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Genetics of Sleep Personality

 

Has anybody ever asked you if were a night owl or a morning lark? Or how much sleep you needed to feel well-rested? While psychologists have been classifying humans into different personality types for decades now, a field of sleep science has emerged which examining the role our genes play in determining different sleep personalities – such as whether you’re a night owl or a short sleeper.

Our genes can determine whether we develop diabetes, cancer, heart disease, or obesity. Not surprisingly, the traits that make up our sleep personality are also genetically determined. As with many things, our environment has an impact on how we sleep, but certain genes (single unit of heritability), and ranges of our chromosomes (containing multiple genes) also influence our sleep personality. This suggests that people who go to bed very late, for example, are much more likely to have genes or sections of chromosome in common with each other than with people who go to bed very early.

There are three primary ways to test how genes influence sleep personality. First, you can compare identical and fraternal twins. Twins are typically raised in the same environment, but identical twins share 100% of their genetic material, and fraternal twins share only 50% of their genetic material, like typical siblings. Therefore, if a certain sleep trait shows up more often in identical twins than in fraternal twins, it is likely to be genetically linked.

Second, you can apply a similar strategy to unrelated people by administering sleep surveys to hundreds or thousands of people, asking detailed questions about their sleep habits, collecting genetic material from them, and looking for matches between self-reported traits such as “long-sleeper” and regions of chromosomes that are linked to this trait. This technique is known as a “genome-wide association study”, or linkage analysis.

Third, you can take a more direct approach and search the genes of people with extreme sleep personalities for mutations, or “polymorphisms” – an alternate form of the gene that usually resides in a smaller percentage of the human population. Mutations and polymorphisms that affect sleep are generally rare, but once the different gene copy has been found, scientists can examine that specific gene and test whether it is the same in other people who share the extreme sleep trait.

Genetic Contribution to Sleep Personality Traits:

Most of what is known about the genetics of sleep personality comes from studying extreme examples (extreme larks/early risers, for example). However, it’s important to remember that while you may not be an extreme lark, or an extremely long-sleeper, the same genes are likely modified in more subtle ways to produce sleep personalities within a normal range as well.

Morning/Evening Preference

The genetic control of morning/evening (M/E) preference is well established. Various twin studies and linkage analyses have shown a genetic linkage to M/E preference (eg. Heath et al., 1990; Koskenvuo et al., 2007). More focused genetic studies have discovered that changes in individual genes that keep the biological clock – the timing mechanism within our body – running on time can greatly impact our M/E preference.

For instance, the circadian disorders known as “advanced sleep phase syndrome (ASPS)” and “delayed sleep phase syndrome (DSPS) both run in families and are caused by genetic mutations of biological clock genes. Those with ASPS fall asleep very early (6-8pm) and wake very early (1-3am). Mutations in the “period 2” and “casein kinase 1” genes are the most common culprit for this disorder (Toh et al., 2001; Xu et al., 2005). Those with DSPS are the opposite, they fall asleep extremely late (5am) and wake up extremely late (2pm). In these people, polymorphisms in the biological clock gene “period 3” have been implicated (Archer et al., 2003). Morning/evening preference has also been associated with polymorphisms in the “clock” gene, (Katzenberg et al., 1998) which as can be deduced from the name, is a central player in the biological clock.

Sleep Duration and Napping

Sleep duration and napping have been shown to be under genetic control in twin studies (e.g. Heath et al, 1990). Other than what has been learned from twin studies, very little is known about the genetic control of napping. As yet, no “napping gene” has been isolated. More is known about the genetic control of sleep duration. In one study, sleep duration was linked to a mutation in a gene that keeps our biological clock running known as “dec2” (He et al., 2009). People with this mutation tend to sleep ~2hr less (about 6 hr) than people without it.

How long we sleep can also be influenced by genes that alter general brain function. “Morvan’s syndrome” is an autoimmune disorder that attacks proteins in neurons that are required to put the brain into a sleep state, causing a marked reduction in sleep (Liguori et al, 2001). “Fatal Familial Insomnia” is another sleep disorder that is caused by a mutation in the “prion” gene, a gene that codes for a protein required for normal neuronal function (Lugaresi and Provini, 2007). Sadly, both Morvan’s syndrome and Fatal Familial Insomnia eventually result in near complete sleeplessness and death.

Sleep Flexibility

Little is known about how sleep flexibility is genetically determined. Flexible sleepers tend to be those that can nap during the day. They also tend to be evening types, which in general are less rigid in sleep/wake times than morning types. It may turn out that these traits are genetically inseparable, however if there is a “sleep flexibility” gene, it is only a matter of time before it is identified.

