetic influences than difficulty falling asleep (0%).

CONCLUSIONS

Sleep reactivity to stress has a substantial genetic component, as well as an environmental component. The finding that FIRST scores and insomnia symptoms share genetic influences is consistent with the hypothesis that sleep reactivity may be a genetic vulnerability for developing insomnia.

摘要

研究目的

确定睡眠反应性和失眠的遗传和环境贡献。

设计

基于人群的双胞胎队列。

参与者

1782 名个体双胞胎(988 对同卵或 MZ;1086 对异卵或 DZ),包括 744 对完整双胞胎(377 对 MZ 和 367 对 DZ)。平均年龄为 22.5±2.8 岁;性别分布为 59%的女性。

测量

使用福特失眠应激反应测试(FIRST)测量睡眠反应性。失眠的标准是入睡困难、保持睡眠或非恢复性睡眠“通常或总是”≥1 个月,且至少“有些”干扰日常功能。

结果

失眠的患病率为 21%。女性睡眠反应性的遗传率估计值为 29%,男性为 43%。女性睡眠反应性的环境方差较大,且完全由非共享效应引起。男性和女性的失眠分别有 43%至 55%是遗传的,性别差异不显著。失眠和 FIRST 评分的遗传方差相关(女性为 r=0.54,男性为 r=0.64),环境方差也相关(女性为 r=0.32,男性为 r=0.37)。就个别失眠症状而言,入睡困难(25%至 35%)和非恢复性睡眠(34%至 35%)比入睡困难(0%)表现出更多的遗传影响。

结论

对压力的睡眠反应具有相当大的遗传成分,以及环境成分。FIRST 评分和失眠症状具有遗传影响的发现与睡眠反应性可能是失眠发生的遗传易感性的假设一致。

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