CIRCADIAN RHYTHMS, SLEEP, AND DEPRESSION RISK AT PUBERTY
CIRCADIAN RHYTHMS, SLEEP, AND DEPRESSION RISK AT PUBERTY
批准号:
2416058
负责人:
Mary A Carskadon
金额:
$51.29万
依托单位国家:
美国
项目类别:
财政年份:
1994
资助国家:
美国
项目状态:
已结题
起止时间:
1994-09-01 至 1999-04-30
关键词:
adolescence (12-20) behavior test biosensor device body temperature case history child behavior circadian rhythms disease /disorder proneness /risk electrocardiography electroencephalography electromyography electrooculography emotions homeostasis human puberty human subject major depression melatonin middle childhood (6-11) psychomotor reaction time sleep sleep deprivation thermometry urinalysis wakefulness
中文摘要
该项目的主要目的是了解青少年的睡眠
模式作为潜在的生物调节过程的函数,
青春期发育一种常见的青春期模式是延迟,
睡眠不足,反映了复杂的生物心理社会相互作用。的
这项研究的重要性源于已知的行为风险,
睡眠不足,包括白天过度嗜睡,学习成绩差
表现、情绪低落、受伤和事故。使用的技术
昼夜节律和睡眠研究,该项目承担三个
研究,每一个重点是基本的睡眠调节问题。
在研究1中,内源性昼夜节律振荡器输出的标记物
在108名10至14岁的女孩和男孩中进行了测量,
阶段睡眠、情绪、表现、嗜睡、深部体温(DBT),
和尿6-硫酸氧褪黑激素(6-SM)在一个周末期间测量
study.在实验室睡了2个晚上后,孩子们仍然保持清醒
在床上半卧位36小时,在“恒定”期间,
照明、食物和液体摄入以及活动受限的“常规”。一
夜复一年。昼夜节律参数包括内源性
DBT的昼夜节律时相(ECP)和振幅,以及6-SM的时间
起始、偏移和峰值。恢复睡眠变量标志着自我平衡
流程.具体的假设是(1)昼夜节律相位延迟,
(2)自我平衡睡眠/觉醒机制的强度在青春期下降。
本研究还获得了独特的昼夜节律发育数据库
青春期的节律和睡眠变量。
在研究2中,60名女孩和男孩在一个为期24天的实验室中进行评估,
despiry”协议,其中内源性的内在周期
可以准确地估计昼夜节律振荡器。措施见研究
1.在2个基线实验室检查日之后和2个恢复日之前,
睡眠/觉醒安排在28小时的一天,内源性
昼夜节律不能夹带,从而从正常的内源性节奏中释放出来,
睡眠和清醒的掩蔽效应。持续进行ECP常规评估,
ECA是连续三次,当身体的槽,
温度与预定的睡眠时段不同步。本研究
检验了内源性昼夜节律周期
振荡器在青春期延长;它还提供了丰富的身体
关于青春期睡眠、觉醒和昼夜节律过程的信息
成熟
研究3是内源性昼夜节律输出的纵向研究
32名正常儿童和40名有发展风险的儿童的起搏器
抑郁症是由于有严重抑郁症的家族史。的
研究1的恒定常规范式用于测量
正常儿童和处于青春期早期和晚期的高危儿童。这
一项研究检验了ECP在高危人群中变化更大的假设
极端的人群可能会表现出不同的睡眠异常。这些
研究结果可能会澄清睡眠,昼夜节律,
青少年情绪障碍
英文摘要
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.
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