Genetic contributions to other equally enigmatic sleep disorders and characteristics have been worked out in recent years, including; narcolepsy - a debilitating disease that causes people to fall asleep as inappropriate times, restless legs syndrome, insomnia, the electroencephalographic (EEG) brain activity pattern during wake and sleep (see Sehgal and Mignot, 2011 for review), and even individual responses to caffeine (Landolt, 2008).

Working With our Sleep Personality:

Genetics are “hard-wired” and cannot be changed in our lifetimes, but behavior can be altered within certain boundaries. It is important to learn your sleep personality, identify your sleep needs, and try to make adjustments to your daily life to maximize your sleep and alertness.

Research has shown that flexible sleepers and those with an evening preference tolerate shiftwork (especially night shifts) well (Costa et al., 1989; Foster & Kreitzman, 2004), since they more quickly adapt to new sleep/wake schedules and resulting sleep loss. Those with a morning preference find nighttime shiftwork more challenging, since they have rigid wake times, and have more difficulty making up for lost sleep (Duffy, Dijk, Hall, & Czeisler, 1999). These people do best with morning shifts, but they can adapt to night shifts.

We’re not all suited to work 9-5 jobs (itself a challenging schedule for a night owl!), so when circumstances dictate that we must work outside of the “normal” work day, it is important to pay attention to what your genes are trying to tell you, and to set yourself up for the best possible chance of success. If you are a shift manager in charge of scheduling employees, it is advisable to get to know your employees, and schedule them at times when they are most efficient.

REFERENCES

Archer SN, Robilliard DL, Skene DJ, Smits M, Williams A, Josephine Arendt J, & von Schantz M (2003) A length polymorphism in the circadian clock gene Per3 is linked to delayed sleep phase syndrome and extreme diurnal preference. SLEEP 26(4): 413-415.
Costa G, Lievore F, Casaletti G, Gaffuri E & Folkard S (1989) Circadian characteristics influencing interindividual differences in tolerance and adjustment to shiftwork. Ergonomics 32(4): 373-385.
Duffy JF, Dijk DJ, Hall EF & Czeisler CA (1999) Relationship of endogenous circadian melatonin and temperature rhythms to self-reported preference for morning or evening activity in young and older people. Journal of Investigative Medicine 47(3): 141-150.
Foster RG & Kreitzman L (2004). Rhythms of life: The biological clock that control the daily lives of every living thing. London: Yale University Press.
He Y, Jones CR, Fujiki N, Xu Y, Guo B, Holder JL Jr., Rossner MJ, Nishino S, & Y-H Fu (2009) The transcriptional repressor DEC2 regulates sleep length in mammals. Science 325(5942): 866-870.
Heath AC, Kendler KS, Eaves LJ, & Martin NG (1990) Evidence for genetic influences on sleep disturbance and sleep pattern in twins. Sleep 13(4): 31S-335.
Katzenberg D, Young T, Finn L, Lin L, King DP, Takahashi JS, & Mignot E (1998) A CLOCK polymorphism associated with human diurnal preference. SLEEP 21(6): 569-576. 
Koskenvuo M, Hublin C, Partinen M, Heikkila K & Kaprio J (2007) Heritability of diurnal type: a nationwide study of 8753 adult twin pairs. Journal of Sleep Research 16(2): 156-162. 
Landolt H-P (2008) Genotype-dependent differences in sleep, vigilance, and response to stimulants. Current Pharmaceutical Design 14(32): 3396-3407.
Liguori R, Vincent A, Clover L, Avoni1 P, Plazzi G, Cortelli P, Baruzzi A, Carey T, Gambetti P, Lugaresi E & Montagna P (2001) Morvan's syndrome: peripheral and central nervous system and cardiac involvement with antibodies to voltage-gated potassium channels. Brain 124(12): 2417-2426.
Lugaresi E & Provini F (2007) Fatal familial insomnia and agrypnia excitata. Reviews in Neurological Diseases 4(3):145-52.
Moore-Ede M & LeVert S (1998) The Complete Idiot’s Guide to Getting a Good Night’s Sleep. Alpha Books, New York, NY. 
Sehgal A & Mignot E (2011) Genetics of sleep and sleep disorders. Cell 146(2): 194-207.
Toh KL, Jones CR, He Y, Eide EJ, Hinz WA, Virshup DM, Ptáček LJ, & Fu Y-H (2001) An hPer2 phosphorylation site mutation in familial advanced sleep phase syndrome. Science 291(5506): 1040-1043
Xu Y, Padiath QS, Shapiro RE, Jones CR, Wu SC, Saigoh N, Saigoh K, Ptácek LJ & Fu Y-H (2005) Functional consequences of a CKId mutation causing familial advanced sleep phase syndrome. Nature 434: 640-644.

 

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