Department of Integrative Physiology, University of Colorado Boulder, Boulder, Colorado.
Department of Applied Mathematics and Statistics, Colorado School of Mines, Golden, Colorado.
J Biol Rhythms. 2023 Feb;38(1):77-86. doi: 10.1177/07487304221134330. Epub 2022 Nov 22.
Late sleep timing is prevalent in early childhood and a risk factor for poor behavioral and health outcomes. Sleep timing is influenced by the phase of the circadian clock, with later circadian timing linked to delayed sleep onset in young children. Light is the strongest zeitgeber of circadian timing and, in adults, evening light produces circadian phase delay in an intensity-dependent manner. The intensity-dependent circadian phase-shifting response to evening light in children, however, is currently unknown. In the present study, 33 healthy, good-sleeping children aged 3.0 to 4.9 years (M = 4.14 years, 39% male) completed a 10-day between-subjects protocol. Following 7 days of a stable sleep schedule, an in-home dim-light circadian assessment was performed. Children remained in dim-light across 3 days (55 h), with salivary melatonin collected in regular intervals throughout each evening. Phase-shifting effects of light exposure were determined via changes in the timing of the dim-light melatonin onset (DLMO) prior to (Day 8) and following (Day 10) a light exposure stimulus. On Day 9, children were exposed to a 1 h light stimulus in the hour before their habitual bedtime. Each child was randomly assigned to one intensity between 5 and 5000 lux (4.5-3276 melanopic EDI). Across light intensities, children showed significant circadian phase delays, with an average phase delay of 56.1 min (SD = 33.6 min), and large inter-individual variability. No relationship between light intensity and magnitude of the phase shift was observed. However, a greater percentage of melatonin suppression during the light exposure was associated with a greater phase delay ( = -0.73, < 0.01). These findings demonstrate that some young children may be highly sensitive to light exposure in the hour before bedtime and suggest that the home lighting environment and its impact on circadian timing should be considered a possible contributor to behavioral sleep difficulties.
晚睡时间在幼儿中很常见，是行为和健康结果不佳的一个风险因素。睡眠时间受生物钟相位的影响，而生物钟相位较晚与幼儿入睡时间延迟有关。光作为生物钟计时的最强 Zeitgeber，在成年人中，傍晚的光会以强度依赖的方式引起生物钟相位延迟。然而，目前尚不清楚儿童在傍晚的光下，强度依赖性的生物钟相位改变反应。在本研究中，33 名健康、睡眠良好的 3.0 至 4.9 岁儿童（M=4.14 岁，39%为男性）完成了一项为期 10 天的被试间方案。在稳定的睡眠时间表进行 7 天后，进行了家庭暗光下的生物钟评估。儿童在暗光下连续 3 天（55 小时），定期采集唾液褪黑素。通过在光暴露刺激之前（第 8 天）和之后（第 10 天）测量暗光下褪黑素开始时间（DLMO）的变化，确定光暴露的相移效应。在第 9 天，儿童在习惯的就寝时间前 1 小时接受 1 小时的光刺激。每个儿童随机分配到 5 到 5000 勒克斯（4.5-3276 个 melanopic EDI）之间的一个强度。在不同的光照强度下，儿童表现出明显的生物钟相位延迟，平均相位延迟为 56.1 分钟（SD=33.6 分钟），个体间差异很大。没有观察到光强度与相移幅度之间存在关系。然而，在光暴露期间，褪黑素抑制的百分比越大，相位延迟越大（=-0.73，<0.01）。这些发现表明，一些幼儿可能对睡前 1 小时的光暴露非常敏感，并表明家庭照明环境及其对生物钟计时的影响可能是行为性睡眠困难的一个潜在因素。
