‘Night owl’ people have a special gene mutation

‘Night owl’ people have a special gene mutation

If you’ve been a night owl all your life and mornings are your nemesis, you may be able to blame a gene mutation for all those late nights.

Researchers at The Rockefeller University have discovered that a variant of the gene CRY1 slows the internal biological clock—called the circadian clock—that normally dictates when you feel sleepy each night and when you’re ready to wake.

People with the “night owl” variant of this gene have a longer circadian cycle than most, making them stay awake later, the team reported in Cell.

“Compared to other mutations that have been linked to sleep disorders in just single families worldwide, this is a fairly impactful genetic change,” says senior author Michael W. Young.

According to the new research, the mutation may be present in as many as one in 75 people in some populations.

Diagnosing night owls

The Centers for Disease Control and Prevention estimate that between 50 and 70 million adults in the US have a sleep or wakefulness disorder.

These conditions—ranging from insomnia to narcolepsy—can predispose people to chronic diseases including diabetes, obesity, and depression.

People who self-categorize as night owls are often diagnosed with delayed sleep phase disorder (DSPD). Their 24 hour sleep-wake cycle is delayed, making them energetic long after most people have fallen asleep.

Going to bed late has its downsides: most people with DSPD are forced to wake up before their bodies tell them to in order to make it to work or school on time, leading not only to insomnia early in the night, but also to fatigue during the day.

In the study, When the researchers examined the DNA from the DSPD patient, one variant stood out; a mutation in CRY1, a gene that had already been implicated in the circadian cycle.

The researchers reached out to other members of the patient’s family and discovered five relatives who shared the mutation in CRY1. All of them had signs of DSPD, or a history of persistent sleep problems, too.

After contacting them and administering interviews and questionnaires, the researchers were able to confirm that people with the mutation had altered sleep behavior, while none of their relatives without the CRY1 mutation had unusual sleep patterns.

The researchers say that right now there’s no established benefit for DSPD patients in being tested for the CRY1 mutation.

For now, many DSPD patients are able to control their sleep cycles—and get to bed earlier than their body wants—by following strict schedules.

“It’s a bit like cigarette smoking in that there are things we can do to help the problem before turning to drugs,” says Young. Some patients seem to be helped by getting strong light exposure during the day, he adds.

The team already has future studies planned to work out whether CRY1 mutations also affect the metabolic cycles of people with DSPD, since the human circadian cycle is known to not only regulate sleep, but also hunger and levels of metabolites and hormones.

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