A Gene Mutation Lets You Function Perfectly on 4 Hours of Sleep
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Without 8 or 9 hours of sleep, most of us end up staggering around like zombies. But according to a new study, some people have a genetic mutation that makes them feel perfectly alive after sleeping only half as much. Lucky.
Sleeping gives the body a chance to detox and clear out junk from the brain. While the human body typically takes about 8 or 9 hours to do this, having what's called the 'short sleep' mutation makes this possible within just 3 to 6 hours. Neuroscientist Ying-Hui Fu, who researches gene mutations related to sleep, has now discovered another mutation that contributes to natural short sleep (NSS), adding to the five already known mutations that she and her team previously discovered. The new mutation affects the gene SIK3, which is involved in regulating metabolism, energy, and circadian rhythm. A study describing the finding appears now in the journal Proceedings of the National Academy of Sciences.
'Our bodies continue to work when we go to bed, detoxifying themselves and repairing damage,' Fu said in a recent press release. 'These people, all these functions our bodies are doing while we are sleeping, they can just perform at a higher level than we can.'
Fu began investigating genetic reasons for needing so little sleep after she and her team were approached by a mother and daughter who felt refreshed after sleeping six hours or less. They would go to bed with the rest of us—around 11 p.m. to midnight—but wake up far earlier without an alarm. Analyzing their genome led to finding a rare mutation in the gene DEC2, which regulates circadian rhythm by binding to the gene MyoD1, which in turn switches on expression of the neuropeptide known as orexin. Orexin is secreted by the hypothalamus and keeps you awake, so when DEC2 inhibits MyoD1, lower levels of orexin promote sleep.
The DEC2 mutation results in increased levels of orexin, which explains why short sleepers can wake up after only a few hours and have no issue with feeling as if they are about to pass out during the day. In contrast, narcolepsy (characterized by excessive sleepiness during the day and disrupted sleep at night) is caused by an orexin deficit.
SIK3 has a part in regulating both the need for sleep and the amount of NREM (non-rapid-eye-movement) sleep we get each night. This gene is active in synapses—spaces between neurons where messages are sent from one neuron to another—and is expressed most in the cerebellum and adrenal glands. When Fu genetically modified mice (which usually need about 12 hours of sleep) to have the SIK3 mutation, she found that they needed half an hour less of sleep to function. That probably means that SIK3 is not the dominant factor in NSS. However, the mutated gene was also most active in synapses, which could mean that it helps reset the brain to decrease the need for sleep.
Another SIK3 mutation was previously found to trigger hypersomnia, or the need for more sleep. This study found that one amino acid in this gene, known as S551, is especially important when it comes to sleep regulation. Future studies might be able to use knowledge about such genetic mutations to help with sleep conditions like narcolepsy or insomnia.
'These findings advance our understanding of the genetic underpinnings of sleep,' Fu and her team said in the study. '[They] highlight the broader implications of kinase activity in sleep regulation across species, and provide further support for potential therapeutic strategies to enhance sleep efficiency.'
Someday, we may never feel undead in the morning again.
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