Sleep Length and Circadian Regulation in Humans

描述（由申请人提供）：数百万美国人患有昼夜节律睡眠障碍，包括倒班睡眠障碍、时差反应、睡眠阶段延迟综合征，可能还有冬季抑郁症。这些疾病的典型特征是持续失眠和/或白天过度嗜睡，表现受损和胃肠道不适。这些负面症状是由于外部社会世界的时间和内部昼夜节律（身体）时钟的时间不一致。明亮的光线可以有效地治疗昼夜节律睡眠障碍，它可以改变生物钟的相位，从而使其与外部社会世界的时间重新调整。人们普遍认为，社会影响导致睡眠限制在现代社会越来越普遍。我们最近首次证明，与长时间睡眠相比，短时间睡眠明显减少了明亮光线的阶段进展。因此，当人们缩短睡眠时间时，他们无意中降低了对强光的昼夜节律反应。这些减少的相移到光的机制是未知的。然而，睡眠不足至少有两个方面可能导致这种影响。首先，短时间睡眠与部分睡眠剥夺有关。其次，由于人类睡觉时闭着眼睛，醒着的时候经常暴露在光线下，所以短时间的睡眠也与短时间的黑暗有关。我们的总体目标是确定短睡眠期影响到明亮光线的相移的生物行为机制。具体目标1是在控制黑暗长度的情况下，确定部分睡眠剥夺对进入光明阶段的影响。具体目标2是确定短黑暗长度对阶段进展的影响，同时最大限度地减少睡眠剥夺。我们将通过测量唾液褪黑激素（松果体释放的一种神经内分泌激素）来估计人类生物钟的时间，并通过活动记录仪收集睡眠数据，通过计算机评估收集睡意、情绪、胃肠不适和认知表现。表征睡眠剥夺和黑暗长度对人类昼夜节律相移到光的不同影响对于理解人类在日常生活活动中如何对光的反应至关重要。此外，本研究的发现将为避免光相移的减少提供重要和实用的建议，从而优化昼夜节律睡眠障碍的强光治疗，从而改善公众健康和安全、福祉、情绪、认知功能和生活质量。

DESCRIPTION (provided by applicant): Millions of Americans suffer from circadian rhythm sleep disorders, which include shift work sleep disorder, jet lag, delayed sleep phase syndrome and possibly winter depression. These conditions are typically characterized by persistent insomnia and/or excessive daytime sleepiness, impaired performance, and gastrointestinal distress. These negative symptoms result from a misalignment between the timing of the external social world and the timing of the internal circadian (body) clock. Circadian rhythm sleep disorders are effectively treated with bright light, which phase shifts the circadian clock, thereby realigning it with the timing of the external social world. It is widely recognized that social influences have led to an increasing prevalence of sleep restriction in modern society. We recently demonstrated for the first time that short sleep episodes, when compared to long sleep episodes, markedly reduce phase advances to bright light. Thus when people cut their sleep short, they inadvertently reduce their circadian responsiveness to bright light. The mechanism(s) behind these reduced phase shifts to light are unknown. However, there are at least two aspects of short sleep episodes that could be responsible for this effect. First, short sleep episodes are associated with partial sleep deprivation. Second, as humans sleep with their eyes closed and are usually exposed to light when awake, short sleep episodes are also associated with short dark lengths. Our overall goal is to determine the biobehavioral mechanisms by which short sleep episodes impair phase shifts to bright light. Specific Aim 1 is to determine the effect of partial sleep deprivation on phase advances to light, while controlling for dark length. Specific Aim 2 is to determine the effect of short dark lengths on phase advances to light while minimizing sleep deprivation. We will estimate the timing of the human circadian clock by measuring salivary melatonin, a neuroendocrine hormone released from the pineal gland, and collecting measures of sleep via actigraphy, and sleepiness, mood, gastrointestinal distress and cognitive performance via computerized assessment. Characterization of the separate effects of sleep deprivation and dark length on circadian phase shifts to light in humans is critical to understanding how humans respond to light during their daily life activities. Furthermore, the findings of this research will produce important and practical recommendations for avoiding decrements to phase shifts to light, thereby optimizing the bright light treatment of circadian rhythm sleep disorders, and thus improving public health and safety, well-being, mood, cognitive function, and quality of life.