Can’t sleep? Your genes could be to blame

Tired/Sleeping Businessman - nyul/iStock/Getty Images Plus/Getty Images
Two new studies identify gene variants that may contribute to common sleep disorders. (nyul/iStock/Getty Images Plus/Getty Images)

Some people burn the midnight oil because they just don’t feel sleepy enough to turn out the lights. Others try to go to sleep at a reasonable hour, but they toss and turn all night, only to wake up feeling as if they didn’t sleep at all. In fact, the Centers for Disease Control estimates that up to 70 million Americans have some sort of sleep disorder.

Now a pair of studies suggests sleep quality may be largely genetic.

On April 5, researchers at Washington State University published research identifying a variant of a gene called FABP7 that plays a major role in governing normal sleep. Lead author Jason Gerstner, assistant research professor in WSU's Elson S. Floyd College of Medicine, had previously observed the brains of mice during sleep and awake time and discovered that the expression of the gene changed over the day. When the gene was knocked out, the mice slept more fitfully, according to a release from the university.

To further elucidate the role of the gene variant in producing sound sleep, Gerstner and his co-authors analyzed data from a sleep study in Japan that included gene testing. They discovered that 29 patients in the study had the FABP7 variant and that they slept more fitfully than people who didn’t have it.

From there, they created transgenic fruit flies by inserting normal and mutated FABP7 genes into astrocytes—cells in the brain that release chemicals that control behavior. They observed that the flies who received the mutant FABP7 did not sleep as well as those that received functional FABP7 genes.

"This suggests that there's some underlying mechanism in astrocytes throughout all these species that regulates consolidated sleep," Gerstner said in the release. The research was published in the journal Science Advances.

On April 6, researchers at Rockefeller University announced that they discovered another sleep variant—this one that regulates the body’s circadian clock. The variant is in the gene CRY1, which normally produces a protein that helps the body’s “clock genes” switch on and off to produce sleep and wakefulness. In people who have the mutation identified by the Rockefeller team, the CRY1 protein is more abundant than it is in people without the variant, which keeps other clock genes off for longer than they should be, according to a press release.

The result? People with the CRY1 variant are prone to delayed sleep phase disorder (DSPD), or as they most likely put it, they’re night owls. That can be a problem, because if they’re forced to wake up early for work or school, they’re likely to suffer from fatigue during the day.

The Rockefeller team discovered the variant when they took volunteers, put them in an apartment for two weeks and isolated them from any cues that would tell them the time of day. Most people slept and woke on a normal schedule, but one study subject stayed up late and slept 30 minutes longer than normal.

By collecting skin cells from each subject, the researchers discovered that the night owl’s levels of melatonin—a hormone essential for regulating normal sleep—didn’t start rising until 2 or 3 in the morning, as compared to 9 or 10 at night for most people. When they sequenced the DNA from that subject, they discovered the variant in CRY1. Five of the patient’s family members also had the gene mutation. They reported their findings in the journal Cell.

So how might these discoveries lead to new treatments for sleep disorders? Researchers at both WSU and Rockefeller say they need to do more work to figure out exactly how these genes—and their variants—control the urges to hit the sack and to get going in the morning. From there, ideas for new therapies could emerge. "Just finding the cause doesn't immediately fix the problem. But it's not inconceivable that one might develop drugs in the future” that target the genes, said Rockefeller research associate Alina Patke.