As important as the air we breathe and the water we drink, sleep is a basic necessity of human life. From giant elephants to microscopic bacteria, all forms of life cycle through activity and rest, and the interruption of such cycles can often have negative consequences. In animals, these phases of rest take the form of sleep, and during sleep a series of complex biological processes occur that serve to repair damaged tissue, clear metabolic waste, and consolidate memories. Although the mechanisms underlying such processes have yet to be fully illuminated, it is clear that sleep plays an important role in the continued survival of animals, and humans are no exception. Animals will die if they are not allowed to sleep, and sleep restriction can severely impede performance of a variety of functions. In humans, these lapses in performance caused by sleep deprivation have led to countless tragedies, including the disaster at Chernobyl and the explosion of the Challenger space shuttle. A growing proportion of the population is sleep deprived; given that humans spend about a third of their lives sleeping, it would be of significant benefit to human society if there existed some means of reducing sleep need and minimizing the effects of sleep deprivation. Although there currently exists no such method of reducing our sleep need, the negative impact of sleep deprivation can be reduced, and investigation of the functional mechanisms of sleep and sleep deprivation may yield further progress.

Animals vary tremendously in their shape, size, diet, and habitat. Similarly, there is a huge variation in the timing and amount of sleep observed in animals. Brown bats sleep 20 hours a day, while giraffes only sleep four hours (Tobler 1996); owls are active hunters at night and sleep during the day, while in eagles these phases of hunting and sleep are reversed. Given this diversity in animal sleeping habits, it is no surprise that sleeping habits among humans also vary considerably. Optimum level of sleep in adult humans can vary from six to nine hours a night, and some disorders like narcolepsy can leave people tired even after a full night’s sleep.

Koalas can sleep over 20 hours a day.

Another parameter of sleep is morningness/eveningness, which refers to whether people tend to sleep in the morning or in the evening (i.e. whether someone is a morning lark or a night owl). Morningness/eveningness is highly variable in humans, and, along with several other characteristics of human sleep, is also highly heritable (Klei 2005). While some aspects of sleep are governed by genetics, others depend on environmental cues. Foremost of these cues is exposure to light, which determines several cycles in the body including the production of melatonin (Lewy 2009).

Although sleep need in humans is variable and governed by several genetic and environmental factors, the basic patterns and function of sleep are consistent across normal adults. Many essential hormones are regulated by sleeping patterns, including growth hormone and prolactin(Sassin 1969). During waking hours, metabolic byproducts accumulate in the fluid surrounding the brain as a result of normal functioning. One such byproduct is adenosine, which is a common organic molecule present in several important biological compounds including adenosine triphosphate (ATP), cyclic adenosine monophosphate (cAMP), and deoxyribonucleic acid (DNA). Elevated adenosine levels in the brain induce sleepiness, and caffeine can improve alertness by blocking adenosine receptors to reduce this effect (Porkka-Heiskanen 1997; Smits 1987). During sleep, intercranial canals (the space between brain lobes) increase in size, allowing increased circulation of cerebrospinal fluid and clearance of accumulated metabolic byproducts (Xie 2013). Clearly, sleep plays a very important role in many processes that are essential to normal function.

During sleep deprivation, most of these processes are impeded or prevented completely, leading to severely-reduced ability to perform. In rats, it has been shown that total sleep deprivation will lead to death in two to three weeks. Although for obvious reasons, such lab experiments are not taken to this extreme in humans, many experiments demonstrate that total sleep deprivation in humans causes dramatic decline — sleep deprivation can reduce cognitive and physical performance by as much as 25% per day (Belenky 1994). Furthermore, many natural experiments have confirmed that total sleep deprivation in humans can lead to death — for example, a Chinese man who attempted to watch every football match in the European Championship died after staying awake 11 consecutive days (Chan 2012). Sleep deprivation in normal life is usually not so extreme, but it can have even more dire and widespread consequences. For example, the meltdown of a nuclear reactor at Chernobyl was one of the worst nuclear disasters in history, causing the deaths of hundreds of people. The two engineers who were supposed to monitor the reactor were sleep deprived, and each had worked for over 13 hours before the meltdown occurred. It is likely that a lapse in concentration due to sleep deprivation was a cause of the disaster (Klein 2013).

