Impact of Well-Timed vs. Mis-timed Sleep Extension on Adolescents’ Dietary Intake

项目摘要 最近的研究表明，睡眠可以在预防肥胖和长期发病方面发挥新的作用。 人口研究发现睡眠过少预示肥胖的发展和实验研究 研究表明，睡眠不足会增加饮食摄入量，而不会增加体力活动。睡眠可能是一种 尤其是针对青少年的有效干预目标。在青春期，睡眠不足是非常重要的。 普遍的，肥胖率上升最多，非睡眠导向的肥胖预防计划最少 成功，年轻人可以发展持久的饮食模式，为终身肥胖奠定基础， 健康风险。我们的实验室已经证明了青少年睡眠时间更长的承诺， 间隙我们发现，通过早睡来延长青少年的睡眠时间， 早睡型（“晨雀”;喜欢早睡早起），而不是晚睡型（“夜雀 猫头鹰”;喜欢晚睡晚起的人）。这种影响不仅在统计上很强，而且在大约400 随着时间的推移，每天的卡路里差异可能会导致体重发生重大变化。除了卡路里之外， 云雀和猫头鹰在睡眠延长后消耗的血糖负荷存在类似的差异， 并且血糖负荷与长期发病率独立相关。我们断言， 云雀和猫头鹰对长时间睡眠的反应是由于昼夜节律失调： 外部睡眠-觉醒需求和内部生物钟的定时。我们建议，对于青少年猫头鹰， 早睡干预会导致睡眠时间失调，从而抵消长时间睡眠的好处。 持续时间在成年人中，严重的昼夜节律失调会大大增加肥胖的风险，甚至 适度的错位与较高的热量摄入有关。如果因果关系在青春期成立， 强调早睡的常见睡眠建议可能会浪费有限的资源，甚至对健康有害。 猫头鹰相比之下，考虑生理时钟类型的方法可能会利用改善的生理时钟类型的潜在影响。 我们为百灵鸟展示的睡眠。在这里，我们提出了一个新的实验研究，其中124名健康的14- 18岁的孩子（62只猫头鹰和62只云雀）完成了为期3周的试验，包括睡眠限制和睡眠时间。 扩展，其中扩展周期被随机分配为相对于 时间型独立关注热量摄入和血糖负荷，我们将评估饮食影响 与青少年的生物钟相比，睡眠时间的长短是有区别的。我们将 测试一个因果模型，其中睡眠时间在促进或否定 睡眠延长。这是我们研究计划的关键下一步，该计划显示了睡眠的前景 扩展，以防止肥胖和发病率，但到目前为止，只有早期的chronotypes（云雀）。于年底 通过这项研究，我们预计将获得更好地利用睡眠的力量来预防肥胖所需的知识 这将有助于降低高危青年的发病率和长期发病率，为更有效的公共卫生干预措施奠定基础。

Project Summary Recent research shows that sleep could play a novel role in preventing obesity and long-term morbidity. Population studies find that too little sleep predicts the development of obesity and experimental studies show that short sleep increases dietary intake without increasing physical activity. Sleep may be a particularly potent intervention target for adolescents. During adolescence, inadequate sleep is very common, obesity rates are rising most, non-sleep-oriented obesity prevention programs have had least success, and young people can develop enduring dietary patterns that set the stage for life-long obesity and health risk. Our lab has shown both the promise of longer sleep for adolescents and a critical knowledge gap. We found that extending adolescents’ sleep via earlier bedtimes impressively reduced caloric intake for early chronotypes (“Morning Larks”; who prefer early bed- and rise times), but not late chronotypes (“Night Owls”; who prefer late bed- and rise times). The effect was not only statistically strong, but at roughly 400 calories difference per day, could add up to major shifts in body weight over time. Beyond calorie counts, there was a similar discrepancy in the glycemic load consumed by Larks and Owls after sleep extension, and glycemic load has been independently linked to long-term morbidity. We assert that the discrepancy in how Larks and Owls responded to longer sleep is due to circadian misalignment: a mismatch between the timing of external sleep-wake demands and internal biological clock. We propose that, for adolescent Owls, an early-to-bed intervention induces misaligned sleep timing that counters the benefits of longer sleep duration. In adults, severe circadian misalignment dramatically increases the risk for obesity, and even modest misalignment is linked to higher caloric intake. If a cause-effect relationship holds in adolescence, common sleep advice emphasizing earlier bedtimes might waste limited resources or even do harm for Owls. In contrast, an approach that considers chronotype might capitalize on the potent effect of improved sleep that we have shown for Larks. Here, we propose a novel experimental study in which 124 healthy 14- 18-year-olds (62 Owls and 62 Larks) complete a 3-week trial involving periods of sleep restriction and sleep extension, in which the extension periods are randomly assigned to be aligned vs. misaligned relative to chronotype. Focusing independently on caloric intake and glycemic load, we will assess the dietary effect of sleep extension when it is well-timed versus poorly-timed relative to adolescents’ internal clocks. We will test a causal model in which sleep timing plays an important role in promoting or negating the benefits of sleep extension. This is pivotal next step for our research program, which has shown the promise of sleep extension to prevent obesity and morbidity, but so far only for early chronotypes (Larks). At the end of this study, we anticipate having the knowledge needed to better harness the power of sleep to prevent obesity and long-term morbidity for at-risk youth, laying the foundation for more effective public health interventions.