By reading and understating the research literature related to FAS will definitely help readers to explore the issue.
The main discussion of the paper comprises that 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 very heavy-drinking mothers produce such infants (Abel, 1996). But although not all the offspring of very heavy drinking mothers exhibit the full-blown FAS, many show signs of damage, for example craniofacial abnormalities.
In summary, the results suggest that since 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, small sample size limits the generalizibility of the results.
This study discusses that teratogenic mechanism of FAS remains unclear but is obviously 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 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.
Fundamental mechanism by which alcohol administration leads to the interruption of brain development has not been described definitively. Studies shows that Teratogenic effects due to FAS may adversely affect 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 gared ion channels, neuro transmitter receptors, signal transduction, transcription of multi genes, trophic support of neurons, and membrane fluidization.
Moreover, 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. Researchers have not yet been able to elucidate these processes, leaving a major gap in their understanding of candidate mechanisms underlying FAS. Although investigators have identified genes