A new study has identified a rare genetic mutation that may explain why some individuals can thrive on just four to six hours of sleep per night without suffering the usual health consequences associated with sleep deprivation. This mutation affects the sleep-wake cycle, reducing total sleep time while potentially enhancing the quality of deep sleep.
While doctors typically recommend seven to nine hours of sleep for optimal health—citing links between chronic sleep deprivation and serious conditions such as Alzheimer’s disease and heart problems—this research suggests that a small group of people, often referred to as "natural short sleepers," may not need as much rest as others.
The findings, published in the journal Proceedings of the National Academy of Sciences (PNAS), highlight how some people’s bodies are able to perform restorative processes more efficiently during sleep.
“Our bodies continue to work when we go to bed. These people [natural short sleepers], all these functions our bodies are doing while we are sleeping, they can just perform at a higher level than we can,” said co-author Ying-Hui Fu, a neuroscientist and geneticist at the University of California, in a statement to LiveScience.
Researchers pinpointed one such mutation, known as SIK3-N783Y, in a human subject classified as a "super-sleeper." To better understand its effects, they introduced the mutation into genetically modified mice and observed its impact on sleep patterns.
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Mice carrying the SIK3-N783Y mutation slept an average of 31 minutes less than non-mutated mice. After being subjected to mild sleep deprivation through gentle handling, the mutated mice still managed to sleep 54 minutes less than the control group, indicating a significant reduction in overall sleep requirement.
“In a mouse model, the presence of the NSS hSIK3-N783Y mutation leads to a decrease in sleep time and an increase in EEG delta power,” the study reported, suggesting that although these mice slept less, their deep sleep—or slow-wave sleep—may have been more intense or efficient.
The researchers further noted that the mutation causes a structural alteration in the protein responsible for transferring phosphate molecules to other proteins, a key process in regulating bodily functions during sleep.
These insights could eventually pave the way for new treatments aimed at improving sleep quality or addressing sleep disorders. The study also identified other kinases—enzymes involved in cellular signaling—that may be part of a larger network influencing sleep duration.
“Further data analyses reveal additional kinases that could participate in the modulating network for sleep duration,” the study concluded, offering hope for the development of future therapeutic strategies for managing sleep health.
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