To examine the causes of variability in the effect of maternal drinking on the foetus, with particular reference to the pattern, frequency and duration of the period of drinking, differences in maternal, foetal and
placental metabolism of ethanol/acetaldehyde, and genetic factors.
Narrative review of published studies of the pathogenesis of foetal alcohol syndrome (FAS) with emphasis in the development of the central nervous system.
Animal models suggest that acetaldehyde, the primary hepatic oxidative metabolite of ethanol, reaches the foetus either by placental production or by placental transference, which in turn could affect foetal growth and development. The most likely hypothesis regarding the decrease of foetal growth is via hypoxia and increased oxidative/nitrative stress, which interfere with cellular processes that require oxygen in order to function adequately, such as placental transport.
There seems to be an association between the teratogenic effect, hypoxia and oxidative stress, the molecular mechanism involved (e.g. apoptosis) and the range of effects. The review sums ups the evidence that could explain some of the abnormalities in the brain development that could be related to behavioural problems observed in individuals with FAS/foetal alcohol spectrum disorder.
This suggests that alcohol consumption produces failures in the normal migration of radial cells, from which the rest of the brain cells would eventually develop.
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