The document discusses why organisms need sleep. The NIH recommends 7-8 hours of sleep per night for adults, but many people report getting less. Fatal familial insomnia is a rare genetic disorder where people are completely unable to sleep, leading to rapid cognitive decline and death within 1-3 years, showing sleep is necessary for survival. Experiments depriving rats of sleep found they all died within 2-4 weeks, though autopsies found no clear cause of death. Several theories for why we sleep are discussed, with the most viable being that sleep has a restorative function, allowing the brain to clear out metabolic waste that builds up during waking hours.

1. Why do we sleep?
The National Institute of Health (NIH) recommends that adults get 7-8 hours of sleep a
night (“How Much Sleep,” 2012). This is not 7-8 hours between the time one sets the alarm and the
time it goes off, but rather the time a person spends cycling through the four stages of sleep. This
discrepancy is important: According to the Bureau of Labor Statistics in the 2014 American Time
Use Survey, it would seem that people are getting an impressive 8.74 hours of sleep per day (2014).
However, this survey doesn’t measure sleep so much as it measures time spent in bed, a portion of
which could be devoted to activities such as reading or getting ready to fall asleep. A Gallup poll
from 2013 finds that people report getting 6.8 hours of sleep, just a little bit shy of the
recommended 7-8 hours, although 56% of the survey respondents indicated that they got enough
sleep as they needed (Jones, 2013). Still, almost half of the population feels that they could benefit
from more sleep.
Getting a lot of sleep is hard, however. As adults, we devote about a third of our time to this
single activity, time we are often willing, or forced, to sacrifice for work, family, or fun. So here is the
big question: Why do we sleep?
Here is the big answer: We don’t know for sure. What we do know is that organisms need it
to survive.
One of the rarest disorders in the world demonstrates the fatality that accompanies complete
sleep deprivation in humans. Fatal familial insomnia is a genetic sleep disorder affecting only a few
dozen families worldwide. The onset of the disease typically begins in middle-to-late adulthood
when a person with the mutated prion protein gene that causes the disease begins to show
symptoms of severe insomnia (Krasnianski, 2008). In as little as half a year or up to three years, the
insomnia develops into a complete inability to sleep. Sleeping pills and barbiturates do not induce
sleep, and while inducing a chemical coma causes the individual to lose consciousness, the brain still
fails to enter into the sleep stages. In the absence of sleep, the individual shows rapid cognitive
decline, with significant memory and other cognitive deficits emerging in early stages of the disease
and signs of dementia appearing in the months preceding death (Cortelli, Gambetti, Montagna,
Lugaresi, & Lugaresi, 1999).
The reason that a lack of sleep causes death remains unknown. Some studies have attempted
to answer this question by conducting total sleep deprivation (TSD) experiments on rats (for the
generative article, see Rechtschaffen, Gilliland, Bergmann & Winter, 1983). The design of these
studies was ingenious: A sleep deprived (SD) rat and a control rat would be placed on a disk
suspended over water and the SD rat’s brain activity was recorded. When the rat began to fall asleep,
the disk would rotate, forcing the rat to wake up and walk to avoid falling into the water
(Rechtschaffen & Bergmann, 1995). See Figure 1. In these studies, all sleep deprived rats died, and in
a surprisingly short amount of time. In a study by Everson, Bergmann, and Rechtschaffen (1989), all
sleep deprived rats succumbed to death within about two to four weeks.
Figure 1.

2. Rechtschaffen etl al., 1983.
Curiously, the researchers could not identify the cause of death. Autopsies of SD rats found
no deterioration of the brain or damage to the internal organs (Carlson, 2010).
There are several theories attempting to answer the question of why we sleep. The early
evolutionary theory of sleep suggested that sleep has an adaptive function and that animals that
could stay still and quiet during periods of the day when they were most vulnerable (at night, when
they could not see) would be more likely to go undetected by predators than animals that were
moving around (“Why do we sleep,” 2007). However, this argument is weakened under the
consideration that all vertebrates, both mammals and birds, including those at the top of the food
chain, sleep. Some species of marine mammals, such as bottlenose dolphins, have evolved to have
cerebral hemispheres that sleep separately rather than at the same time so that one hemisphere is
always alert (Carlson, 2010). This makes for strong evidence against the claim that sleep is merely an
adaptive behavior to avoid predation.
A more viable theory for the need to sleep is that is has a restorative function. A recent study
from 2013 suggests that sleep has a restorative function. During wakefulness, metabolic activity in
the brain produces chemicals that are cleared out through the exchange of fluid in the brain and
spine, termed cerebrospinal fluid (CSF) and fluid that resides between the cells, termed interstitial
fluid (ISF). During sleep, extracellular space expands and contracts, increasing the efficiency of the
clearance of metabolic waste (Xie et al., 2013). The waste that builds up is toxic to the brain, and
offers a solid explanation for the cognitive decline that occurs with sleep deprivation. While this area
of research is new, it provides the most promising explanation to the question of why we sleep.
References
American time use survey news release. (2014). Bureau of Labor Statistics. Retrieved from
http://www.bls.gov/news.release/atus.htm.
Carlson, N. R. (2010). Physiology of behavior. Boston, MA: Pearson.
Cortelli, Gambetti, Montagna, Lugaresi, & Lugaresi, E. (1999). Fatal familial insomnia: clinical
features and molecular genetics. Journal Of Sleep Research, 823-29.

3. Everson, C. A., Bergmann, B. M., & Rechtschaffen, A. (1989). Sleep deprivation in the rat: III. Total
sleep deprivation. Sleep: Journal Of Sleep Research & Sleep Medicine, 12(1), 13-21.
How much sleep is enough? (2012). National Institute of Health. Retrieved from
http://www.nhlbi.nih.gov/health/health-topics/topics/sdd/howmuch.html
Jones, J.M. (2013). In U.S., 40% get less than recommended amount of sleep. Gallup. Retrieved from
http://www.gallup.com/poll/166553/less-recommended-amount-sleep.aspx.
Krasnianski, A., Bartl, M., Juan, P., Heinemann, U., Meissner, B., Varges, D., & ... Zerr, I. (2008).
Fatal familial insomnia: Clinical features and early identification. Annals Of Neurology, 63(5), 658-661.
doi:10.1002/ana.21358
Rechtschaffen, A., & Bergmann, B. M. (1995). Sleep deprivation in the rat by the disk-over-water
method. Behavioural Brain Research, 69(1-2), 55-63. doi:10.1016/0166-4328(95)00020-T
Rechtschaffen A, Gilliland M, Bergmann B, Winter J. (1983). Physiological correlates of prolonged
sleep deprivation in rats. Science, 221(4606):182-184. Available from: PsycINFO, Ipswich, MA.
Accessed July 31, 2014.
Why do we sleep, anyway? (2007). Division of Sleep Medicine at Harvard Medical School. Retrieved from
http://healthysleep.med.harvard.edu/healthy/matters/benefits-of-sleep/why-do-we-sleep.
Xie, L., Hongyi, K., Qiwu, X., Chen, M. J., Yonghong, L., Thiyagarajan, M., & ... Nedergaard, M.
(2013). Sleep Drives Metabolite Clearance from the Adult Brain. Science, 342(6156), 373-377.
doi:10.1126/science.1241224
by Suzanne Crockett
for John G. Kuna, Psy.D. & Associates
http://drjohngkuna.com/blog/
570-961-3361