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A Genetic Mutation Causes ‘Night Owl’ Disorder, Study Finds

Woman staying up late at night.

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Key Takeaways

  • For those with delayed sleep phased disorder, a genetic mutation elongates the body’s biological clock.
  • This disorder causes people to stay up late at night and sleep later into the morning.
  • The mutation impacts the production of hormones like melatonin, which is important for regulating the sleep cycle.

If you’ve ever wondered whether your body is wired to stay up into the wee hours of the night and sleep late into the morning, you may have delayed sleep phase disorder. 

Delayed sleep phase disorder is defined as a kind of insomnia in which a person’s sleep is delayed by two hours or more beyond what is considered a healthy bedtime. People with the disorder, which is also called ‘night owl disorder,' typically stay up long past 2 a.m. In a recent study, researchers show how a genetic mutation can change the timing of a person’s biological clock. A longer clock means people go to sleep later and have difficulty waking up in the morning.

“It’s like being in permanent daylight savings time—being off by an hour, but every single day,” Carrie Partch, PhD, professor of chemistry and biochemistry at the University of California, Santa Cruz, tells Verywell.

For the October study, published in Proceedings of the National Academy of Science, Partch and her team investigated how variation in the tail region of one of the four key clock proteins, cryptochrome, affects a person’s circadian rhythms. She says the work is inspired by a 2017 paper that reported the discovery of the mutation and its effect on the biological clock. This research dives deeper into the molecular mechanisms behind this process.

What This Means For You

If you suffer from delayed sleep phase disorder, consider reducing your light intake at night. You can also speak with your doctor about taking supplemental hormones like melatonin to help induce sleepiness earlier in the evening.

How It Works

Humans and most other vertebrates operate on a circadian rhythm. This is a biological ‘clock’ which moderates periods of activity and inactivity. This clock operates with what scientists call a ‘feedback loop.’ Transcription factors act like a gas pedal, turning on the expression, or creating certain proteins during the day. At night, these proteins turn these transcription factors off, working like a brake.

Researchers found that a mutation can cause the tail of the protein cryptochrome to be snipped. When this happens, it binds more tightly with a complex of other proteins responsible for regulating the function of the clock. Partch says the effect is similar to holding down a brake for longer than is typical. When this happens, the body does not cycle between an active and inactive phase normally.

“It gets a little complicated because this process controls almost 10,000 genes in your body including the protein that makes the hormone melatonin,” Partch says. “When your clock doesn’t run in time with the 24-hour day, it’s hard sometimes to get lined up with the light-dark cycle so that your behavior matches the normal experience that we have as humans on earth of being active at day and sleeping at night.”

This research tells scientists they should be looking for drugs that can serve the same purpose as the cryptochrome tail, according to Partch. Her lab is in the process of doing just that, looking for molecules that can fill this gap.

Delayed sleep phase disorder is hereditary. It’s a common form of insomnia that affects about 1 in 75 people of European descent.

“This is remarkably prevalent,” Partch says. “If you’re in a crowded room, someone probably has it.”

Researchers have conducted similar studies to understand the mechanisms behind night owl disorder's inverse, which is commonly called the ‘morning lark’ disorder. People with this genetic variation go to sleep early in the evening and wake up early in the morning.

Functioning As a Night Owl

People who live with delayed sleep phase disorder typically still need eight hours of rest per night, though this period begins later than most people. Because of the way schools and workplaces structure their day—like following the standard 9 a.m. to 5 p.m. workday—it can be challenging to get the full amount of recommended sleep.

“Though intrinsically, it doesn’t impact your sleep need or how much sleep you need to feel well-rested, there are practical limits that society puts on us,” Partch says. “We have to get up, regardless of how well we feel in the morning, and go to work and school.”

Humans’ circadian rhythms are highly responsive to light. When the sun sets at night and rises in the morning, the change in light signals our bodies to shut down or start up.

When society's clock competes with the body’s natural clock, biological processes connected to circadian rhythms, like melatonin production and metabolism, are adversely affected. Many people experience this during daylight savings time, and people who suffer delayed sleep phase disorder feel this discord daily.

“Almost none of this is by choice," Partch says. "Time coding is encoded in our biology and we are kind of slaves to our internal clock, whether they run fast or long."

To help maintain a sleep schedule consistent with those who don’t have the disorder, Partch recommends limiting light exposure at night. This will help encourage melatonin production. To further spur sleepiness, you can also take a melatonin supplement at 9 or 10 p.m. to help your body fall asleep earlier.

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  1. Stephens T. Scientists discover how a common mutation leads to ‘night owl’ sleep disorder. University of California, Santa Cruz. Updated October 26, 2020.

  2. Parico G, Perez I, Fribourgh J, Hernandez B, Lee H, Partch C. The human CRY1 tail controls circadian timing by regulating its association with CLOCK:BMAL1. Proceedings of the National Academy of Sciences. 2020;117(45):27971-27979. doi:10.1073/pnas.1920653117

  3. Patke A, Murphy PJ, Onat OE, et al. Mutation of the human circadian clock gene cry1 in familial delayed sleep phase disorderCell. 2017;169(2):203-215.e13. doi:10.1016/j.cell.2017.03.027