Some people really are fine with remarkably little sleep. But it can be hard to tell if you’re one of those people.
For as long as she can remember, Aimee Pugh Bernard hasn’t needed much sleep. Today she tends to go to bed around 22:00 and wake up around 04:30. “I’m wide awake. I cannot stay in bed,” she says.
Sometimes Bernard, an immunology professor at the University of Colorado, can’t fall asleep right away. Then she’ll log only five hours’ slumber.
Perhaps most surprisingly, Bernard usually still feels energised the next day. She’ll walk her dog, sweat through an hour-long gym session, and clock 1.5 hours of work before 08:00. Friends gawk at Bernard’s ability to do so much on so little sleep. But in her family, it’s normal – her father and brother are the same.
Most of us, of course, require more. The average adult aged 26-64 years needs about seven to nine hours of sleep in every 24, according to the US National Sleep Foundation’s latest review of the evidence.
Why there is such a wide variation in how much sleep people need has been a long-standing mystery. Yet over the last few years, scientists have pinpointed a wealth of ways in which genetics play a role. From the rare mutations carried by people like Bernard, to hundreds of much more common variants, here’s why some people get away with very little sleep. In the future, these findings could be used to help protect those who can’t get enough from some of the usual consequences.
The first clues
In 2019, Bernard learned the likely reason for her own sleep superpower.
A research team from the University of California, San Francisco had discovered a genetic mutation related to sleep duration in humans. Although the people who carried it went to bed at fairly conventional times, they woke up very early, often getting anywhere from four to six-and-a-half hours’ sleep a night. After sending a blood sample to the research team, Bernard found out that she was one of them.
This rare, heritable condition is called familial natural short sleep (FNSS). In the years since, several other mutations associated with FNSS have been identified.
One of the biggest mysteries about FNSS is that those who have it seem “fine” on so little sleep, says the team’s lead investigator, molecular biologist Ying-Hui Fu. Exactly why is still being worked out.
There is intriguing evidence that FNSS-linked genetic variations might not only cause short sleep but protect those who have it from the consequences. This includes memory impairment, for example.
One 2019 experiment led by Fu introduced a mutation linked to FNSS in mice. The team found that the mice with a related variant not only slept less, but seemed to be protected from memory deficits. Another test found that mice with some of these variants were less likely to develop a mouse version of Alzheimer’s.
In 2014, an international research team investigated a pair of human fraternal twins where one twin had a short-sleep mutation and the other did not. They found that the carrier twin regularly slept about an hour less than their sibling. They also discovered that when both twins were kept continuously awake for 38 hours, the carrier twin had about 40% fewer performance lapses than the other twin.
The researchers also found some intriguing differences between how the two twins slept. Even though the carrier twin slept less, he had almost the same amount of non-REM sleep as his brother. This includes slow-wave or “deep” sleep, which could mean that he was, in some ways, getting more benefits from the sleep he did obtain.
Pharmaceutical dreams
Still, research in the area is ongoing – and critical, says Fu.
Over the last few years, there has been increasing interest in how our understanding of these genetic variations could be harnessed to help people. Within the pharmaceutical industry, there are hopes that one day discoveries about short sleepers could lead to drugs for treating sleep disorders or help military personnel to get by on less sleep, for example.
For that, scientists not only need a clear idea of whether the variants protect short sleepers from negative consequences, but also exactly how they do so. Without this information, you could wind up creating a drug with unexpected side effects. “You have to understand how it works,” says Fu. “You don’t want to sleep less and then get Alzheimer’s or Parkinson’s or cancer after 10 years, or five years, or 20 years.”
While the genetic mutations associated with FNSS are one of the more extreme and exciting examples, they are only a handful of those that can shape our sleep duration.
Overall, how long we sleep for is estimated to be anywhere from 30 to 65% heritable, meaning that up to 65% of the difference in sleep duration between us can be explained by genetics. So far, several hundred different parts of the genome have been identified as influencing sleep duration. In one new analysis that looked at data from nearly 650,000 adults, there were around 244. (The research has not yet been published and is currently in preprint.)
If you took any single one of these common mutations on its own, it would only be linked to a difference in sleep duration of about a minute, says the paper’s lead author, geneticist Isabelle Austin-Zimmerman at King’s College London.
But combined, the effects can add up. For the average person, genetic differences might account for around 20 minutes’ difference in sleep duration between us, says Austin-Zimmerman.
But there hasn’t yet been much research on which of these more common variations can help to protect people from the effects of short sleep.
However, a recent study led by Chiara Petrosellini, a clinical academic obstetrician and gynaecologist at University College London, found evidence of one. The research team investigated the genetics of 343 women with bipolar disorder who had given birth.
Their genetics were scored for their likelihood of being a short sleeper, based on the presence of mutations suspected to be involved. Those who scored as most likely to be short sleepers had half the risk of developing postpartum psychosis, compared to women who scored as least likely to be short sleepers. The same trend was found for insomnia.
More studies are needed, but it’s possible that these individuals may have developed a higher tolerance to sleep disruption earlier in life, suggested the researchers. That may be mitigating the impact of disrupted sleep in the postnatal period on their mood.
Unfortunately, though, being genetically susceptible to short sleep isn’t always good for you. In fact, research by Austin-Zimmerman and her team on a much larger population (not specifically mothers with bipolar disorder) has found that, in general, genetic variants associated with shorter sleep were associated with a higher risk of insomnia and of feeling tired. They were also linked to various mental and physical health conditions. This included ADHD, depressive symptoms and type 2 diabetes.
This doesn’t necessarily mean that short sleep or being predisposed to it causes these conditions. But it does mean that a genetic predisposition to short sleep isn’t always protective from any of these risks.
The illusion of being OK
Making matters more complicated, even those of us who think we function fine on little sleep aren’t always the best judges.
One study, for example, found that when healthy adults were curtailed to just four or six hours in bed per night, their performance on various cognitive tests kept worsening.
Yet, two weeks in, participants rated themselves as feeling only “slightly” sleepy.
You become progressively more impaired, but also increasingly unaware of the impairment, says Hans van Dongen, a sleep scientist at Washington State University’s Sleep and Performance Research Center, who co-authored the research.
It’s still true that many people need less sleep than others. Other research by van Dongen himself has found that some people are more resilient to sleep deprivation. But it means that understanding these differences is more complicated than asking how many hours someone sleeps, or how they feel the next day.
Over the long term, genetic findings like those from Austin-Zimmerman and Fu may help pinpoint which people really are fine on little sleep. It could also help to sift out those of us who may feel fine but are still at greater risk of impairment. Eventually, it’s hoped that they might lead to drugs that can help people who have short sleep bolster their resilience to it.
But in the meantime, these findings can help people to understand why they sleep the way they do.
For Bernard, learning she carried one of the variations for FNSS took some pressure off, she says. As a scientist, she’d already known there were natural variations between us, including with our sleep. She has also always appreciated the extra time it gave her to get ahead of her workday, particularly while her husband and children were still fast asleep.
Even so, Bernard had wondered if she was just particularly bad at relaxing, or whether her inability to sleep more indicated that she was juggling too much.
“Now I have an answer,” says Bernard. “I know, genetically, it’s just the way that I am – and I’m just going to have to embrace it.”
Amanda Ruggeri is a science, psychology and history journalist. She writes the six-part How to Sleep Better newsletter course, and her forthcoming book, The Sleep Myth, will be published in summer 2027.
