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group_3_presentation_3_-_sleep_deprivation [2016/04/01 22:59] wajaa |
group_3_presentation_3_-_sleep_deprivation [2018/01/25 15:18] (current) |
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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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| 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> | 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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| 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 | 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 | ||
| - | 23. | + | 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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