WASHINGTON – A groundbreaking study has identified a genetic mutation that may explain why some individuals can function optimally on as little as three hours of sleep per night. The research, published on May 5 in the journal Proceedings of the National Academy of Sciences (PNAS), pinpoints the SIK3-N783Y mutation in the SIK3 gene, a key regulator of sleep and wakefulness.

This finding bolsters the growing body of research on natural short sleepers (NSS), individuals who thrive on significantly less sleep than the average person without experiencing adverse health effects. Previously, scientists had linked mutations in four genes-DEC2, NPSR1, GRM1, and ADRB1-to this rare trait.

In the recent study, researchers analyzed the DNA of volunteers who identified as natural short sleepers. One participant, a healthy 70-year-old woman, reported needing only three hours of sleep nightly. However, actigraphy recordings revealed her average sleep duration to be 6.3 hours. Whole-exome sequencing of her DNA led to the discovery of the SIK3-N783Y mutation.

To validate the mutation’s effects, scientists introduced the genetic alteration into laboratory mice. The genetically modified mice slept an average of 30 minutes less per night compared to their normal counterparts. Following induced sleep deprivation, these mice slept up to 54 minutes less, confirming the mutation’s impact on sleep duration.

The SIK3 gene encodes a protein kinase, an enzyme that transfers phosphate molecules to other proteins, thereby influencing their function. The N783Y mutation appears to induce structural changes in the SIK3 protein, impairing its ability to transfer these molecules. This alteration affects biochemical processes at synapses-the connections between neurons-and consequently, sleep duration.

Implications for Sleep Disorder Treatments

“these findings advance our understanding of the genetic underpinnings of sleep,” the researchers stated. Understanding how the SIK3-N783Y mutation reduces the natural need for sleep could pave the way for new therapeutic strategies to improve sleep efficiency and treat common sleep disorders like insomnia.

“the body finishes processes like detoxification, cell repair, and brain cleaning in a shorter time, allowing them to function with less sleep than usual.”

Natural short sleepers not only thrive on less sleep but also tend to feel worse if they oversleep. Despite getting only four to six hours of sleep, they do not experience daytime sleepiness or cognitive deficits, suggesting that specific genetic factors regulate their need for rest. The discovery of the SIK3-N783Y mutation highlights the genetic diversity that explains why sleep needs vary among individuals.

Ying-Hui Fu,a researcher involved in the study,explained that these individuals “can perform at a higher level than we do all the functions that our body performs while we sleep,” because “the body finishes processes like detoxification,cell repair,and brain cleaning in a shorter time.”

Medical professionals typically recommend seven to nine hours of sleep each night for adults to function optimally. For most people, sleep deprivation is linked to increased risks of chronic diseases, including diabetes, heart disease, and dementia. the SIK3-N783Y mutation could make some individuals more resistant to the negative effects of insufficient sleep.

The researchers hope that unraveling the genetic mechanisms of natural short sleepers could help identify new drug targets for treating sleep disorders. By understanding how certain genetic mutations reduce the need for sleep without compromising health, new therapeutic approaches could be developed to improve sleep efficiency and mitigate the impacts of sleep deprivation.

While the SIK3-N783Y mutation is highly likely rare, its discovery is a critically important step in understanding how the brain regulates sleep. The study underscores that sleep,far from being a simple biological routine,is a complex function influenced by genetic factors that are still largely unknown.