"Animal studies suggested that sleep intensity is under genetic control, yet the physiological mechanisms remain unknown," explained study author Hans-Peter Landolt, an associate professor at the University of Zurich. His report appears in this week's issue of the Proceedings of the National Academy of Sciences.

Landolt and his colleagues focused on the adenosine neurotransmitter system in the brain, and isolated the gene that regulates adenosine. Adenosine is a compound believed to act on specific receptors that induce sleep. Compounds known as antagonists that block the receptors, such as caffeine, increase alertness.

"These effects of caffeine supported a role for adenosine and adenosine receptors in sleep regulation," Landolt said. "The present study provides the first direct evidence in humans that the adenosinergic system indeed modulates sleep...."

High adenosine levels are believed to make people sleepy. "This relationship is assumed, based on animal experiments," Landolt said. "It was shown in cat and rat studies that the concentration of adenosine increased locally in the basal forebrain with increasing duration of wakefulness. Whether it holds true in humans is not known."

In all, Landolt's team evaluated 32 people, finding that those with the gene variant associated with reduced metabolism of the adenosine -- meaning they have higher levels of it -- slept more deeply than those who did not have the variant.

The study, Landolt said, indicated that adenosine plays a direct role in people's sleep quality. These genetic differences, he said, contribute to the variability in brain electrical activity during sleep and wakefulness.

While there is no immediate relevance for consumers, Landolt said, the research suggests the adenosinergic system may be an important target for drugs that would improve sleep disturbances.

Dr. Flavia Consens, associate director of the Sleep Disorders Center at the University of Michigan, praised the paper. For the first time, she said, the researchers have isolated a gene involved in the individual variability in human sleep. Now that this has been accomplished, she said, "potentially there is always a role for a drug or intervention."

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