Gene mutation may explain why some people need less sleep

US scientists have discovered a gene involved in regulating how much sleep is required by a person, providing the first genetic insight into unravelling the regulatory mechanisms of sleep.

Scientists believe that sleep is regulated in part by two processes: circadian rhythms and sleep homeostasis. Interactions between these two phenomena influence the timing, duration and quality of sleep and wakefulness. However, ‘the details in the process are really completely unknown’ says Ying-Hui Fu, PhD, a professor of neurology at the University of California, San Francisco.

The team of scientists led by Fu in this study used blood samples from families to look for variations is several genes that were thought to be related to sleep patterns and requirements. They found a mutation in the DEC2 gene, a transcription factor that has been implicated in circadian rhythms, in two DNA samples and, working backwards, found that the samples were from a mother and daughter from one family who were both naturally short sleepers. This meant they required on average two hours less sleep per night than the other family members; they routinely function on only six hours of sleep a night rather than the eight to eight and a half hours for the average person.

Having isolated the variation, the researchers then genetically engineered mice to have the mutation in the DEC2 gene. They found that mice with the mutation slept less than normal mice, and also did not need as much compensation after sleep deprivation as normal mice. The results were also replicated in fruit fly studies.

While some people claim they only need six hours sleep per night rather than eight to eight and a half, they usually use stimulants, such as coffee, and alarm clocks to maintain a short sleep schedule. The difference in the women from the studied family is that they awoke naturally after six hours with enough sleep, were up and about doing things, and were still perfectly healthy and active.

'Short term and chronic disruptions in the length of optimal sleep can have serious consequences on cognition, mood and physical health, including cancer and endocrine function', says Fu. 'These changes in sleep homeostasis in the mutant mice could provide an explanation for why human subjects with the mutation are able to live unaffected by shorter amounts of sleep throughout their lives.'

The next step to be taken by the scientists would be to determine the exact role of DEC2, which could add to the findings. The current study, however, provides an exciting probe towards a better understanding of what regulates sleep quality and quantity, and could possibly lead to new treatments for sleep disorders or a safe treatment for people who want or need to stay awake for longer without harming their health.