Night owls, rejoice! The tendency to stay up late at night, delaying sleep, may be blamed on a gene mutation, according to a study from Rockefeller University. According to the team of researchers, led by Michael W. Young, head of the Rockefeller’s Laboratory of Genetics and Richard and Jeanne Fisher Professor, found that a mutation on the gene CRY1 slows the circadian clock making the person affected stay up later into the night. The mutation, according to the researchers may be present in 1 in 75 people in certain populations. The study was recently published in the journal Cell.
The circadian clock or circadian rhythm is a biological process that prompts a person, animal, plants, fungi or cyanobacteria to go to sleep. Circadian rhythms adjust to the surrounding environment including light, temperature, and reduction-oxidation reaction or redox cycles. Circadian rhythms are important to animals, including humans, because during sleep biological processes occur that do not happen while the animal is awake. In humans, sleep helps repair the damage done to the body, clear away harmful chemicals, and refreshes people for another day.
According to the Rockefeller University, Young and his team of researchers researched circadian rhythms for over thirty years. During that time, they identified genes in “keeping flies, humans, and other animals on schedule when it comes to eating and sleeping.” Collaborating with researchers from Weill Cornell Medical College, Young and company asked study participants to spend two weeks in their lab and studying their reactions when “all cues to the time of day, eating, and sleeping” were removed. Skin cells were also collected from each participant.
The participants, most of which had delayed sleep phase disorder (DSPD), stayed up late with a sleep cycle that was “30 minutes longer,” according to the press release from Rockefeller University. DSPD is a “common form of insomnia.” The participants were also found to have body temperature and hormone changes that were delayed as well as their sleep cycle. Young stated that “melatonin levels start to rise around 9 or 10 at night in most people, “ but those with DSPD the melatonin levels started at 2 or 3 in the morning. Melatonin is a hormone that regulates sleep and wakefulness in humans and other animals.
The CRY1 gene mutation means that the protein made by the gene was “more active than usual” and prevented other genes from switching off and promoting sleep. Young and his team also discovered that those with the mutation also had family members with the same mutation, meaning they had DSPD as well. Taking this knowledge, the team turned to genetic databases to identify those with the sleep gene mutation. They were able to identify almost 40 other people with the mutation.
The researchers, however, cautioned that just because the gene mutation was found, does not mean an automatic fix. More research and tests must be done to help DSPD in people. Alina Patke, co-lead author and research associate at the Laboratory of Genetics at Rockefeller University said that even with this mutation, “there are steps [a person] can take to try to match [their] internal rhythms to the outside world.”
By Cheryl Werber