Discovered: The 'insomnia' gene that means you sleep two-thirds less than normal (… and don't live as long)

Last updated at 8:31 AM on 22nd February 2012

An 'insomnia gene' has been discovered by scientists.

Experiments on fruit flies found those carrying a mutation in the protein slept two thirds less than normal – and also had much shorter lifespans.

Previous studies have found men, in particular, are significantly more likely to die early if they suffer from chronic shortage of sleep with the problem linked to conditions such as high blood pressure and diabetes.

Man Counting Sheep.

Man Counting Sheep.

The latest research says although flies and humans have little in common when it comes to lifestyle, the mechanisms of sleep and wakefulness are likely to be quite similar.

Dr Nicholas Stavropoulos, of Rockefeller University in New York, said: “Sleep is a fundamental behaviour in all animals, and it is poorly understood from a scientific standpoint.

“This work gives us several new clues about how sleep is controlled at the molecular level, and could prove useful in understanding and treating sleep disorders.”

By cloning and testing the gene, known as insomniac, in more than 20,000 fruit flies his team say they have discovered an entirely new mechanism by which sleep is regulated.

Using an infrared beam to detect when the flies nodded off, they discovered those with the variant slept for an average of just 317 minutes a day instead of the typical amount of 927 minutes. The mutant flies also snoozed for shorter periods, and slept and woke more frequently.

Dr Stavropoulos said: “The results showed a dramatic loss of both the duration of the flies' sleep and their ability to remain asleep after they dozed off.

“But what's especially interesting is the insomniac gene may function through homeostatic mechanisms.

“These are distinct from the well-studied circadian clock pathways linked to sleep, and have an effect on the body regardless of the time of day.”

The scientists believe the gene works by eliminating specific proteins within brain cells that help in the onset of sleep.

The researchers also found flies with mutations lived only about two thirds as long as others.

But when the scientists eliminated the gene from neurons – allowing it to remain in the rest of the flies' bodies – this disparity was eliminated. The resulting animals slept poorly but lived just as long.

Dr Stavropoulos said: “This suggests reduced sleep can be 'uncoupled' from reduced lifespan, supporting the idea some disruptions of sleep do not effect overall health, at least as far as lifespan is concerned.”