Thriving on little sleep? Scientists think it might be your genetic mutation

If your friends are giving you odd looks when you tell them you only slept for four hours last night again and you’re still your energetic self, it could be your genes, or specifically a genetic mutation, that’s responsible for your reduced need for sleep.

Indeed, while most folks need at least eight hours of slumber every night to function like normal human beings, a rare genetic condition allows some to doze for as little as three hours, and that’s enough for them, according to a report published by Nature on May 5.

As Ying-Hui Fu, a neuroscientist and geneticist at the University of California, San Francisco, and the co-author of the study, explained, understanding the genetic changes in people who sleep between three and six hours per night with no consequences could aid in treatments for sleep disorders.

According to her, “our bodies continue to work when we go to bed”, detoxifying themselves and repairing damage. “These people, all these functions our bodies are doing while we are sleeping, they can just perform at a higher level than we can.”

The genetic mutation at work

Back in the 2000s, Fu and her colleagues discovered a rare mutation in a gene that helps regulate our circadian rhythm – the body’s internal clock controlling our sleep-wake cycle – when analyzing the genomes of a mother and daughter who slept six hours or less each night.

Upon this finding, they came to believe that their genetic variation contributed to their short sleep needs, which prompted others with similar sleeping habits to come forward for DNA testing as well, leading to as many as several hundred naturally short sleepers identified by the research team.

Thanks to such a large body of evidence, the researchers have so far been able to determine five mutations in four genes that seem to have an effect on the trait, although different families have different mutations. 

One of the identified mutations was in salt-induced kinase 3 (hSIK3-N783Y) gene, and it was confirmed in a mouse model carrying the homologous mutation, confirming its connection to the short sleep duration trait. Specifically, it led to decreased SIK3 gene activity and altered global phosphorylation profiles, especially for synaptic proteins.

Meanwhile, a common gene mutation that puts people at risk of a punctured lung or pneumothorax could be present in as many as one in 3,000 individuals, raising concerns over effective diagnosis and treatment of the condition called Birt-Hogg-Dubé syndrome, which may cause lung collapse.