Huang Tianyi, Poole Elizabeth M, Vetter Celine, Rexrode Kathryn M, Kubzansky Laura D, Schernhammer Eva, Rohleder Nicolas, Hu Frank B, Redline Susan, Tworoger Shelley S
Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, United States; Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA, United States.
Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, United States.
Psychoneuroendocrinology. 2017 Oct;84:172-180. doi: 10.1016/j.psyneuen.2017.07.484. Epub 2017 Jul 19.
Dysregulation of the hypothalamus-pituitary-adrenal (HPA) axis has been suggested as a potential mechanism linking sleep and cardiometabolic disorders. However, the associations of two primary outputs of the HPA axis, cortisol and its antagonist dehydroepiandrosterone (DHEA), with sleep are less well studied. In the Nurses' Health Study II, 233 postmenopausal women provided five timed saliva samples over one day (immediately upon waking, 45min, 4h, and 10h after waking, and prior to going to sleep) to measure cortisol and DHEA. Of these, 209 completed assessment of their habitual sleep patterns using the Pittsburgh Sleep Quality Index (PSQI). We used piecewise linear mixed models to compare cross-sectional associations of slopes reflecting diurnal cortisol and DHEA rhythms with overall sleep quality and with seven sub-components. Overall, we observed no differences in the diurnal patterns of cortisol or DHEA between good versus poor sleepers as assessed by the global PSQI score. However, longer sleep latency was associated with significantly reduced cortisol awakening rise (p=0.02). Poorer subjective sleep quality (p=0.02), shorter sleep duration (p=0.02), and lower sleep efficiency (p=0.03) were associated with slower rate of cortisol decline later in the day. Women reporting daytime dysfunction had a sharper cortisol decline early in the day (p=0.03) but a flattened decline later in the day (p=0.01). The differences in diurnal patterns of DHEA between good versus poor sleepers, though less pronounced, were similar in direction to those of cortisol. Self-reported sleep duration, efficiency, latency and daytime dysfunction were associated with altered diurnal rhythms of cortisol and, to a lesser extent, DHEA. These findings provide support for the interplay between sleep and the HPA axis that may contribute to cardiometabolic disease.
下丘脑 - 垂体 - 肾上腺(HPA)轴功能失调被认为是连接睡眠与心脏代谢紊乱的一种潜在机制。然而,HPA轴的两个主要输出产物,皮质醇及其拮抗剂脱氢表雄酮(DHEA)与睡眠之间的关联研究较少。在护士健康研究II中,233名绝经后女性在一天内提供了五个定时唾液样本(醒来后即刻、醒来后45分钟、4小时、10小时以及睡前)以测量皮质醇和DHEA。其中,209名女性使用匹兹堡睡眠质量指数(PSQI)完成了对其习惯性睡眠模式的评估。我们使用分段线性混合模型来比较反映昼夜皮质醇和DHEA节律的斜率与整体睡眠质量以及七个子成分之间的横断面关联。总体而言,根据全球PSQI评分评估,睡眠良好者与睡眠不佳者之间的皮质醇或DHEA昼夜模式没有差异。然而,较长的入睡潜伏期与皮质醇觉醒升高显著降低相关(p = 0.02)。较差的主观睡眠质量(p = 0.02)、较短的睡眠时间(p = 0.02)和较低的睡眠效率(p = 0.03)与当天晚些时候皮质醇下降速度较慢相关。报告白天功能障碍的女性在当天早些时候皮质醇下降更明显(p = 0.03),但在当天晚些时候下降变平缓(p = 0.01)。睡眠良好者与睡眠不佳者之间DHEA昼夜模式的差异虽然不太明显,但方向与皮质醇相似。自我报告的睡眠时间、效率、潜伏期和白天功能障碍与皮质醇昼夜节律改变有关,在较小程度上也与DHEA有关。这些发现为睡眠与HPA轴之间的相互作用提供了支持,这种相互作用可能导致心脏代谢疾病。