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Library Source-Reproductive Toxicology - Essay Example

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The paper "Library Source-Reproductive Toxicology " discusses that generally, studies support earlier reports documenting the adverse effects of prenatal alcohol exposure in children who lack the physical features necessary to warrant a diagnosis of FAS…
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Library Source-Reproductive Toxicology
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Extract of sample "Library Source-Reproductive Toxicology"

This essay aims to critically evaluate original research articles that have utilized different methodologies.

All research journals discussed a similar issue of ‘FAS’ that is based on extrapolation from epidemiological studies of pregnant women. Reading and understating the research literature related to FAS will help readers to explore the issue. The main discussion of the paper comprises how alcohol consumption during pregnancy can result in a child being born with FAS. It is noted that British experiences show that only about 2.5% of heavy-drinking mothers produce such infants (Abel, 1996). But although not all the offspring of very heavy-drinking mothers exhibit full-blown FAS, many show signs of damage, for example, craniofacial abnormalities.

In summary, the results suggest that the results of the current study indicate that mothers of FAS children had more neuropsychological deficits than control mothers, leading to diminished self-regulation and alcohol abuse. There exists, also, the possibility that mothers of FAS children had more social and emotional problems than controls. The data suggest that mothers of FAS children felt socially more isolated and "more stressed" during pregnancy. The association between maternal depression, self-esteem, emotions, and drinking was not assessed.

Finally, a small sample size limits the generalizability of the results. This study discusses that the teratogenic mechanism of FAS remains unclear but is not solely dependent on alcohol. Experimental studies in animals point to mineral deficiency, particularly zinc, which in combination with alcohol intake may lead to serious birth defects. However, some women who have produced children with the syndrome have normal plasma zinc levels. Britain's experience suggests that FAS is more commonly found among the offspring of very heavy-drinking mothers who are also socially and materially deprived.

Confusion over the relative contribution of alcohol in causing this syndrome has led to the suggestion that titles such as 'Fetal Poverty Syndrome' or 'Foetal Alcohol Lifestyle Syndrome' may be more appropriate than Fetal Alcohol Syndrome. However, although the relative contribution of alcohol may eventually be shown to be less than that of other variables, the fact that reduction of intake in alcoholic women has been of demonstrable benefit to their offspring suggests that heavy drinking remains an integral factor.

The fundamental mechanism by which alcohol administration leads to the interruption of brain development has not been described definitively. Studies show that Teratogenic effects due to FAS may adversely affect the growing brain in multiple ways. These include direct effects such as ephemeral impairment of uterine vessels and reduced fetal cerebral metabolic rate. It also affects voltage-gated ion channels, neurotransmitter receptors, signal transduction, transcription of multi-genes, trophic support of neurons, and membrane fluidization.

Moreover, the mechanism through which prenatal alcohol exposure could damage the CNS and lead to such devastating consequences as FAS is through interfering with the normal regulation of the genes that control brain development. 

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