Drake Christopher L, Cheng Philip, Almeida David M, Roth Thomas
Henry Ford Health System, Detroit, MI.
Pennsylvania State University, University Park, PA.
Sleep. 2017 Oct 1;40(10). doi: 10.1093/sleep/zsx143.
Abnormalities in the stress system have been implicated in insomnia. However, studies examining physiological stress regulation in insomnia have not consistently detected differences in the hypothalamic-pituitary-adrenal (HPA)-axis response to stress. One explanation may be that deficits in the stress system are associated specifically with a biological vulnerability to insomnia rather than the phenotypic expression of insomnia. To examine stress response as a function of vulnerability to insomnia, this study tested response to the Trier Social Stress Test in a sample of healthy sleepers with varying familial risks for insomnia.
Thirty-five healthy individuals with and without familial risk for insomnia were recruited to complete a laboratory stressor. Participants with one or both biological parents with insomnia were categorized as positive for familial risk, whereas those without biological parents with insomnia were categorized as negative for familial risk. Participants completed the Trier Social Stress Test in the laboratory, and psychological and physiological (autonomic and HPA-axis) responses were compared.
Despite self-reported increases in anxiety, those positive for familial risk exhibited a blunted cortisol response relative to those without familial risk for insomnia. Individuals with blunted cortisol also reported heightened reactivity to personal life stressors, including increased sleep disturbances, elevated cognitive intrusions, and more behavioral avoidance.
Findings from this study provide initial evidence that abnormal stress regulation may be a biological predisposing factor conferred via familial risk for insomnia. This deficit may also predict negative consequences over time, including insomnia and the associated psychiatric comorbidities.
应激系统异常与失眠有关。然而，研究失眠患者生理应激调节的研究并未始终检测到下丘脑-垂体-肾上腺（HPA）轴对应激反应的差异。一种解释可能是，应激系统的缺陷与失眠的生物学易感性有关，而不是失眠的表型表达。为了检验应激反应作为失眠易感性的函数，本研究在具有不同失眠家族风险的健康睡眠者样本中测试了对特里尔社会应激测试的反应。
招募了35名有或没有失眠家族风险的健康个体来完成一项实验室应激源测试。有一个或两个亲生父母患有失眠的参与者被归类为家族风险阳性，而没有亲生父母患有失眠的参与者被归类为家族风险阴性。参与者在实验室完成了特里尔社会应激测试，并比较了心理和生理（自主神经和HPA轴）反应。
尽管自我报告的焦虑增加，但与没有失眠家族风险的人相比，家族风险阳性的人皮质醇反应迟钝。皮质醇反应迟钝的个体还报告了对个人生活应激源的反应性增强，包括睡眠障碍增加、认知侵入增加和更多的行为回避。
本研究结果提供了初步证据，表明异常应激调节可能是通过失眠家族风险赋予的生物学易患因素。随着时间的推移，这种缺陷也可能预测负面后果，包括失眠和相关的精神共病。
