The molecular basis of intrauterine growth retardation in cases of SIDS

The molecular basis of intrauterine growth retardation in cases of sudden and unexpected death in infancy (SIDS)
Dr Anne Burchell, Professor Robert Hume (University of Dundee), Dr Fiona Drimmie (Tayside University Hospitals NHS Trust), Dr Allan Howatson
Royal Hospital for Sick Children, Glasgow
(2000: £43,300 over 2 years)

Glucose is the primary source of energy for the brain. The brain cannot make sufficient glucose for its needs by itself, so it must obtain glucose from the blood. It is therefore vital that blood glucose concentrations are maintained within a restricted range – neither too high or too low. Episodes of low blood glucose can lead to brain damage and, in extreme cases, even to death.

Low birth weight infants are particularly vulnerable to low blood glucose levels; low birth weight is also a risk factor for SIDS. Research has previously shown that some infants dying suddenly and unexpectedly have defects in liver glucose production, which could lead to low blood glucose at times of stress or reduced milk intake.

The researchers in Dundee believe that many of these defects in liver glucose production result from failures to regulate this system at birth. They have investigated the molecular nature of this regulation, and have shown that subtle alteration in the structure of regulatory regions of genes that control glucose levels occur in some infants.

The next phase of this work is to identify these changes in genes at the time of birth, to determine which infants are at greatest risk at times of stress. Once we have the knowledge of which infants are at risk, then simple preventative measures (such as changes in feeding patterns, combined with emergency action plans to deal with the normal minor ailments of infancy) will lower the risks.