Although studies of total sleep deprivation have helped illuminate the necessity of sleep and its role in supporting life, most of the population isn’t subjected to continuous total sleep deprivation. Rather, most of us suffer from a different type of sleep deprivation — chronic sleep restriction — that has a different but significant negative impact on performance. In total sleep deprivation, performance declines rapidly but is usually recovered after one to two full nights of sleep (Jewett 1999). During chronic sleep restriction, the onset on performance deficit is less rapid, but performance loss also takes much longer to regain during recovery. For people who sleep less than four hours a night, the effects of sleep deprivation will accumulate indefinitely, and performance will steadily decline after each night of sleep restriction. Those who sleep more than four hours but less than seven hours a night are still considered to be sleep-restricted, and in these subjects performance initially declines. However, after a few nights, performance stabilizes, and does decrease with further sleep restriction (Belenky 2003). This result, combined with the result that performance deficits caused by chronic sleep restriction are not rapidly recovered, suggests that chronic sleep restriction can induce neuromodulatory changes in the brain. These changes help achieve stable performance during sleep restriction, but they also take some time to reverse, leading to a slower recovery of optimal performance. Over longer periods, chronic sleep deprivation is correlated with an extensive list of diseases and conditions, from diabetes to hypertension to mood disorders (Yaggi 2006; Cappuccio 2008). In an era when more than 39% of American adults get less than 7 hours of sleep a night, this news is rather troubling — nearly half of the population is suffering from chronic sleep deprivation (National Sleep Foundation 2002). Therefore, any method of reducing the impact of sleep deprivation would have tremendous implications across society.

For certain segments of the population — for example, people in the military — sleep deprivation cannot be avoided, and the resulting reduced performance can have disastrous consequences. “The most immediate human performance factor in military effectiveness is degradation of performance under stressful conditions, particularly sleep deprivation” (Williams 2008). Sleep deprived soldiers are less effective, have a higher mortality rate, and can even have increased incidences of friendly fire. Combatants go through intense training in sleep-deprived circumstances before entering the war zone; Navy SEALs are required to stay awake for five days straight under extreme duress as a part of training, while the average daily sleep during Army Rangers training school is 3.2 hours (Barzilay 2015 ; Pleban 1990). However, training alone simply cannot compensate for the reduction in performance capacity caused by sleep deprivation. Although there are currently no means of actively reducing the need for sleep, there are methods of delaying the effects of sleep deprivation until a later time, when accepting the negative impact on performance might be acceptable.

By far the most common way of putting off the negative impact of sleep deprivation is the use of stimulants. Such stimulant use can delay the effective need for sleep, creating a “sleep debt,” but this effect is not indefinite. Over the years, the military has tested over 86 drugs for their efficacy in reducing the impact of sleep deprivation, and in 2000 it was found that “90% of Special Forces soldiers and 76% of support soldiers used supplements” (Williams 2008). But should the general population use these same substances to combat sleep deprivation to a similar extent? Extensive research indicates that the drug most widely used by soldiers to stay awake also happens to be available in nearly every supermarket in America: caffeine. So while 90% of Special Forces soldiers use supplements to combat drowsiness, 80% of the US population also enjoys a cup of coffee for the same effect (FDA 2007). In fact, during the Gulf War, gum was infused with caffeine and distributed to soldiers because caffeinated gum has a faster onset than orally consumed caffeine(Kamimori 2002).

U.S. soldiers in the Gulf War relied on caffeinated gum to stay awake.

Caffeine remains the gold standard for fighting sleep deprivation, and it has been proven effective time and time again, even keeping air force pilots alert and capable after 87 hours awake (Darlington 2006). Recently, military researchers have been experimenting with new, nootropic drugs to combat sleep deprivation. Nootropic drugs such as modafinil and dextroamphetamine are usually prescribed to treat certain conditions (narcolepsy and ADHD, respectively), and, unlike caffeine, these drugs can actually improve cognition in well-rested subjects (Kelley 2012). The newest class of nootropic drugs, ampakines, is being developed for the treatment of Alzheimers, but ampakines also show tremendous potential to fight sleep deprivation. In Rhesus monkey trials, the use of ampakines brought the cognitive performance of severely sleep-deprived monkeys to levels above that of their baseline, well-rested performance (Porrino 2005). Although these new classes of nootropic drugs may be in the future for soldiers facing sleep deprivation, it is unlikely that they will ever be available to the public, as such drugs often impact dopamine transmission, which is a hallmark of addictive potential.

Sleep deprivation in humans has wide-ranging effects that negatively impact measures of health, physical stamina, and cognitive performance. Although a large proportion of the modern American population suffers from sleep deprivation, very few methods exist for counteracting the negative effects of it. Among the most effective methods to minimize these effects is the use of caffeine — a method utilized by the majority of the US population. Although other drugs might better minimize the impact of sleep deprivation and improve performance, these drugs also have many negative side effects and can be addictive, and so they will likely remain restricted to military use. Therefore, it is unlikely that there will be any better alternative for combatting sleep deprivation in the near future — only sleep can eliminate sleep deprivation, while caffeine can only delay the effects. Further research into the neurological mechanisms of sleep might hold answers, and it will likely be the discovery of a method of reducing overall sleep need that will have the greatest impact on reducing the negative effects of sleep deprivation in humans.

