The technique measures attention, rather than sexual desire specifically, but Yoram Vardi, at Rambam Hospital and the Technion, both in Haifa, Israel told NewScientist: “We found that sexual stimuli are the most potent.”

So far 30 people with normal sexual function have been tested, but if further tests are successful, Vardi hopes his method will have many applications. These could include quantitatively analysing the libido-lowering (or enhancing) side effects of medication or even supporting legal claims of a reduction in sex drive after an accident.

But he cautions that it is too early to say for sure whether it will be possible to establish an absolute measurement scale for libido.

David Ralph, chairman of the British Society for Sexual Medicine, says the technique is “an interesting concept and the first of its kind – there has never been any quantitative measurement of libido”.

He told 91av further tests are needed involving people with sexual dysfunction to indicate the potential of the approach, but adds that “another tool to help diagnose patients is always helpful”.

Random clips

Vardi conducted experiments on 14 male and 16 female volunteers with normal sexual function. Using standard EEG equipment, a pair of headphones and a computer monitor, the subjects listened to music and other sounds to stimulate p300 brain waves. These waves, produced 300 milliseconds after an event, are the brain’s normal response to stimuli.

The subjects were then shown a random selection of 40-second film clips, which mixed erotic clips in amongst footage of sports, nature and romantic vistas. The reduction in amplitude of the p300 waves was recorded and provides a measure of how much someone was distracted by a clip.

The reduction in amplitude was significantly greater for the sexual clips than for the others. Vardi then compared the results with questionnaires the subjects filled in afterwards about how much each erotic clip had aroused them. He found a strong correlation between their description and the drop in p300 amplitude, and the results were similar for men and women.

Standard stimulation

Vardi acknowledges that the measurement of p300 reduction is not specific to libido and has been used by researchers for other purposes for many years. He was inspired to use it in a sexual context by a neurologist colleague who was using the technique to measure the attention capabilities of people involved in car accidents.

Vardi, who presented his research at the recent European Society for Sexual Medicine Congress, is now preparing to test patients whose libido has been lowered by prescribed drugs, such as antidepressants.

One of the challenges, he says, is to find a standard measure of how stimulating a particular piece of erotic footage is to viewers. “To have a standardised sexual clip is very problematic,” Vardi said. The footage he used had been tested in Italy by 25 men and women. “Only the clips that were the most arousing were used,” he says.

AT causes brain degeneration and loss of muscular control and speech. Children with AT are also unusually sensitive to X-rays and are a thousand times more likely than normal to develop cancer. Biologists now hope that by studying the gene’s precise function they will learn more about the causes of cancer.

The discovery of the gene is particularly important because the 1.5 per cent of the population who are AT carriers – with just one copy of the mutated gene – are also particularly sensitive to X-rays, and are four times more likely than normal to develop cancer. For female carriers, the risk of developing breast cancer is five times the norm. The carriers’ sensitivity to X-rays means that radiotherapy to treat cancer can do more harm than good, causing large wounds. Now that the gene has been discovered, it should be possible to identify AT carriers and advise them to avoid radiotherapy.

Yosef Shiloh of Tel-Aviv University, who led the international team that made the discovery, has been hunting the gene for 10 years. It sits on chromosome 11, and the researchers have now determined its sequence of bases. This is providing some clues about its function. Parts of the gene’s sequence resemble those of genes that regulate cell division and growth (Science, vol 268, p 1749). Shiloh and his colleagues believe that the gene codes for a protein similar to proteins found in yeast, which are responsible for temporarily halting the division of cells whose DNA has been damaged by ultraviolet light or X-rays.

This implies that the AT gene’s protein may act as a lookout to spot damaged DNA, or else is the “brake” that halts the cycle of cell division and growth. When the gene is mutated, therefore, cells with damaged DNA may continue to divide, and so go on to form tumours. But Shiloh warns that a great deal still needs to be done to confirm this picture: “It’s a big gene with a lot of mutations.”

How the gene could lead to the neurological symptoms of AT is still a mystery. These symptoms arise from the death of neurons called Purkinje cells in the brain’s cerebellum. Purkinje cells do not normally grow and divide, so it is not obvious how a fault in a gene that regulates this cell cycle could cause their death.