If you go to bed late and have trouble getting up in the morning, it might be no fault of yours. It could be written in your DNA.
A new study on 70 people has found a link between delayed sleep phase disorder (DSPD) and a gene called CRY1. A mutation on the gene is believed to change the human circadian clock that tells our body when to wake up and when to fall asleep. For people with this condition, the internal clock is delayed compared to the day/night rhythms and they end up having trouble falling asleep until the early morning.
The research, published in Cell, looked at six families of Turkish individuals – 39 carrying the CRY1 variant and 31 without. The people with the mutated gene felt sleepy later than the people without the mutation, with the average mid-point of sleep for carriers at 6-8am compared to 4am for non-carriers.
The circadian clock is regulated by a protein cycle. It begins when cells produce a particular protein known as call activators – proteins that increase the activities of the cell. These proteins, in turn, produce inhibitors, which over the course of the day, reduce the effectiveness of the activators until they are all stopped. At that point, no more inhibitors are produced and those that are there begin to degrade. When they are gone, the activators surge once more and the clock starts again.
The CRY1 has the instructions to produce one of the inhibitor proteins. The mutation changes a single letter in the genetic instruction, resulting in inhibitors that are active for longer than in people without DSPD. The paper suggests that the more active inhibitors extend this protein cycle for an extra 30 minutes.
“Carriers of the mutation have longer days than the planet gives them, so they are essentially playing catch-up for their entire lives,” first author Alina Patke, from The Rockefeller University, said in a statement.
“It’s as if these people have perpetual jet lag, moving eastward every day,” added senior author Professor Michael Young. “In the morning, they’re not ready for the next day to arrive.”
DSPD affects about 10 percent of the general population, but based on a database of non-Finnish, European individuals, only one in 75 people have the CRY1 variation. Clearly, CRY1 plays a role, but that’s not the end of the story.
According to the researchers, DSPD can be managed. One of the 39 people sporting the CRY1 variation stated they enforce regular sleep cycles on themselves to fight off DSPD.
“An external cycle and good sleep hygiene can help force a slow-running clock to accommodate a 24-hour day,” says Patke. “We just have to work harder at it.”