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group_3_presentation_3_-_sleep_deprivation [2016/04/01 22:49] wajaa |
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| ===== Introduction ===== | ===== Introduction ===== | ||
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| ==== Diabetes ==== | ==== Diabetes ==== | ||
| - | Diabetes is another major disease that is caused by sleep deprivation. To begin with, obesity is heavily linked with Type 2 diabetes but it is evident that a lack of sleep may impair glucose metabolism which increases the chance of diabetes.<sup>14</sup> Sleep deprivation can negatively impact one`s energy balance which can cause weight gain because of an upregulation of appetite, an increase in time to eat and a decline in energy output.<sup>14</sup> If an excessive amount of weight is gained there is potential that insulin resistances may increase coupled with a loss in glucose tolerance, which is a condition that increases the risk of developing diabetes potentially causing more weight gain to occur.<sup>14</sup> Further research was done to test the effects of sleep restriction on patients rather than patients who incurred sleep disorders.<sup>14</sup> The results of the experiments were consistent with the initial hypothesis as sleep loss resulted in an upregulation of appetite and increased Body Mass Index (BMI).<sup>14</sup> An increase level of sleepiness and fatigue coupled with a lower level of energy expenditure was also found due to the loss of glucose metabolism that occurred from the lack of sleep, thus justifying the linked causation of diabetes from sleep deprivation.<sup>14</sup> | + | There is a greater risk of about 50-150% in contracting Type 2 diabetes for those who are sleep deprived.<sup>14</sup> To begin with, obesity is heavily linked with Type 2 diabetes but it is evident that a lack of sleep may impair glucose metabolism which increases the chance of diabetes.<sup>14</sup> Sleep deprivation can negatively impact one`s energy balance which can cause weight gain because of an upregulation of appetite, an increase in time to eat and a decline in energy output.<sup>14</sup> If an excessive amount of weight is gained there is potential that insulin resistances may increase coupled with a loss in glucose tolerance, which is a condition that increases the risk of developing diabetes potentially causing more weight gain to occur.<sup>14</sup> Glucose tolerance is the mechanism that links sleep deprivation and Type 2 diabetes.<sup>14</sup> Further research was done to test the effects of sleep restriction on patients rather than patients who incurred sleep disorders.<sup>14</sup> The results of the experiments were consistent with the initial hypothesis as sleep loss resulted in an upregulation of appetite and increased Body Mass Index (BMI).<sup>14</sup> An increase level of sleepiness and fatigue coupled with a lower level of energy expenditure was also found due to the loss of glucose metabolism that occurred from the lack of sleep, thus justifying the linked causation of diabetes from sleep deprivation.<sup>14</sup> |
| ==== Heart Disease ==== | ==== Heart Disease ==== | ||
| - | With heart disease there is a 2x increase in short sleepers’ risk of developing CVD and hypertension.<sup>15</sup> Essentially a loss in sleep will result in an increase in blood pressure as well as a decrease in the sympathetic system (ANS).<sup>15</sup> The sympathetic system is the mechanism that links sleep deprivation and heart disease.<sup>15</sup> Also, stress hormones are regulated during sleep and with sleep being deprived this can cause a lot of harmful issues with the regulation of blood pressure.<sup>16</sup> Sleeping for less than 5 hours on a consistent basis causes high blood pressure and if this occurs during sleep there is a potential risk of myocardial infarction.<sup>16</sup> With these combined there is an increased risk of getting heart disease due to sleep deprivation.<sup>15</sup> | + | With heart disease there is a 2x increase risk of developing CVD and hypertension for those who are sleep deprived.<sup>15</sup> Essentially a loss in sleep will result in an increase in blood pressure as well as a decrease in the sympathetic system (ANS).<sup>15</sup> The sympathetic system is the mechanism that links sleep deprivation and heart disease.<sup>15</sup> Also, stress hormones are regulated during sleep and with sleep being deprived this can cause a lot of harmful issues with the regulation of blood pressure.<sup>16</sup> Sleeping for less than 5 hours on a consistent basis causes high blood pressure and if this occurs during sleep there is a potential risk of myocardial infarction.<sup>16</sup> With these combined there is an increased risk of getting heart disease due to sleep deprivation.<sup>15</sup> |
| ==== Psychopathological ==== | ==== Psychopathological ==== | ||
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| ====The Effects on Cognition ==== | ====The Effects on Cognition ==== | ||