Works Cited

Barzilay, Julie. “Extreme Sleep Deprivation: How Navy SEALs Handle No Sleep.” ABC News. ABC News Network, 18 Nov. 2015. Web. 18 Oct. 2016.

Belenky, Greg, et al. “The effects of sleep deprivation on performance during continuous combat operations.” Food components to enhance performance (1994): 127–135.

Belenky, Gregory, et al. “Patterns of performance degradation and restoration during sleep restriction and subsequent recovery: A sleep dose‐response study.” Journal of sleep research 12.1 (2003): 1–12.

Cappuccio, Francesco P., et al. “Meta-analysis of short sleep duration and obesity in children and adults.” Sleep — 31.5 (2008): 619.

Chan, Amanda L. “Man Dies After Going 11 Days Without Sleep: What Are The Health Risks Of Sleep Deprivation?” The Huffington Post. TheHuffingtonPost.com, 27 June 2012. Web. 18 Oct. 2016.

Darlington, K., et al. Situational Awareness, Crew Resource Management and Operational Performance in Fatigued Two-Man Crews Using Three Stimulant Countermeasures. Army Aeromedical Research Lab, Fort Rucker, AL. 2006

Food and Drug Administration. “Medicines in my home: Caffeine and your body.” US Food and Drug Administration Home Page (2007).

Jewett, Megan E., et al. “Dose-response relationship between sleep duration and human psychomotor vigilance and subjective alertness.” Sleep: Journal of Sleep Research & Sleep Medicine (1999).

Kamimori, Gary H., et al. “The rate of absorption and relative bioavailability of caffeine administered in chewing gum versus capsules to normal healthy volunteers.” International Journal of Pharmaceutics 234.1 (2002): 159–167.

Kelley, Amanda M., et al. “Cognition enhancement by modafinil: a meta-analysis.” Aviation, space, and environmental medicine 83.7 (2012): 685–690.

Klei, Lambertus, et al. “Heritability of morningness‐eveningness and self‐report sleep measures in a family‐based sample of 521 hutterites.” Chronobiology international 22.6 (2005): 1041–1054.

Klein, Sarah. “5 Other Disastrous Accidents Related To Sleep Deprivation.” The Huffington Post. TheHuffingtonPost.com, 12 Mar. 2013. Web. 18 Oct. 2016.

Lewy, Alfred J., Robert L. Sack, and Clifford M. Singer. “Melatonin, light and chronobiological disorders.” Photoperiodism, melatonin and the pineal (2009): 231–252.

National Sleep Foundation. 2002 “Sleep in America” Poll. (2002)

Pleban, Robert J., et al. “Characterization of sleep and body composition changes during ranger training.” Military Psychology 2.3 (1990): 145.

Porkka-Heiskanen, Tarja, et al. “Adenosine: a mediator of the sleep-inducing effects of prolonged wakefulness.” Science 276.5316 (1997): 1265–1268.

Porrino, Linda J., et al. “Facilitation of task performance and removal of the effects of sleep deprivation by an ampakine (CX717) in nonhuman primates.” PLoS Biol 3.9 (2005): e299.

Sassin, J. F., et al. “Human growth hormone release: relation to slow-wave sleep and sleep-waking cycles.” Science 165.3892 (1969): 513–515.

Smits, Paul, et al. “Evidence for an antagonism between caffeine and adenosine in the human cardiovascular system.” Journal of cardiovascular pharmacology 10.2 (1987): 136–143.

Tobler, Irene, and B. Schwierin. “Behavioural sleep in the giraffe (Giraffa camelopardalis) in a zoological garden.” Journal of sleep research 5.1 (1996): 21–32.

United States of America. Pentagon. Office of Defense Research and Engineering. Human Performance. By E. Williams et al. Washington D.C.: JASON, 2008. Print.

Van Dongen, Hans PA, et al. “The cumulative cost of additional wakefulness: Dose-response effects on neurobehavioral functions and sleep physiology from Chronic sleep restriction and total sleep deprivation.” Sleep 26.2 (2003): 117–126.

Xie, Lulu, et al. “Sleep drives metabolite clearance from the adult brain.” science 342.6156 (2013): 373–377.

Yaggi HK, Araujo AB, McKinlay JB. Sleep duration as a risk factor for the development of type 2 diabetes. Diabetes Care 2006; 29:657–61.

Originally published at medium.com