Boy, some people have all genetic luck. In a recent study, scientists describe a newly discovered mutation which allows humans to sleep naturally much less hours per night without any negative health effect.
Researchers in China conducted the study, published in Acts of the National Academy of Sciences. The mutation was found in a healthy woman of 70 years who lived his whole life barely. The results could one day help us understand how to better treat sleep disorders that afflict the rest of humanity, say the researchers.
Most people need about seven to nine hours of sleep per night for optimal health. But there are some who are so-called natural short sleeps, capable of resting between four and six hours each night without experiencing the symptoms of sleep deprivation (so as not to confuse with about a third of people who sleep less than seven hours per night and suffer). Research has revealed that these individuals tend to transport unique genetic mutations.
So far, scientists have found mutations in four different genes (DEC2, NPSR1, GRM1 and ADRB1) linked to natural short sleep. But the researchers behind this new study have now found another: Kinase 3 inducted by salt, or SIK3, gene, named after the protein it makes. SIK3 is a kinase protein, a type of enzyme. It is believed that to play a role in our metabolism, but previous research (mainly in mice) also suggested that it helps influence the duration of sleep.
The team analyzed the sleep models and the DNA of their volunteer. Although she declared that she generally needed that three hours of sleep per night, the activation recordings (movement at night generally captured via the wristwatch) revealed that it was sleeping on an average of 6.3 hours per night very windy. The genetic exploration of the team also identified a particular mutation in the SIK3 – Dubbed N783Y gene – which seemed to explain its natural natural sleep.
To confirm their discovery, they designed mice with the same mutation, and found that they also slept less as normal mice. The mutation seems to inhibit SIK3’s ability to transfer certain molecules to other proteins as usual, in particular important proteins for synapses, connections that form between neurons.
“These results underline the preserved function of SIK3 as a critical gene in the regulation of human sleep,” wrote the authors.
Perhaps about 1% of the world’s population are natural short sleepers. But the lessons we learn by disentangling their unique genetic gift could help scientists find new drug targets to treat sleep disorders. Study researchers have already found evidence that other kinase proteins similar to SIK3 also play a role in assigning our sleeping time.
“These results advance our understanding of the genetic foundations of sleep, highlight the broader implications of the Kinase activity in the regulation of sleep between species and provide additional support for potential therapeutic strategies to improve sleep efficiency,” they wrote.
In any case, we hope that scientists will also discover the genetic reason for which my cat must wake me up at 6 am, despite the fact that breakfast is a few hours.
