How does your DNA affect your sleep?
Some people just seem to be able to roll out of bed at sunrise and jump right into the day. Others are slower to wake up, but are able to be productive well into the night. Why do our sleeping habits vary so much from person to person? Scientists have asked this same question, and their research shows that DNA is part of the reason.
To say the least, sleep is a popular activity. We need it to live, and we spend about a third of our lives doing it1. We’re not alone, either—sleep has been described (in some form or another) in many different animals including birds, dolphins, flies, worms, lizards, snakes, and fish2. Researchers believe that sleep evolved millions of years ago to help animals conserve energy, improve mental cognition, or simply pass the time between periods of feeding2.
Sleep varies from species to species. Consider the difference between dolphins and humans. Dolphins engage in a form of sleep where the two halves of their brain alternate between a sleep-like state and a more alert, awake state. Dolphins don’t have an REM cycle (the stage of sleep where we dream), possibly because REM sleep is often accompanied by muscle relaxation—which would be bad for an animal that is perpetually swimming2. In contrast, humans typically have a solid block of time where our bodies become temporarily paralyzed and the majority of our brain goes through cycles of REM and non-REM (NREM) sleep2,3. It may not be surprising that humans and dolphins sleep differently, but even among people, there’s wide variation in sleep patterns.
“Early birds” have a natural tendency to wake up earlier than most people, but are also prone to feeling sleepy earlier in the day. In contrast, the so-called “night owls” prefer to go to bed later and wake up later. Scientists studying these traits have found that the DNA we inherit may affect which category we fall into4-6.
Studies both large and small have aimed to explain how a person’s genetics might influence their sleep habits. Researchers have found that whether a person is likely to wake up early or later is partially determined by genes involved in setting their circadian rhythm—their internal clock.
Nearly every cell in the human body has its own rhythm that controls when (and to what extent) some parts of the DNA will be used. These individual rhythms are synchronized by signals sent from part of the brain known as the suprachiasmatic nucleus (SCN). Together with input from environmental factors like food, light, and temperature, the SCN helps our body know when to wake up and when to go to sleep. Critical to this process are genes like CLOCK, CRY, PER, CK1ẟ/ϵ, and DEC2, which collectively build and maintain a cell’s circadian rhythm3,4,6.
Variants—heritable changes in the DNA—that are found in these genes affect sleep to different degrees. For example, some variants in the PER2 gene have been found to increase a person’s likelihood of having Familial Advanced Sleep Phase Syndrome. People with this condition exhibit an extreme shift in their sleep cycle, resulting in a drive to fall asleep between 1:00 am and 3:00 am, and wake up between 6:00 pm and 8:00 pm4,6. But there are also less severe effects related to variants in the circadian rhythm genes. Variants in the CLOCK gene have been associated with a shift of only half an hour in sleep duration7. This highlights the fact that there’s a wide spectrum of ways that DNA can potentially influence a person’s sleep.
An emerging area of focus for researchers relates to sleep and the immune system. The link between them is somewhat intuitive because most people are familiar with the sluggish, tired feeling that comes with illness. It’s not clear what that link is or why exactly its there, but genetic studies have found evidence that variants in the DNA affecting our immune system may also lead to changes in our sleep habits4. Good examples of this are changes in the HLA genes, genes that help our body produce antibodies to fight infections. Variants in these genes have been associated with the occurrence of narcolepsy with cataplexy, which is when an individual experiences excessive daytime sleepiness, disrupted sleep at night, and moments of temporary paralysis that’re often brought on by sudden, strong emotions4,8. Research has found that many people with narcolepsy have altered levels of a signaling protein known as orexin which helps stabilize a person in the wakefulness state8. Importantly, many people with these variants never develop narcolepsy, suggesting to researchers that narcolepsy may be the result of both environmental and genetic factors.
After decades of research, it’s clear that sleep is an important and complex activity that’s influenced by the foods we eat and drink, the environments we live in, and—to some extent—our DNA. With much left to learn, we look forward to discovering more about the latest sleep science for a long time to come.
2Joiner, William J. “Unraveling the Evolutionary Determinants of Sleep.” Current biology : CB 26.20 (2016): R1073–R1087. PMC. Web. 11 Sept. 2018.
3Wright, Kenneth P., Christopher A. Lowry, and Monique K. LeBourgeois. “Circadian and Wakefulness-Sleep Modulation of Cognition in Humans.” Frontiers in Molecular Neuroscience 5 (2012): 50. PMC. Web. 10 Sept. 2018.
4Sehgal, Amita, and Emmanuel Mignot. “Genetics of Sleep and Sleep Disorders.” Cell 146.2 (2011): 194–207. PMC. Web. 10 Sept. 2018.
5Kalmbach, David A. et al. “Genetic Basis of Chronotype in Humans: Insights From Three Landmark GWAS.” Sleep 40.2 (2017): zsw048. PMC. Web. 11 Sept. 2018.
6Andreani, Tomas S. et al. “Genetics of Circadian Rhythms.” Sleep medicine clinics 10.4 (2015): 413–421. PMC. Web. 10 Sept. 2018.
7Landgraf, Dominic, et al. “Clock Genes and Sleep.” SpringerLink, Springer, Dordrecht, 11 Aug. 2011, link.springer.com/article/10.1007/s00424-011-1003-9.
8Leonard, C S, and J P Kukkonen. “Orexin/hypocretin Receptor Signalling: A Functional Perspective.” British Journal of Pharmacology 171.2 (2014): 294–313. PMC. Web. 12 Sept. 2018.
9Hublin, Christer, et al. “Parasomnias: Co-Occurrence and Genetics.” Psychiatric Genetics, vol. 11, no. 2, 2001, pp. 65–70., doi:10.1097/00041444-200106000-00002.
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