| - | Frequently disrupted and restricted sleep is a common problem for many people in our modern around-the-clock society (Meerlo et. al, 2008). Deficits in daytime performance due to sleep loss are experienced universally, and associated with significant effects on the human body. The first known study addressing the negative effects of sleep deprivation was published in the late 1800s. Since then, hundreds of studies have established that sleep loss impairs various cognitive functions and behaviours. Sleep deprivation studies repeatedly indicate a (variable) impact on mood, cognitive performance, and motor function due to destabilization of the body's wake state. It has been shown that specific neurocognitive domains including, executive attention, working memory, and higher cognitive functions (e.g. emotional intelligence and decision making), are particularly vulnerable to sleep loss (Durmer et. al, 2005). Recent chronic partial sleep deprivation studies, which more closely mimic the sleep loss experienced in society today, demonstrate that neurocognitive deficits are capable of accumulating over time, due to the body adapting or altering its response to the sensation of sleepiness (Durmer et. al, 2005). | + | Frequently disrupted and restricted sleep is a common problem for many people in our modern around-the-clock society.<sup>20</sup> Deficits in daytime performance due to sleep loss are experienced universally, and associated with significant effects on the human body. The first known study addressing the negative effects of sleep deprivation was published in the late 1800s. Since then, hundreds of studies have established that sleep loss impairs various cognitive functions and behaviours. Sleep deprivation studies repeatedly indicate a (variable) impact on mood, cognitive performance, and motor function due to destabilization of the body's wake state. It has been shown that specific neurocognitive domains including, executive attention, working memory, and higher cognitive functions (e.g. emotional intelligence and decision making), are particularly vulnerable to sleep loss.<sup>18</sup> Recent chronic partial sleep deprivation studies, which more closely mimic the sleep loss experienced in society today, demonstrate that neurocognitive deficits are capable of accumulating over time, due to the body adapting or altering its response to the sensation of sleepiness.<sup>18</sup> |
| ====The Effects on the Neuroendocrine Stress Systems==== | ====The Effects on the Neuroendocrine Stress Systems==== | ||
| - | Along with its effect on cognitive function, it is important to determine how sleep loss affects the stress systems of the body, since these are the systems that help individuals deal with everyday challenges. Sleep has a mild suppressive effect on the basal activity of the major autonomic neuroendocrine stress systems, i.e., the autonomic sympatho-adrenal system and the hypothalamic-pituitary-adrenal axis (Meerlo et. al, 2008). Studies on both humans and rodents have shown that sleep deprivation raises the activity of these stress systems. The extent to which it raises the activity is dependent upon both the mental load (sensory input, thoughts, emotions) and physical activities (voluntary or forced) that the individual experiences following sleep deprivation. The activity of the stress systems most often rapidly returns to baseline during subsequent recovery sleep. However, if recovery sleep is insufficient, stress systems may display a mild recurrent activation the following day (Meerlo et. al, 2008). Sleep deprivation may not only affect the basal activity of neuroendocrine systems, but in the long run, it may also affect the reactivity of these systems to new challenges and stressors. Ultimately, this will alter the way an individual responds to the new challenges and stressors. The first sign of this alteration in response, appears at the level of emotional perception. Though most of the effects of acute sleep deprivation on the neuroendocrine stress systems seem to be transient, chronic partial sleep deprivation studies in rodents show that too little sleep may gradually cause fundamental changes in the brain systems, that are involved in the regulation of stress responses (Meerlo et. al, 2008). For example, chronic partial sleep deprivation can cause a reduction in the number or sensitivity of corticotropin releasing hormone receptors and serotonin receptors. Sleep restriction gradually changes these brain systems in a direction that is similar to what is seen in mood disorders such as depression. This data supports the idea that insufficient sleep, by acting on stress systems, may sensitize individuals to stress-related disorders. However, it is important to note that few controlled studies in humans have been completed, as such, further research in this area is required (Meerlo et. al, 2008). | + | Along with its effect on cognitive function, it is important to determine how sleep loss affects the stress systems of the body, since these are the systems that help individuals deal with everyday challenges. Sleep has a mild suppressive effect on the basal activity of the major autonomic neuroendocrine stress systems, i.e., the autonomic sympatho-adrenal system and the hypothalamic-pituitary-adrenal axis.<sup>20</sup> Studies on both humans and rodents have shown that sleep deprivation raises the activity of these stress systems. The extent to which it raises the activity is dependent upon both the mental load (sensory input, thoughts, emotions) and physical activities (voluntary or forced) that the individual experiences following sleep deprivation. The activity of the stress systems most often rapidly returns to baseline during subsequent recovery sleep. However, if recovery sleep is insufficient, stress systems may display a mild recurrent activation the following day.<sup>20</sup> Sleep deprivation may not only affect the basal activity of neuroendocrine systems, but in the long run, it may also affect the reactivity of these systems to new challenges and stressors. Ultimately, this will alter the way an individual responds to the new challenges and stressors. The first sign of this alteration in response, appears at the level of emotional perception. Though most of the effects of acute sleep deprivation on the neuroendocrine stress systems seem to be transient, chronic partial sleep deprivation studies in rodents show that too little sleep may gradually cause fundamental changes in the brain systems, that are involved in the regulation of stress responses.