Sleep is a crucial element of every person’s condition that allows everyone to, when obtained in the correct quantity, perform essential day-to-day functions at peak optimization. It is often believed that people need approximately 7-8 sleep hours every night as this is the sufficient duration that the sleep will undertake its restorative function (Nagai, Hoshide, & Kario, 2010). Many people think that missing this mind and body restoration period may bear immediate health threats or that chronic sleep loss may shorten one’s lifespan or increase morbidity. When people stay awake at night, their bodies miss the surge of putatively restorative human growth hormone which occurs during nocturnal sleep and, at the same time gets an overabundance of stressor substances such as corticosteroids as well as norepinephrine (Nagai, Hoshide, & Kario, 2010).
Sleep Deprivation
Sleep medicine experts recommend that grown-ups should sleep for a period not less than seven hours per night for optimal health (Altevogt, & Colten, 2016). However, for the last fifty years, average sleep duration has dramatically reduced with most American at the risk of maintaining a chronic sleep debt state of six or fewer hours of sleep per night. Everyone has experienced sleep deprivation at one time or another either partially or entirely for a number of days. The most common causes of sleep loss are the ones related to modern lifestyle and work-related factors. Ordinary events such as working overtime to meet job deadlines, working at night or spending many hours managing a family as well as business emergencies often lead to temporary or partial sleep loss.
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Researchers in the field of sleep deprivation have identified three kinds of sleep loss which have varying effects on human health. They are total sleep deprivation, partial sleep deprivation, and selective sleep deprivation. Total sleep deprivation implies that a person gets no sleep period a one 24-hour cycles. For instance, an individual who sleeps typically from 0000 hrs to 0800 hrs awakens one morning at 0800 but stays awake until the following day at 0000 hrs; this individual has gone without sleep for 40 hours during which he or she missed one-8-hour sleep. Partial sleep deprivation which is common with most people implies that a person sleeps less than the recommended 8 hours. In some instances, the sleep-duration is gradual or sudden. In the gradual case, individuals reduce their sleep duration by a certain time, for example, 30-minutes every one or two weeks which gives them ample time to adjust to longer working hours every day. On the other hand, in sudden sleep reduction, a person will reduce their sleep period from 8 hours to, for instance, 5 hours and try this short sleep regime for a few days or a long period until they adapt to the new lifestyle (Mullington et al., 2009). Unlike partial and total sleep loss, clear-cut selective sleep deprivation does not happen in real-world situations. It is a laboratory-created sleep manipulation that is used to study the different stages of sleep in which the occurrence of particular sleep stage is prevented (Nagai, Hoshide, & Kario, 2010).
Effects of Sleep Loss
Both total deprivation and partial sleep deprivation are a worrisome phenomenon in the modern world because of their association with a wide range of psychological as well as cognitive defects. The psychological effects of sleep deprivation include impairments in glucose metabolism, cardiovascular health, immune functions, increased inflammation, hypertension, and activation of the sympathetic nervous system.
Sleep Deprivation and Metabolic Changes
Sleep deprivation also alters Anabolic hormones. Growth hormone attains its daily maximum in the initial half of the sleeping duration as well as up to approximately 70% of the daily growth hormone secretion takes please during the same period in health 35 to 40 years aged men (Chaput, & Dutil, 2016). During sleep loss, the-sleep associated growth hormone pulse is significantly abolished or dampened resulting to hypothalamic-pituitary-adrenal axis activation. In addition, sleep loss changes the output of key metabolic hormones such as the glucose metabolism, hence, resulting in insulin resistance.
Endogenous circadian component and sleep affect the levels of glucose and insulin. Human sleep consolidated in the medically recommended duration of seven to nine hours means that extended duration of fast must be maintained over the night. In normal people, the levels of glucose in the blood remain stable or fall minimally despite the extended period without eating while in people awake fasting with no physical activity, the blood glucose level falls by an average 10-20 mg/dl over the 12-hour period (Copinschi, 2015). As such, numerous mechanisms operative during nocturnal sleep must intervene to ensure the glucose level are stable during the overnight fasting.
