Some people genuinely function well on far less sleep than the rest of us, and scientists are now tracing that ability to their DNA, the BBC reports. The findings centre on a rare inherited condition called familial natural short sleep (FNSS), in which carriers go to bed at ordinary hours but wake very early, often after only four to six-and-a-half hours.
One of them is Aimee Pugh Bernard, an immunology professor at the University of Colorado. According to the BBC, she typically goes to bed around 22:00 and is up by about 04:30, wide awake and unable to stay in bed. On nights when she cannot fall asleep promptly, she may log just five hours — yet she still walks her dog, completes an hour-long gym session and puts in 90 minutes of work before 08:00. Her father and brother share the pattern, the BBC reports.
Why it matters
Most adults between 26 and 64 need roughly seven to nine hours of sleep in every 24, according to the latest review of the evidence by the US National Sleep Foundation, as cited by the BBC. People like Bernard sit well outside that range, and understanding why could eventually help everyone else.
The BBC reports that how long we sleep is estimated to be between 30 and 65 percent heritable, meaning genetics can explain up to 65 percent of the differences in sleep duration between individuals. Researchers have so far identified several hundred regions of the genome that influence how long people sleep. If scientists can work out exactly how the protective variants operate, the knowledge could feed into treatments for sleep disorders or help people who cannot get enough rest avoid the usual consequences.
The discovery behind familial short sleep
The trail began with a research team at the University of California, San Francisco, which found a genetic mutation in humans linked to sleep duration. Carriers kept fairly conventional bedtimes but rose very early, the BBC reports. Bernard sent the team a blood sample and learned she was among them. Several further mutations tied to FNSS have been identified since.
Ying-Hui Fu, the molecular biologist who leads the team, told the BBC that one of the biggest puzzles is why people with FNSS appear fine on so little sleep. The answer is still being worked out.
What has emerged is suggestive. A 2019 experiment led by Fu introduced an FNSS-linked mutation into mice; the animals slept less but also seemed shielded from memory deficits, according to the BBC. Another test found that mice carrying some of these variants were less prone to developing a mouse form of Alzheimer's.
Human evidence exists too. In 2014, an international team studied a pair of fraternal twins, only one of whom carried a short-sleep mutation. The BBC reports that the carrier routinely slept about an hour less than his sibling. When both were kept awake continuously for 38 hours, the carrier showed roughly 40 percent fewer performance lapses. Despite sleeping less, he also recorded nearly the same amount of non-REM sleep as his brother, including deep slow-wave sleep — a possible hint that his shorter night delivered more benefit per hour.
Hundreds of common variants, and a note of caution
The rare FNSS mutations are the most dramatic example, but they are only a small part of the picture. According to the BBC, a new analysis examining data from nearly 650,000 adults identified around 244 genome locations tied to sleep duration. The work has not yet been published and is currently available as a preprint.
Isabelle Austin-Zimmerman, a geneticist at King's College London and the paper's lead author, told the BBC that any single common variant on its own is associated with a difference of only about a minute in sleep duration. Taken together, though, such variants might account for roughly 20 minutes of variation between average people.
Less is known about which common variants might protect short sleepers. The BBC reports that a recent study led by Chiara Petrosellini, a clinical academic obstetrician and gynaecologist at University College London, examined the genetics of 343 women with bipolar disorder who had given birth, scoring them for their likelihood of being short sleepers.
Fu cautioned that any drug development must rest on a full understanding of the mechanisms. Speaking to the BBC, she warned that without that knowledge you could create a treatment with unexpected side effects — and that nobody wants to sleep less only to face Alzheimer's, Parkinson's or cancer years down the line.
For now, the practical message is that most people who feel they run fine on very little sleep are probably not carriers of these rare mutations. The BBC frames the research as an ongoing effort to separate genuine short sleepers from those simply accustomed to too little rest.
Watch for the preprint on common variants to go through peer review, and for further work on how FNSS mutations confer their apparent protection.
