May 9 2007
Researchers in Scotland have found what they believe is a link between infant cot deaths and low blood glucose levels.
Each year in the UK as many as 300 babies die from sudden infant death syndrome (SIDS) where there is no apparent reason and understanding why some babies and not others are more susceptible to sudden infant death syndrome is a complex puzzle.
But now a team led by Dundee University professors have found what they believe could be a key piece in the puzzle.
The team have identified defects in glucose production, particularly in premature and small babies, which make infants more prone to risk factors linked to cot death.
Low birth-weight babies are particularly vulnerable to low blood glucose levels and sudden death in infancy.
Earlier research has shown that some infants who died unexpectedly had defects in liver glucose production, which could lead to low blood glucose at times of stress or reduced milk intake.
It appears that in some babies key liver genes making and transporting glucose around the body were not "switched on" soon enough after birth.
The researchers say the findings do not explain cot death and that many other genetic faults and environmental factors could be linked to the syndrome.
The Scottish Cot Death Trust-funded study was led by Professors Ann Burchell and Robert Hume, together with colleagues from Edinburgh University and Glasgow's Royal Hospital for Sick Children.
Professor Hume says this research has concentrated on a system called hepatic glucose-6-phosphatase, which we all have, but unfortunately in some babies this system does not work correctly in that it doesn't start working soon enough after they are born and this delay causes low blood glucose levels in the baby and places the child at risk.