Partial sleep deprivation has been established to affect glucose metabolism in human. Sleep loss decreases glucose tolerance and increases concentrations of blood cortisol (Chaput, & Dutil, 2016). In an experiment conducted by Spiegel et al. (1999) in which a number of young men were subjected to 6 and seven nights of 4 and 12 hours of sleep respectively, glucose tolerance was established to be lower in sleep debt condition. The glucose tolerance decreased by more than 40% after the partial sleep deprivation while glucose effectiveness and the acute insulin response to glucose decreased by 30% (Chaput, & Dutil, 2016). Disposition index, a product of acute glucose-insulin response and glucose effectiveness is used to estimate beta cell functioning to the prevailing insulin resistance level, and it is used as a marker of diabetic risk (Chaput, & Dutil, 2016). In healthy people, insulin resistance is complemented by compensatory hyperinsulinemia which is responsible for maintaining a constant deposition index. Since sleep deprivation lowers both acute glucose insulin resistance and glucose effectiveness, it reduces the deposition index. Low values of deposition index imply that a person has a high risk of type II diabetes. According to (Copinschi, 2015), deposition index in 1000 implies that an individual has a high risk of conducting diabetes.
Sleep deprivation is also associated with certain body hormonal imbalances which have dire consequences for human beings. Hormones such as leptin and ghrelin play an important role in the central control of appetite and energy expenditure. On one side, sleep loss reduces leptin levels, the hormones responsible for reducing appetite, while on the other hand, it increases ghrelin levels, the hormone responsible for stimulating appetite. As such, people experience sleep deprivation eat more as they have higher hunger level than those who sleep adequately. This implies that that sleep loss is a risk factor for obesity. According to Chaput, & Dutil (2016) controlled studies with healthy males have established that a 4-hour sleep increased their craving for high-calorie foods with high carbohydrate contents such as salty, starchy foods and sweets.
Sleep plays a crucial role in thermoregulation and as such sleep loss results in a reduction in the normal nocturnal drop in body temperature. In connection with this temperature drop, the thyroid-stimulating hormone such as T3 and T4 levels increase during sleep loss. Although these increases observed in short-term sleep deprivation cases bear no clinical sequelae and are easily resolved with sleep recovery, thyroid is a crucial regulator of metabolic rate, modulating oxygen consumption, cardiac output, and heart contractility, as well as affects every aspect of carbohydrate metabolism. Moreover, thyroid plays a key role in gastrointestinal tract glucose absorption hence increasing insulin resistance (Copinschi, 2015). If the thyroid-stimulating hormone changes resulting from sleep loss are chronic, they will contribute to the development of the disease.
Sleep Loss, Cardiovascular Diseases, and Inflammation
For a long time, researchers in the medical field have been investigating the causes behind inflammation in asymptomatic people who later proceed to develop cardiovascular disease. Several factor lead to heightened inflammatory markers as well as mediators, including injuries and infections. Adiposity, chiefly visceral adiposity directly contributes to IL-6 production among other inflammatory mediators that in turn stimulate C-reactive protein (CRP) production. Hypoxia, which is found in people suffering from sleep apnea syndrome is strongly linked to increases in inflammatory mediators (Tobaldini, Pecis, & Montano, 2014). Sleep loss, as well as poor sleep quality, directly contribute to the development of the elevated inflammatory state in people without cardiovascular diseases and sleep disorders. Sleep deprivation experimental studies conducted on healthy participants have established that white blood cells, as well as other inflammatory markers, increase in the range of those connected with the future development of cardiovascular diseases (Mullington et al., 2009).
