Scientists find genetic links to cot death risk

Abnormal lung development could be responsible for some cases of cot death, a genetic study suggests.

Scientists at the University of Manchester analysed DNA from 25 babies who died from Sudden Infant Death Syndrome (SIDS).

The samples were compared with DNA from normal babies.

Significant differences between the two were seen in a gene that produces VEGF, a growth-factor protein vital to lung development.

Differences were also seen in the gene for the cytokine IL-6, a cell-signalling chemical that promotes an inflammatory immune response.

Previous research has linked abnormalities in the gene for a different cytokine, IL-10, with SIDS.

One theory is that cot death results from babies being unable to produce a proper immune reaction to bacteria in their upper airways.

Dr David Drucker, who led the Manchester team, believes a combination of impaired lung function and wrong immune response may place babies at risk between the ages of two and four months, when they are most vulnerable.

He told New Scientist magazine: "There are now three genes that are very strongly associated with SIDS.

"These may make the baby less able to cope with infection at a time when its immunity is low."

A baby with all three harmful forms of the genes would be about 14 times more likely to succumb to cot death as an infant with other versions, he said.

Other known risk factors, such as being exposed to cigarette smoke or being placed in the "wrong" cot position, would increase the danger still further.

George Haycock, scientific director of the Foundation for the Study of Infant Deaths, said: "The finding is interesting, given that the final event in cot death is thought to be termination of breathing, and VEGF is important in lung development. But you would probably need some kind of environmental trigger as well."