Sleep loss alters both the concentration and activity of various aspects of the immune system. These alterations lead to increased susceptibility to infection and the progression of pathologies such as insulin resistance and atherosclerosis. Two proposed mechanisms of this alteration in immune function are the changes in both cortisol and sympathetic nervous system activity that accompany sleep deprivation. This work reviewed literature that measured the effects of periods of sleep restriction upon both cortisol and catecholamine concentrations within human subjects. Furthermore, studies which measured the effects of sleep loss upon these hormone levels and the associated changes in immune parameters were included. This thesis asserts that there is no defined pattern in reference to alterations of cortisol levels as a result of sleep deprivation. Furthermore, more evidence must be collected before implementing cortisol as a main effector of sleep loss upon immune system function. This dissertation, although repeatedly noting increased levels of norepinephrine following periods of sleep restriction, similarly argues that more research must be completed in order to declare that altered catecholamine concentrations as a result of sleep loss is a mechanism for altered immune function.
Identifer | oai:union.ndltd.org:bu.edu/oai:open.bu.edu:2144/17016 |
Date | 18 June 2016 |
Creators | Kennedy, James Morgan |
Source Sets | Boston University |
Language | en_US |
Detected Language | English |
Type | Thesis/Dissertation |
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