Have you ever talked to someone who claimed they were on just a few hours of sleep but seemed to be functioning fine? New studies have shown that some individuals have a mutation in their gene that allows them to function perfectly fine with up to half the amount of sleep as a regular individual.
The first study of a mutation that affected sleep length in individuals was conducted in 2009 by Dr. Ying-Hui Fu at the University of California at San Francisco. Studying a family with two exceptionally early risers, they studied their DNA, finding that the “385th amino acid of the DEC2 protein” switched from “proline to arginine,” a report by the National Institutes of Health explains. Scientists then treated lab mice, replacing their version of the same amino acid with the one found in humans. “Mice carrying the arginine version…were awake about 8% longer during their light period.”
A later study arose from the same lab on March 12, 2018, finding that the DEC2 mutation could additionally allow “human short sleepers…to survive and thrive on just a few hours of sleep,” according to UCSF. “They discovered that DEC2 helps control levels of orexin, a hormone involved in maintaining wakefulness.” Orexins, which are brain chemicals that regulate your sleep, are “most active during the day,” according to Sleep Foundation. “These neuropeptides stimulate other neurons to release neurotransmitters that promote alertness, such as dopamine, serotonin and norepinephrine…[and] people with…narcolepsy have an 85-95% reduction in the number of neurons that produce” these.
DEC2 was found to control the prepro-orexin promoter, which represses orexin. However, the mutation results in “increased orexin expression,” according to the National Library of Medicine, by not allowing the promoter to bind with itself.
Furthermore, in 2023, a study was conducted on fruit flies, which were treated with the DEC2 genes. The “DEC2 mutants lived significantly longer with improved health despite sleeping less. In particular DEC2 mutants were more stress resistant and displayed improved mitochondrial fitness in flight muscles,” said NLM. “Several altered transcriptional pathways related to stress response, including detoxification and xenobiotic stress pathways” were also found. The DEC2 mutation shows that there are increased health benefits to having this mutation.
Earlier this year, Ying-Hui Fu made another discovery of a mutation in Salt-Induced Kinase 3 (SIK3), a protein kinase involved in regulating various cellular processes, including metabolism, circadian rhythms and cell divisions, according to eLife. This mutation was found to be correlated with “natural short sleep,” NLM reports. This mutation resulted in “diminished kinase activity” and “decrease in sleep time.”
“In recent years, natural short sleepers have even been identified in the human population that, despite sleeping less, do not exhibit adverse health issues that are typically associated with sleep deprivation,” NLM reports. By studying these people, scientists can help “reveal strategies that can sustain health in sleep-deprived states as well as promote more general health.” Fu was quoted on UCSF as saying that natural short sleepers “aren’t people who’ve trained themselves to wake up early. They’re born this way.”