<sup>20</sup> For example, chronic partial sleep deprivation can cause a reduction in the number or sensitivity of corticotropin releasing hormone receptors and serotonin receptors. Sleep restriction gradually changes these brain systems in a direction that is similar to what is seen in mood disorders such as depression. This data supports the idea that insufficient sleep, by acting on stress systems, may sensitize individuals to stress-related disorders. However, it is important to note that few controlled studies in humans have been completed, as such, further research in this area is required.<sup>20</sup> |
| ====The "All Nighter": Effects on Academic Performance==== | ====The "All Nighter": Effects on Academic Performance==== | ||
| + | The relationship between sleep, memory and learning capacity is well-known. Sleep plays an important role in learning processes and memory consolidation, and studies clearly show that sleep deprivation can impair both.<sup>21</sup> Due to this relationship, exploration of the effects of sleep deprivation on student learning ability and academic performance was inevitable. Most studies have been correlative investigations, where sleep schedules were correlated with school and academic achievement.<sup>21</sup> For example, a study completed by Thacher<sup>19</sup>, assessed the correlation between engaging in a single night of total sleep deprivation (SN-TSD), and sleep schedule parameters, circadian preference, academic performance, and depressive symptoms. The study involved 120 university students, of a mean age of 20 years. Measures included the Owl-Lark Scale of circadian preference, the Beck Depression Inventory, Pittsburgh Sleep Quality Index (PSQI), as well as, self-reported usual bedtime, rise time, and total sleep time. Students' cumulative grade point averages (GPAs) were also obtained from the university registrar. Of the 120 students, 60% reported engaging in SN-TSD once or more since coming to university. Engagement in SN-TSD was found to be correlated with later self-reported bedtimes, evening preference, and poorer academic achievement as measured by GPA.<sup>19</sup> Some studies, however, have been able to actively manipulate sleep in order to observe neurocognitive and behavioural consequences, such as learning, memory capacity and school performance. The findings from these studies strongly suggest that: | ||
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| + | 1. Students of different education levels (from school to university) are chronically sleep deprived or suffer from poor sleep quality.<sup>21</sup> | ||
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| + | 2. Sleep quality and quantity induce several effects on a student's life: increased day-time sleepiness, impaired mood, neurocognitive deficits, and behavioural changes.<sup>21</sup> | ||
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| + | 3. The effects of sleep loss are mainly evident on higher cognitive functions (attention, memory, problem-solving, etc.); as a result, learning capacity and academic performance may seriously be affected.<sup>21</sup> | ||
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| + | One of the most crucial findings of these studies suggests that the negative effects of sleep deprivation can be reversed. Studies in which sleep was actively restricted or optimized showed, respectively, a worsening and an improvement in neurocognitive and academic performance. This indicates the possibility of an improvement in neurocognitive function (and thus of learning capacity and academic performance) as a result of healthy sleep schedules.<sup>21</sup> | ||
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| + | ====Is it possible for sleep deprivation to be beneficial?==== | ||
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| + | Major depressive disorder (MDD) is the leading cause for illness-related reduction of quality of life worldwide, and current first-line treatments show a long-latency (slow-acting) response. Therapeutic sleep deprivation (SD) is a fast-acting anti- depressant intervention that leads to a rapid decrease of depressive symptoms in 50-60% of patients with MDD. It has been shown to improve the clinical symptomatology that is related to impaired associative synaptic plasticity in MDD. However, the effect is temporary, only lasting until the next time the individual falls asleep.<sup>22</sup> | ||
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| + | Neuronal plasticity or remodeling, is a fundamental process by which the brain acquires information and makes the appropriate adaptive responses in future-related settings. Dysfunction of these fundamental processes could thereby contribute to the pathophysiology of mood disorders. Recovery could occur by the induction of the appropriate plasticity or remodeling. These possibilities are supported by preclinical and clinical studies, demonstrating that there are structural alterations that occur in response to stress and in patients with mood disorders, such as MDD.<sup>23</sup> | ||
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| + | In the case of this study, it is proposed that prolonged wakefulness (sleep deprivation) shifts the initially deficient inducibility of associative synaptic long-term potentiation in patients with MDD, into a more favorable window of associative plasticity.<sup>22</sup> In other words, it remediates the deficient neuroplasticity in individuals with MDD. | ||
