Though an overwhelming number of people in the modernized world are running on less sleep than is ideal, for a very small percentage of the population a restricted sleep lifestyle is in their genes—literally. Mutations to the gene DEC2 have been shown in both humans and mice to allow individuals to run sustainably on only about six hours of sleep a night.
The gene in question, DEC2, is a transcriptional repressors that helps to regulate a host of other functions relating to an animal’s circadian clock. It is important to realize that this means that the genetic mechanism underlying this phenomenon is a little more complex than simply “turning on a switch” for less sleep. It is also possible that other genes are involved in producing the short-sleeper phenotype, and currently researchers are exploring other contributing genetic factors. Though the full effect of the DEC2 mutation is not clear, experts in the subject have suggested that the mutation lends itself to more intense periods of rapid eye movement (REM) sleep.
The prevalence of the short-sleeper DEC2 mutation is rare, but scientists are as of yet not sure exactly how rare. For decades researcher have been aware that some people just need less sleep than the general populace. For example, back in 1997 a team of researchers led by Professor Dinges estimated that only one person out of every 1,000 can function optimally on six or fewer hours of sleep. Others think that the disposition towards less sleep is at least an order of magnitude more common—about one to three percent of the population.
To be clear, genetically pre-disposed short-sleepers are not to be confused with insomniacs or people who willfully stay awake for longer than they intend. Experts say that only about five to six percent of the population who regularly run on less than six hours of sleep a night are true short-sleepers. The vast majority of this demographic are actually normal people with normal sleep requirements that cannot (or choose not) to acknowledge the harsh lifestyle that they lead.
Short sleepers are still a largely mysterious demographic, but some preliminary research suggests that the condition does not come without strings attached. Of particular note is a short communication issued in April of 2014 to the journal Sleep Medicine in which researchers noted that short sleepers may have a greater physiological propensity towards ischemic stroke than the rest of the population.
A question that is sure to follow in discussions about DEC2 mutations is “could people in the future have this mutation artificially created?” Surely in the modern world being able to function on less sleep would be an advantage that willful individuals might seek to obtain for themselves or their children. Though some researchers are tentatively exploring this possibility, science’s understanding of the effects of this genetic mutation, not to say anything of sleep itself, leaves flippant genetic tinkering in humans out of the question.
By Sarah Takushi