Kuolema kuittaa univelat? : effects of cumulative sleep loss on immune functions and lipid metabolism

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Sleep is an essential physiological function. It is conserved across the animal kingdom; no animal species studied has been shown not to sleep. The timing of sleep and wakefulness is regulated by two processes. The circadian process works like a clock and accounts for the timing of sleep and arousal, synchronised by the light dark rhythm. The homeostatic process acts like an hourglass balancing the amount of sleep vs wakefulness. In case waking is prolonged, the homeostatic sleep need drives more sleep to take place, i.e. the sleep rebound. The homeostatic aspect of sleep can be studied by restricting sleep in laboratory conditions and assessing the effects on e.g. cognitive functions and physiological processes. Sleep is not merely a function of the brain, occurring in the brain and for the brain. The brain acts in concert with other organs and tissues in physiological and pathophysiological processes. During the recent decades, epidemiological studies have suggested ! that there is a connection between short or insufficient sleep with higher mortality. Increased risk for cardiovascular diseases, atherosclerosis, type II diabetes, and obesity has been reported in individuals who sleep less than the average. Laboratory studies have partly supported these findings, suggesting a causative role of sleep loss in the development of metabolic diseases, particularly type II diabetes. Experimental sleep restriction has been shown to alter glucose metabolism towards insulin resistance. Studies on the effects of sleep loss on lipid metabolism have been more inconclusive. Sleep is tightly interconnected with the immune system. Experimental sleep restriction increases proinflammatory cytokines, which in turn promote sleep. Atherosclerosis is the pathophysiological process underlying ischaemic heat disease and stroke, the two leading causes of death worldwide. The immune system plays a major role in the development of this metabolic disease characteris! ed by plaque-formation in the arterial walls. Altered choleste! rol tran sport by low density and high density lipoproteins (LDL and HDL) triggers an immune response involving macrophages and other white blood cells. Chronic low-grade inflammation has been shown to in turn predict future cardiovascular diseases. Thus, the development of atherosclerosis is a complex process with both metabolic and immunological components. In the current thesis, I have investigated the effects of sleep loss on gene expression and metabolites in the blood, focusing on changes that may participate in the development of cardiovascular diseases, especially atherosclerosis. Short-term sleep loss was studied in carefully controlled laboratory conditions with an experimental protocol simulating a working week with restricted sleep (4 h sleep/night for 5 nights; N=21). Sleep loss occurring chronically in real-life conditions was assessed in two Finnish
Tryckta ISBN978-951-51-2613-9
Elektroniska ISBN978-951-51-2614-6
StatusPublicerad - 2016
MoE-publikationstypG5 Doktorsavhandling (artikel)


  • 3111 Biomedicinska vetenskaper

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