McEwen Bruce S
Harold and Margaret Milliken Hatch, Laboratory of Neuroendocrinology, The Rockefeller University, New York, NY 10021, USA. mcewenmail.rockefeller.edu
Metabolism. 2006 Oct;55(10 Suppl 2):S20-3. doi: 10.1016/j.metabol.2006.07.008.
Sleep has important homeostatic functions, and sleep deprivation is a stressor that has consequences for the brain, as well as many body systems. Whether sleep deprivation is due to anxiety, depression, or a hectic lifestyle, there are consequences of chronic sleep deprivation that impair brain functions and contribute to allostatic load throughout the body. Allostatic load refers to the cumulative wear and tear on body systems caused by too much stress and/or inefficient management of the systems that promote adaptation through allostasis. Chronic sleep deprivation in young healthy volunteers has been reported to increase appetite and energy expenditure, increase levels of proinflammatory cytokines, decrease parasympathetic and increase sympathetic tone, increase blood pressure, increase evening cortisol levels, as well as elevate insulin and blood glucose. Repeated stress in animal models causes brain regions involved in memory and emotions, such as hippocampus, amygdala, and prefrontal cortex, to undergo structural remodeling with the result that memory is impaired and anxiety and aggression are increased. Structural and functional magnetic resonance imaging studies in depression and Cushing's disease, as well as anxiety disorders, provide evidence that the human brain may be similarly affected. Moreover, brain regions such as the hippocampus are sensitive to glucose and insulin, and both type 1 and type 2 diabetes mellitus are associated with cognitive impairment and (for type 2 diabetes mellitus) increased risk for Alzheimer's disease. Animal models of chronic sleep deprivation indicate that memory is impaired along with depletion of glycogen stores and increases in oxidative stress and free radical production. Taken together, these changes in brain and body are further evidence that sleep deprivation is a chronic stressor and that the resulting allostatic load can contribute to cognitive problems, which can, in turn, further exacerbate pathways that lead to disease.
睡眠具有重要的稳态功能,而睡眠剥夺是一种应激源,会对大脑以及许多身体系统产生影响。无论睡眠剥夺是由焦虑、抑郁还是忙碌的生活方式引起的,慢性睡眠剥夺都会产生后果,损害大脑功能并导致全身的应激负荷增加。应激负荷是指由于压力过大和/或通过适应性稳态促进适应的系统管理效率低下而导致的身体系统累积损耗。据报道,年轻健康志愿者的慢性睡眠剥夺会增加食欲和能量消耗,提高促炎细胞因子水平,降低副交感神经张力并增加交感神经张力,升高血压,提高夜间皮质醇水平,以及升高胰岛素和血糖水平。动物模型中的反复应激会导致参与记忆和情绪的脑区,如海马体、杏仁核和前额叶皮质,发生结构重塑,结果是记忆力受损,焦虑和攻击性增加。对抑郁症、库欣病以及焦虑症患者进行的结构和功能磁共振成像研究提供了证据,表明人类大脑可能受到类似影响。此外,海马体等脑区对葡萄糖和胰岛素敏感,1型和2型糖尿病都与认知障碍有关(对于2型糖尿病),并且患阿尔茨海默病的风险增加。慢性睡眠剥夺的动物模型表明,记忆力受损伴随着糖原储备的耗尽以及氧化应激和自由基产生的增加。综上所述,大脑和身体的这些变化进一步证明睡眠剥夺是一种慢性应激源,由此产生的应激负荷会导致认知问题,进而可能进一步加剧导致疾病的途径。