Fetal Alcohol Syndrome Essay

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Fetal Alcohol Syndrome

Many studies have established that a developing organism is susceptible to exogenous and endogenous factors during certain stage of the organism’s development. The effects of ethyl alcohol or ethanol on the developing fetus, which manifest a variety of characteristic abnormalities, are collectively called Fetal alcohol Syndrome. Ethanol exposure to the fetus causes various malformation ranging from the cellular to the organismic levels with the eventual results frequently being different levels of mental retardation (3).

Chick embryo studies provide a relatively good model for defining the effects of ethanol at many organizational levels of neurogenesis, cell death, neuronal migration and differentiation,
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The consequences of ethanol are dependent on the time of administration and duration of treatment (3).

Animal models have displayed conclusively that alcohol can alter normal development of the central nervous system. Alcohol exposure during development has been shown to modify brain growth, neuronal number, myelination, neurotransmitter levels and receptor binding, synaptogenesis, and many other aspects of neuronal metabolism and morphology. There are indications of alcohol’s immediate or short term teratogenic effects, typically recounting deficits or delays in brain growth parameters, measured in the animals that were still in early stages of development (2).

Most infants identified with FAS are microcephalic, hyperactive, and mentally retarded by age four to ten. This persistence of brain dysfunction is what causes the highest human and economic toll (2).

Several studies have exhibited reductions in neuronal number in developing animals following alcohol exposure. However, neuronal death is a consequence of normal development. Some neuronal populations maintain a fifty percent reduction in the number before stabilizing in an adult configuration. The possibility exists that developmental alcohol exposure may in at least some circumstances, be accelerating the deaths of only those neurons that

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