Several studies have also established a causative link between sleep loss and aberrant cardiovascular functioning. Acute surges in diastolic and systolic blood pressure take place following 24 to 88 hours of sleep loss (Tobaldini, Pecis, & Montano, 2014). According to Mullington et al. (2009), healthy people subjected to prolonged sleep loss experience increases in nocturnal blood pressure along with an amplified morning surge as well as dampened nocturnal dipping in the absence of substantial increases in diurnal resisting blood pressure (Mullington et al., 2009). Moreover, sleep loss provokes early deterioration of vascular structure as well as a function which promotes cardiovascular risk. Sleep deprivation results in increased arterial stiffness are resulting in impaired endothelial function which reflects poor vascular health that in turn if not checked leads to atherosclerosis. People exposed to sleep loss showed reduced endothelium-dependent vasodilation which results from decreased acetylcholine-induced cutaneous as well as venous vasodilation and diminished branchial flow-mediated vasodilation (Tobaldini, Pecis, & Montano, 2014). Sleep loss deteriorates the coronary microcirculation and causes the systematic endothelial dysfunction resulting from the increased release of cellular adhesion molecules and selectins from activated endothelial cells (Mullington et al., 2009).
Sleep is crucial for sympathetic nervous system regulation of the heart. As such, the sympathoexcitatory effect of sleep deprivation has been proposed to explain why blood pressure increases in individuals exposed to prolonged sleep loss. Blood pressure increases due to increased sympathetic outflow to the periphery or heart that results from baroreflex resetting to higher levels or changes in baroreflex sensitivity or a combination of both (Mullington et al., 2009). Research conducted on hemodynamics and neural circulatory control supports the increased release of plasma and urinary norepinephrine after a long period of sleep deprivation. Sleep loss results in inhibited muscle sympathetic nerve activity of the heart as indicated by the variation in baroreflex sensitivity. In the case of individuals taking adequate sleep, the resetting of the blood pressure works well as there are no interruptions in the signal. However, for individuals experiencing sleep loss, the sensing of blood pressure in the heart, the carotid artery and aortic arch is compromised which sends the wrong information to the nucleus tractus solitarius resulting in irregularities in blood pressure control.
Sleep Loss Effects on Blood Pressure
Numerous studies have established that experimental sleep results in increased blood pressure, as well as half a night sleep loss, has been cited as a key risk factor that increases blood pressure in individuals suffering from hypertension or pre-hypertension. Physiologically, blood pressure is regulated through numerous mechanisms. Renal fluid filtration as well as reabsorption control the volume of blood and are subject to hormonal control, most significantly the renin-angiotensin system (Mullington et al., 2009). Cardiac contractility which is defined as the force with which the cardiac ejects blood into the circulation system and cardiac output which is the rate of blood pumped in liters per minute, as well as peripheral vascular resistance, is also the other crucial determinants of a person’s blood pressure. The three determinants are under the control of the autonomic nervous system and are connected to blood pressure through the baroreflex which is a feedback loop. The baroreflex comprises of a series of receptors located in heart, carotid artery and aortic arch that sense the pressure of the blood and deliver the information to the nucleus tractus solitarius in the medulla (Mullington et al., 2009). If the pressure of blood requires an adjustment, the sympathetic or the parasympathetic output then influences cardiac contractility, the heart rate, and peripheral vascular resistance.
Sleep Loss and Immune Functions
Sleep is a very important aspect of how human immune system functions. Sleep loss results in significant reduction of cellular immunity as indicated by reduction in NK activity and IL-2 production. The production of IL-2 is driven by shortages in the function of monocyte and lymphocyte cell population in human (Besedovsky, Lange, & Born, 2012). As such, individuals who are exposed to prolonged sleep loss have lower production of this important interleukin-2 which is produced during sleep. Sleep loss also results in an acute reduction of T-cells as well as the functions of monocyte function. This has adverse repercussion as these crucial components of the immune system play an important role in protecting the body against certain infections. For instance, the NK cells mediate protection against primary herpes virus infection (Besedovsky, Lange, & Born, 2012). Sleep loss also affects important functions of the immune system such as the production of cytokines which are protective proteins. These cytokines usually increase in the cases that the body is faced with inflammation or infection and hence since their releasing reduces during sleep loss, the immunity system’s ability to fight infections is compromised. The immune system also relies on blood circulatory system to redistribute these protective cells throughout the entire body. Since sleep loss also results in irregulates in blood circulation through increasing or reducing blood pressure and interfering with its regulation, it hinders the way in which these protective components of the immune systems are distributed to different parts of the body (Besedovsky, Lange, & Born, 2012).
