New research found the “night owlgene, the gene that allows some people to work their best at night and struggle to wake up in the morning.

In the new research, scientists looked at 70 people from different families and discovered that a mutation in a gene called CRY1 was present among those who have a condition called delayed sleep phase disorder (DSPD).

The variant of the gene CRY1 slows down the internal biological clock, known as the circadian clock, which dictates when you want to sleep every night and when you’re ready to wake up in the morning. The study found that people with the “night owl” gene mutation have a longer circadian cycle, which allows them to stay awake during the nights.

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

Night Owl gene variant could cause people to stay up late
The alleged gene variant gets its name for the owl’s commonly known habit of hunting at night. Image Source: YouTube

‘Night owls’ biological clock runs slower than most people

The study was published Thursday in the journal Cell, and it was conducted by scientists from The Rockefeller University.

Researchers explained that the circadian clock is an internal biological clock that guides nearly all life forms on Earth. The circadian clock in humans dictates when a person feels tired, hungry, awake and it even regulates body temperature. A 24-hour biological clock regulates most humans, but almost 10 percent in human beings have DSPD, which makes their biological clock run on a longer loop.

“A person like a bartender, for example, might not experience any problem with the delayed sleep cycle,” explains lead author Alina Patke, a research associate in the Laboratory of Genetics at The Rockefeller University, according to Live Science. “But someone like a surgeon who has to be in the OR in the early morning – that’s not compatible.”

Patke and other colleagues at the University first discovered the DSPD mutation seven years ago. They came across a 46-year-old woman who had come to a sleep clinic after struggling for years with her late sleep cycle.

Patke’s team along with other researchers studied the woman’s sleep patterns. The woman was placed in an apartment for two weeks, and they isolated her from time cues.

The apartment didn’t have windows, TV or internet, according to Patke, and they instructed the woman to live on her timeline and to perform the necessities, like eating or sleeping, that her body told her to do.

The researchers found that in isolation, the woman settled into a routine that was about 1 hour longer than the typical 24-hour circadian cycle, and they also noticed that her sleep was fragmented.

Study identifies Night Owl gene
Patke and her team ran tests to sequence the woman’s genes, and they identified the CRY1 mutation. Image Source: Medical Xpress

They identified the mutation as a single-point mutation in the CRY1 gene, which means that one “letter” in the gene’s instructions is off.

Better ‘sleep hygiene’ could help night owls

In the new study from The Rockefeller University, Patke and her team confirmed the CRY1 genetic mutation as responsible for delayed sleep phase disorder. To find this, they looked for the mutation in the woman’s extended family, along with other population samples.

The team used a database of genomic information from people in Turkey, and they were able to identify individuals who carried the CRY1 mutation. They contacted researchers from Bilkent University in Ankara, Turkey, and in a conjoint effort they tracked down the people from the database and conducted interviews with members of six families as well as DNA sequencing tests.

The study found that among the families studied, 39 carried the CRY1 mutation and 31 did not. Furthermore, data revealed that people who carried the gene mutation were more likely to stay up later than those who didn’t have it. Their midpoint of sleep fell between 6 a.m. and 8 a.m., whereas the midpoint for people without the mutation fell around 4 a.m.

Their midpoint of sleep fell between 6 a.m. and 8 a.m., whereas the midpoint for people without the mutation fell around 4 a.m.Other clinical studies estimate that over 10 percent of people have delayed sleep phase disorder, and the new study says that the CRY1 mutation may not cause all of the cases.

Other clinical studies estimate that over 10 percent of people have delayed sleep phase disorder, and the new study says that the CRY1 mutation may not cause all of the cases. To exemplify this, Patke noted that she is a night owl, as she often works late nights, but she does not carry the gene mutation.

Patke believes that there are probably other underlying genetic causes for the sleep condition, but she noted that identifying at least one genetic mutation represents an important step.

“Understanding how the rhythms are controlled opens the door to eventually manipulating them with drugs,” said Patke.

She added that if in the future a drug is developed to help night owls align their sleep schedules to regular schedules, a similar drug could be used to help travelers deal with jet lag.

However, until that time comes, she believes that there are other things people with DSPD can do to try to reset their clocks. She recommended practicing good sleep hygiene, which means going to bed at the same time every night, including on weekends, and waking up at a set time in the mornings.  Patke also recommended avoiding bright lights at night, such as laptops or smartphones, as well as avoiding exposure to sunlight first thing in the morning.

Source: Live Science