Science in the News — A Passport to Never-Never Land

Sarah Taber, World Almanac Newsletter

Forget white noise machines and warm milk before bed. According to researcher Hans-Peter Landolt, the key to a good night's sleep may be in your genes. Landolt and his team at the University of Zurich, Switzerland, have identified the "slumber gene" - a particular variant of a gene that produces an enzyme called adenosine deaminase (ADA). In a groundbreaking study published in the October 25, 2005 issue of the Proceedings of the National Academy of Sciences (PNAS), Landolt demonstrated that individuals carrying the slumber variant ADA gene sleep considerably more soundly than everyone else. In addition to providing new insight into the biological mechanisms surrounding sleep, Landolt's work may someday lead to new treatments for insomnia and other sleep disorders.

Most of us sleep for several hours each night; however, only a part of that slumber is slow-wave sleep (also known as deep sleep). During slow wave sleep (SWS), the brain's electrical activity is at its lowest. As Malcolm von Schwantz of the Surrey Sleep Research Center in the U.K. told NewScientist.com, "Slow-wave sleep is beyond dreaming. You're completely knocked out, and it takes noise greater than 65 decibels to waken you." (Decibels are a standard unit of loudness; 65 decibels is approximately the level of normal conversation.) Though no one knows exactly why slow wave sleep is so important, body temperature and immune system functions become unstable without it.

Although everyone gets some deep sleep, the amount of time spent in SWS differs from person to person. Researchers believe that this variation is due at least in part to the activity of a neurotransmitter called adenosine. While a person is awake, adenosine builds up in his or her brain as a natural product of the breakdown of adenosine triphosphate and adenosine monophosphate (two molecules that release energy). Once the person goes to bed, the adenosine binds to special receptors that facilitate SWS. Caffeine, the well-known accessory to all-nighters and long drives, blocks adenosine receptors and thus prevents the neurotransmitter from inducing slow wave sleep.

Many of us are roused each morning by alarm clocks; however, even under the most optimal sleeping conditions, no one would sleep forever. So what wakes us up? An enzyme called adenosine deaminase (ADA) breaks down the adenosine in the brain. Since adenosine receptors, when bound to adenosine, cause slow wave sleep, this has the effect of a wake-up call. Roughly ten percent of the population has a mutant variant of the gene that produces ADA, and as a result, has a less efficient version of the enzyme. The mutant ADA breaks down adenosine more slowly, allowing neurotransmitter to remain bound to the deep sleep receptors longer. Landolt and his team postulated that people with the mutant ADA variant - the slumber gene - would get more zzz's than their fellow sleepers.

To test his theory, Landolt determined the genotypes of almost 120 individuals. He selected 32 subjects - half with the normal ADA gene and half with the slumber gene - to sleep over in his lab, and hooked them up to machines that measured their brain waves. Landolt found that the subjects with the slumber gene spent roughly 30 minutes more in slow wave sleep than their normal counterparts. They also reported far fewer awakenings during the night.

As Landolt told MedicineNet.com, "The study provides the first direct evidence in humans that the adenosinergic system indeed modulates sleep." Not only does the research give scientists a better understanding of how we slumber, it may also hold the key to ending those sleepless nights. As Landolt wrote in PNAS, "The adenosinergic system may be an important target for the pharmacological improvement of disturbances of sleep and alertness, which are highly prevalent in the general population." Until then, those of us without the slumber gene will just have to hope the sandman comes on his own.