Conclusion
Unlike other disorders, sleep loss is a relatively young disease that is rapidly affecting the current generation everywhere in the world. Interests in the field of sleep date back to 20 th century when electroencephalograph was used to observe the brains electrical activities during nonrapid eye movement sleep by Loomis and colleagues in 1937. Their work opened the field to research as Kleitman and friends used the rapid eye movement to study its correlation with dreams, hence, advancing the understanding of sleep physiology by defining different stages of sleep (Altevogt, & Colten, 2016). Since the 1950s, research in the field has established sleep as an important biological process required in the functioning of many organ systems.
Sleep loss is a modern phenomenon that has been advanced majorly by the current way of life in most countries. In the contemporary world, people are more determined than ever to become successful in their endeavors. Unlike in the previous centuries, the 21 st first century is characterized by advanced economic competition which has made people work harder to sustain their lifestyles. The high cost of basic needs such as education, food, and shelter has seen many people undertake more than one job to earn enough capital to foot the bills. As such they are left with very limited time to sleep and spend with their families. The nature of the economy has also evolved. Most developed countries are running on a 24-hour economy which requires increased output to meet the ever-growing demand resulting in work-shifts that require people to perform both day and night shifts. This leads to disruption in sleeping patterns and eventually results in sleep loss if not well managed. Other issues such as the parenthood and old age result are sleep loss. For instance, working parents with young children spend most parts of their sleeping time taking care of the young ones while menopausal women and the elderly have difficulties in sleeping.
Sleep loss a number of symptoms that are easily identifiable. Individuals are suffering from sleep loss experience prolonged sleepiness from time to time. In extreme cases, people experience mood changes as well as have difficulties in concentrating which results in impaired performance and decision making. Sleep loss is also characterized by memory and thinking problems which result in poor planning, increased risk-taking, disorganization, poor prioritization, decreased judgment and tendency to focus on short-term rewards. Individuals with acute sleep loss also experience disorientation, paranoia, and hallucinations.
As a disorder, sleep loss has no correct medication, and its remedies are straightforward. The first remedy is to encourage the affected people to revert to 7-8 hour sleeping program. In acute cases, sleeping pills may be used to enhance their sleeping. Parents should also ensure their children sleep for at least 8 hours so that they learn and adopt this schedule from a young age. This is because, the effects of sleep loss which include impairments in glucose metabolism, cardiovascular health, immune functions, increased inflammation, hypertension, and activation of the sympathetic nervous system are more detrimental to young children than in adults.
References
Altevogt, B. M., & Colten, H. R. (Eds.). (2016). Sleep disorders and sleep deprivation: an unmet public health problem . National Academies Press.
Besedovsky, L., Lange, T., & Born, J. (2012). Sleep and immune function. Pflügers Archiv-European Journal of Physiology , 463 (1), 121-137.
Chaput, J. P., & Dutil, C. (2016). Lack of sleep as a contributor to obesity in adolescents: impacts on eating and activity behaviors. International Journal of Behavioral Nutrition and Physical Activity , 13 (1), 103.
Copinschi, G. (2015). Metabolic and endocrine effects of sleep deprivation. Essential Psychopharmacology , 6 (6), 341-347.
Mullington, J. M., Haack, M., Toth, M., Serrador, J. M., & Meier-Ewert, H. K. (2009). Cardiovascular, inflammatory, and metabolic consequences of sleep deprivation. Progress in cardiovascular diseases , 51 (4), 294-302.
Nagai, M., Hoshide, S., & Kario, K. (2010). Sleep duration as a risk factor for cardiovascular disease-a review of the recent literature. Current cardiology reviews , 6 (1), 54-61.
Tobaldini, E., Pecis, M., & Montano, N. (2014). Effects of acute and chronic sleep deprivation on cardiovascular regulation. Archives italiennes de Biologie , 152 (2-3), 103-110.
