Sleep Quality and Depressive Symptoms After Prostate Cancer: The Mechanistic Role of Cortisol
Sleep Quality and Depressive Symptoms After Prostate Cancer: The Mechanistic Role of Cortisol
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DOI：
10.1037/bne0000107
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发表时间：
2016-06-01
影响因子：
1.9
通讯作者：
Stanton, Annette L.
中科院分区：
文献类型：
--
作者：
Hoyt, Michael A.;Bower, Julienne E.;Stanton, Annette L.
在接受前列腺癌治疗的男性中，很大一部分人报告了临床上严重的睡眠问题，睡眠质量的紊乱对幸存者发展抑郁症状构成了重大风险。生物应激过程中的失调是睡眠不良对抑郁症状发生和/或发展的影响的基础，然而很少有研究试图确定PC幸存者这种联系的潜在神经生物学机制(例如，HPA轴激活)。本研究调查了接受前列腺癌治疗的男性患者的睡眠障碍、抑郁症状和每日皮质醇模式指数之间的关系。总共有66名男性(84.8%的白人；平均年龄=65.8岁，SD=9.04)在过去两年中因局限性前列腺癌而接受治疗。他们完成了问卷调查，以测量研究开始时(T1)和4个月后(T2)的睡眠质量和抑郁症状。他们还在T1的3天内每天提供4份唾液样本。计算三个皮质醇指数：昼夜斜率、曲线下面积(AUC(G))和皮质醇唤醒反应(CAR)。分析表明，控制体重指数和年龄，T1时睡眠质量较差与T2时抑郁症状水平较高显著相关。皮质醇斜率(间接效应=-.17，95%CI[-.61，-.01])和AUC(G)(间接效应=-.14，95%CI[-.43，-.01])有显著的间接效应，但CAR没有。结果表明，HPA活性的失调是睡眠中断对前列腺癌男性抑郁症状影响的神经生物学机制。
A substantial portion of men treated for prostate cancer report clinically significant sleep problems and disturbance in sleep quality constitutes significant risk for the development of depressive symptoms in survivors. Dysregulation in biological stress processes underlies the impact of poor sleep on the onset and/or progression of depressive symptoms, yet few studies have sought to identify potential neurobiological mechanisms (e.g., HPA axis activation) underlying this association in PC survivors. The present study examines the relationships between sleep disturbance, depressive symptoms, and indices of diurnal cortisol patterns among men treated for prostate cancer. In total, 66 men (84.8% White; mean age = 65.8 years, SD = 9.04) treated in the prior 2 years for localized prostate cancer were recruited. They completed questionnaires to measure sleep quality and depressive symptoms at study entry (T1) and 4 months later (T2). They also provided 4 saliva samples per day, over 3 days, at T1. Three cortisol indices were computed: diurnal slope, area under the curve (AUC(g)), and cortisol awakening response (CAR). Analyses indicate that, controlling for body mass index and age, worse sleep quality at T1 was significantly associated with higher levels of depressive symptoms at T2. Significant indirect effects were observed for cortisol slope (indirect effect = -.17, 95% CI [-.61, -.01]) and AUC(g) (indirect effect = -.14, 95% CI [-.43, -.01]), but not CAR. Results suggest that dysregulation in HPA activity acts as a neurobiological mechanism of the impact of sleep disruption on depressive symptoms in men with prostate cancer.