CIRCADIAN RHYTHMS, SLEEP, AND DEPRESSION RISK AT PUBERTY

该项目的主要目的是了解青少年的睡眠。 作为潜在生物调节过程的函数的模式及其 青春期发育。一种常见的青春期模式被推迟并 睡眠不足，反映了复杂的生物、心理和社会互动。这个 这项研究的重要性源于已知的行为风险 睡眠不足，包括白天过度困倦，学校条件不佳 表现、情绪低落、受伤和意外。使用以下技术 昼夜节律和睡眠研究，该项目进行了三项 研究，每一项都集中在基本的睡眠调节问题上。 在研究1中，内源性昼夜节律振荡器的输出的标记 对108名10至14岁的青春期女孩和男孩进行了测量 各阶段。睡眠、情绪、表现、困倦、深层体温(DBT)、 并在周末测定尿中6-硫氧基黑素(6-SM) 学习。在实验室里睡了两个晚上后，孩子们仍然醒着 在床上以半卧位卧床36小时 照明、食物和液体摄入以及限制活动的例行公事。 接下来是康复之夜。昼夜节律参数包括内源性 DBT的昼夜节律相(ECP)和波幅以及6-SM的时间 起始值、偏移值和峰值。恢复期睡眠变量标志着体内平衡 流程。具体的假设是(1)昼夜节律、相位延迟和 (2)动态平衡睡眠/觉醒机制强度在青春期下降。 本研究还获得了一个独特的昼夜节律发育数据库 青春期的节奏和睡眠变量。 在研究2中，60名女孩和男孩在一个24天的实验室里接受了评估 “去同步化”协议从其中内源性的内在周期 昼夜节律振荡器可以被准确地估计。措施如研究中 1.在两个基线实验室之后，即恢复前两天， 睡眠/醒来被安排在28小时的一天中，内源性 昼夜节律不能缠绕，从而将内生节律从平日中解放出来。 掩盖睡眠和清醒的效果。持续的ECP和ECP例行评估 ECA分三次连续制作，当身体的低谷 体温与预定的睡眠时段不一致。本研究 检验了内源性昼夜节律周期的假设 振荡器在青春期延长；它还提供丰富的 有关青春期睡眠、觉醒和昼夜节律过程的信息 成熟。 研究3是对内源性昼夜节律输出的纵向研究。 32例正常儿童和40例高危儿童的起搏器 由于有严重抑郁障碍家族史而导致的抑郁症。这个 使用研究1的常量常规范式来测量ECP和ECA 青春期早期和后期的正常儿童和高危儿童。这 一项研究验证了ECP在高危人群中更具变异性的假设 极端人群可能会表现出不同的睡眠异常。这些 这些发现可能会澄清睡眠、昼夜节律和 青少年的情绪障碍。

The chief purpose of the project is to understand adolescent sleep patterns as a function of underlying bioregulatory processes and their pubertal development. A common adolescent pattern is delayed and insufficient sleep, reflecting complex biopsychosocial interactions. The importance of this research stems from the known behavioral risk of insufficient sleep, including excessive daytime sleepiness, poor school performance, depressed mood, injuries and accidents. Using techniques of circadian rhythms and sleep research, the project undertakes three studies, each focusing on basic sleep regulatory issues. In Study 1, markers of the output of the endogenous circadian oscillator are measured in 108 girls and boys ages 10 to 14 years spanning pubertal stages. Sleep, mood, performance, sleepiness, deep body temperature (DBT), and urinary 6-sulphatoxymelatonin (6-SM) are measured during a weekend study. After sleeping in the laboratory on 2 nights, children remain awake in bed in a semi-recumbent position for 36 hours during a "constant routine" of lighting, food and fluid intake, and restricted activity. A recovery night follows. Circadian rhythm parameters include endogenous circadian phase (ECP) and amplitude of DBT, as well as times of 6-SM onset, offset, and peak. Recovery sleep variables mark homeostatic processes. Specific hypotheses are (1) circadian rhythms phase delay and (2) intensity of homeostatic sleep/wake mechanisms declines at puberty. This study also obtains a unique developmental data base of circadian rhythm and sleep variables across puberty. In Study 2, 60 girls and boys are evaluated in a 24-day laboratory "forced desynchrony" protocol from which the intrinsic period of the endogenous circadian oscillator can be accurately estimated. Measures are as in Study 1. After 2 baseline laboratory, days and before 2 recovery days, sleep/wake are scheduled on a 28-hour-day to which the endogenous circadian cannot entrain, thus freeing the endogenous rhythm from usual masking effects of sleep and wake. Constant routine assessment of ECP and ECA are made serially on three occasions when the trough of body temperature is out of phase with the scheduled sleep episode. This study tests the hypothesis that the period of the endogenous circadian oscillator lengthens at puberty; it also provides a rich body of information regarding sleep, wake, and circadian processes during pubertal maturation. Study 3 is a longitudinal study of the output of the endogenous circadian pacemaker in 32 normal children and 40 children at risk to develop depression by virtue of a family history of major depressive disorder. The constant routine paradigm Of Study 1 is used to measure ECP and ECA in normal and at-risk children at early and late stages of puberty. This study tests the hypothesis that ECP is more variable in the at-risk group and that extreme groups may show different sleep abnormalities. These findings may clarify the relationships of sleep, circadian rhythms, and mood disorder in adolescents.