Barely Sleep and Still Feel Fine? Thank Your Lucky Genes

Boy, some people have all the genetic luck. In a recent study, scientists describe a newly discovered mutation that allows humans to naturally sleep much fewer hours a night without any negative health effects.

Researchers in China conducted the study, published in Proceedings of the National Academy of Sciences. The mutation was found in a 70-year-old healthy woman who’s lived her whole life barely sleeping. The findings could someday help us understand how to better treat sleep disorders that plague the rest of humanity, the researchers say.

Most people need around seven to nine hours of sleep a night for optimal health. But there are some out there who are so-called natural short sleepers, able to rest between four and six hours every night without experiencing the symptoms of sleep deprivation (not to be confused with the roughly one-third of people who sleep less than seven hours a night and suffer for it). Research has found that these individuals tend to carry unique genetic mutations.

So far, scientists have found mutations in four different genes (DEC2, NPSR1, GRM1, and ADRB1) tied to natural short sleep. But the researchers behind this new study have now found another: the salt-inducible kinase 3, or SIK3, gene, named after the protein it makes. SIK3 is a protein kinase, a type of enzyme. It’s thought to play a role in our metabolism, but past research (mostly in mice) has also suggested that it helps influence sleep duration.

The team analyzed the sleeping patterns and DNA of their volunteer. Though she reported usually only needing three hours of sleep a night, actigraphy recordings (movement at night typically captured via wristwatch) found that she actually slept a still very breezy 6.3 hours a night on average. The team’s genetic exploration also identified a particular mutation in the SIK3 gene—dubbed N783Y—that seemed to explain her natural short sleep.

To confirm their discovery, they engineered mice with the same mutation, and found that they too slept less than normal mice did. The mutation appears to inhibit SIK3’s ability to transfer certain molecules to other proteins as usual, particularly proteins important to the synapses, the connections that form between neurons.

“These findings underscore the conserved function of SIK3 as a critical gene in human sleep regulation,” the authors wrote.

Perhaps only around 1% of the world’s population are natural short sleepers. But the lessons we learn from unraveling their unique genetic gift could help scientists find new drug targets for treating sleep disorders. The study researchers have already found some evidence that other protein kinases similar to SIK3 also play a part in affecting our sleep duration.

“These findings advance our understanding of the genetic underpinnings of sleep, highlight the broader implications of kinase activity in sleep regulation across species, and provide further support for potential therapeutic strategies to enhance sleep efficiency,” they wrote.

In any case, here’s hoping scientists also discover the genetic reason why my cat has to wake me up at 6 in the morning rain or shine, despite knowing that breakfast is hours away.