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| + | The synaptic plasticity model of sleep deprivation in MDD suggests a novel framework for a potential mechanism of action of therapeutic sleep deprivation that can be further tested in humans through non-invasive measures, and in animals (i.e. rodents) based on synaptic plasticity studies. Further determining the mechanism of action of sleep deprivation might contribute to the development of novel fast acting treatments for MDD, one of the major health problems world wide.<sup>22</sup> | ||
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| + | ===Potential underlying molecular mechanisms=== | ||
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| + | **Brain Derived Neurotrophic Factor (BDNF):** Plays a key role in synaptic plasticity in the adult brain. Decreased BDNF expression is associated with reduced synaptic plasticity and neuronal atrophy, while increased BDNF expression is associated with neuronal survival and differentiation. BDNF levels increase with prolonged periods of wakefulness, facilitating associative synaptic plasticity. This could potentially provide a mechanism for the clinical improvement after therapeutic sleep deprivation in MDD.<sup>22</sup> | ||
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| + | **Adenosine:** Adenosine is important in sleep regulation, and its absence has also been implicated in a greater risk for depression. Adenosine release is increased the longer you're awake (to a point), making you feel less aroused and more tired, and acting as part of your normal sleep-wake cycle. A beneficial side effect of its release also appears to be an alleviation of depressive symptoms. Several animal studies suggest that activation of adenosine A1 receptors in the brain has an antidepressant effect.<sup>22</sup> | ||
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| + | **Monoaminergic:** The therapeutic effects of SD are comparable to the rapid onset of mood changes after the treatment with psychostimulants. Psychostimulants increase the release of all monoamines or inhibit the reuptake of these neurotransmitters, leading to the net effect of increased synaptic dopamine, noradrenaline and serotonin. The therapeutic effects of SD may be mimicking the effects of psychostimulants.<sup>22</sup> | ||
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| + | **Glutamatergic System:** Under physiological conditions, glutamate has a prominent role in synaptic plasticity, learning and memory. Therapeutic sleep deprivation may have various effects on glutamate transmission.<sup>22</sup> | ||
| =====Treatments===== | =====Treatments===== | ||
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| 17. Luby, E. D., Grisell, J. L., Frohman, C. E., Lees, H., Cohen, B. D., & Gottlieb, J. S. (1962). Biochemical, psychological, and behavioral responses to sleep deprivation. Annals of the New York Academy of Sciences, 96(1), 71-79. | 17. Luby, E. D., Grisell, J. L., Frohman, C. E., Lees, H., Cohen, B. D., & Gottlieb, J. S. (1962). Biochemical, psychological, and behavioral responses to sleep deprivation. Annals of the New York Academy of Sciences, 96(1), 71-79. | ||
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| + | 18. Durmer, J. S., & Dinges, D. F. (2005). Neurocognitive Consequences of Sleep Deprivation. Seminars in Neurology, 25(01), 117-129. | ||
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| + | 19. Thacher, P. V. (2008). University students and the “All Nighter”: Correlates and patterns of students' engagement in a single night of total sleep deprivation. Behavioral Sleep Medicine, 6(1), 16-31. | ||
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| + | 20. Meerlo, P., Sgoifo, A., & Suchecki, D. (2008). Restricted and disrupted sleep: effects on autonomic function, neuroendocrine stress systems and stress responsivity. Sleep Medicine Reviews, 12(3), 197-210. | ||
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| + | 21. Curcio, G., Ferrara, M., & De Gennaro, L. (2006). Sleep loss, learning capacity and academic performance. Sleep Medicine Reviews, 10(5), 323-337. | ||
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| + | 22. Wolf, E., Kuhn, M., Norman, C., Mainberger, F., Maier, J. G., Maywald, S., ... & Riemann, D. (2016). Synaptic plasticity model of therapeutic sleep deprivation in major depression. Sleep Medicine Reviews, 30, 53-62 | ||
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| + | 23. Duman, R. S. (2002). Pathophysiology of depression: the concept of synaptic plasticity. European psychiatry, 17, 306-310. | ||
| 24. Peters, B. (2016, January 27). What Is the Treatment for Sleep Deprivation? Retrieved March 30, 2016, from http://sleepdisorders.about.com/od/sleepdisorderstreatment/ss/What-Is-The-Treatment-For-Sleep-Deprivation.htm | 24. Peters, B. (2016, January 27). What Is the Treatment for Sleep Deprivation? Retrieved March 30, 2016, from http://sleepdisorders.about.com/od/sleepdisorderstreatment/ss/What-Is-The-Treatment-For-Sleep-Deprivation.htm | ||
| 25. Feature, M. J. (2005, June 29). How to Sleep Better: Sleep Deprivation Solutions. Retrieved March 30, 2016, from http://www.webmd.com/sleep-disorders/features/sleep-hygiene | 25. Feature, M. J. (2005, June 29). How to Sleep Better: Sleep Deprivation Solutions. Retrieved March 30, 2016, from http://www.webmd.com/sleep-disorders/features/sleep-hygiene | ||
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