What if the amount of sleep you need isn’t just a matter of lifestyle, but is partly coded in your DNA?

Most people know that consistently getting insufficient sleep affects cognitive performance, emotional regulation, and nearly every major system in the body.

Yet some rare individuals, known as natural short sleepers, appear to require only about six hours of sleep per night while maintaining normal cognitive function.

Researchers believe that genetic differences help explain this unusual ability.

The DEC2 Gene

One of the first genetic discoveries involved a variant in the DEC2 gene, identified in families with naturally short sleep patterns.

Researchers studied twins who differed in whether they carried this genetic variant.

Sleep patterns were measured both in everyday life and under controlled laboratory conditions.

The results showed that the twin carrying the DEC2 mutation (also known as BHLHE41) naturally slept approximately 30 to 60 minutes less than the noncarrier twin.

But the researchers didn’t stop at measuring how long the twins slept. They wanted to know what happened when the twins were pushed beyond their normal sleep limits.

After 38 hours without sleep, the twin carrying the DEC2 mutation showed greater resilience to sleep deprivation.

Compared with the non-carrier twin, the mutation carrier did better on cognitive testing.

The difference continued during recovery sleep. Normally, after losing sleep, the body responds with a strong recovery process. The longer a person remains awake, the greater the pressure to sleep longer and more deeply afterward.

However, the DEC2 mutation carrier showed a much smaller sleep rebound, suggesting that their biological need for sleep was genuinely lower.

These findings suggest that, for some rare individuals, a lower biological need for sleep may be influenced by specific genetic variants.

How Can Someone Sleep Less Without Becoming Sleep-Deprived?

Researchers have created genetically engineered mice that carry the same short-sleeping DEC2 mutation found in some humans.

Studying these mice has helped researchers investigate how this mutation may alter the regulation of sleep and wakefulness.

The DEC2 mutation increases the expression of orexin, a brain chemical involved in promoting wakefulness.

As a result, mice carrying the mutation are able to remain awake longer and sleep less than normal mice.

However, increased wakefulness alone doesn’t fully explain why these mice appear to tolerate less sleep, particularly after sleep deprivation.

Interestingly, the DEC2 mutation is also associated with greater slow-wave activity, a brain-wave pattern characteristic of deep, restorative sleep.

The stronger slow-wave activity raises the possibility that the mutation may allow some restorative aspects of sleep to occur more intensely during a shorter sleep period.

In other words, the biology may involve more than simply staying awake longer.

The mutation may alter both the drive to remain awake and the architecture of sleep itself.

This combination may help explain why mice carrying the DEC2 mutation can function with less total sleep.

Whether the same mechanism fully explains the reduced sleep need observed in humans with DEC2 mutations remains an important question for researchers.

But does needing less sleep come with a cost?

What Happens to Their Long-Term Health?

Although natural short sleepers do not appear to show obvious cognitive deficits, scientists still do not know whether there are long-term health consequences.

Most studies have focused on short-term measurements of performance.

However, researchers have not yet conducted long-term studies examining whether natural short sleepers experience the same health span or life span as people who sleep longer.

Evidence from other organisms suggests that reduced sleep may sometimes come with hidden costs.

For example, fruit flies with a genetic mutation that shortened sleep duration experienced shorter life spans compared with normal flies.

This suggests that genetic variations that reduce sleep need may appear harmless in the short term but have consequences that only become visible over time.

One possibility worth considering is whether sleeping less could affect some of the cellular maintenance processes that normally take place during sleep, such as DNA repair.

Sleep Protects Your DNA

Genes not only influence sleep, but sleep also influences the health of your DNA.

During wakefulness, DNA, especially within neurons, accumulates damage in the form of double-strand breaks.

These breaks represent a significant challenge because neurons are highly active cells with demanding metabolic requirements.

During sleep, these DNA breaks are rapidly repaired.

This suggests that sleep provides a critical period of cellular maintenance, allowing the brain to restore genetic integrity after the demands of waking life.

Without sufficient sleep, excessive DNA damage may accumulate, potentially increasing the risk of cellular dysfunction.

Researchers have also discovered that the relationship works in reverse: the body’s response to DNA damage can influence sleep itself.

The expression of PARP1, an enzyme involved in DNA repair, can promote sleep, suggesting that cellular damage signals may help communicate the need for rest.

Could You Be a Natural Short Sleeper?

Genuine natural short sleepers are rare, have a lifelong pattern of naturally sleeping less, and don’t simply force themselves to function on less sleep.

But if you’re curious about the similarities between your own sleep habits and those of natural short sleepers, answer the following questions:

• Have you naturally needed relatively little sleep for years, rather than recently cutting your sleep down?
• Do you consistently wake after your shorter sleep without an alarm and without having to drag yourself out of bed?
• During the day, do you remain alert, cognitively sharp, emotionally stable, and physically functional without relying heavily on caffeine or other stimulants?
• If you’re given the opportunity to sleep in, do you naturally continue sleeping significantly longer?
• Are you accumulating signs of sleep deprivation?
• Do any close relatives share the same sleep pattern?

While answering these questions, keep in mind that this isn’t a way to diagnose a genetic short-sleep trait.

A clinical evaluation by a physician can establish whether you have a specific genetic variant associated with natural short sleep.

Also, uploading your raw DNA file from 23andMe, AncestryDNA, or MyHeritage onto Genetic Lifehacks can help you determine if you carry the variant.

Why This Matters

While the study of natural short sleepers has revealed that sleep can be shaped by your genes, scientists still don’t know whether natural short sleepers experience long-term health consequences.

What we do know is that, during sleep, the brain carries out essential maintenance, including repairing DNA damage that accumulates during waking life.

Your DNA helps determine how you sleep. And sleep helps protect your DNA.

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This article was excerpted and adapted from “The new science of sleep: From cells to large-scale societies” by Omer Sharon, et al. published in PLoS Biology. It is presented here under the terms of the Creative Commons Attribution License CC BY 4.0.