Dose and time dependence of alcohol exposure in relation to craniofacial dysmorphisms in fetal alcohol syndrome
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The National Institutes of Health defines Fetal Alcohol Syndrome (FAS) as a debilitating collection of birth defects that include craniofacial dysmorphisms, neurological and motor insufficiencies, growth retardation, and behavioral and social discrepancies. Characteristic craniofacial abnormalities, which include smooth philtrum, thin vermillion border, short palpebral fissures, and microcephaly, are used as a diagnostic tool for FAS. There is agreement across the literature that the characteristic craniofacial dysmorphisms are induced as a result of prenatal alcohol exposure in very specific doses, and during very particular time periods during embryonic development. However, ambiguity still exists about the critical time and dose relationship of prenatal alcohol exposure in the production of FAS. In regards to the critical timing, researchers have concluded that prenatal alcohol exposure during the second half of the first trimester, defined as days 43-94 postconception, was found to cause an increased incidence of smooth philtrum, thin vermillion border, microcephaly and reduced birth weight. Conversely, other studies found that prenatal alcohol exposure on day 7 of gestation in mice, which corresponds to week 3 of human gestation, induced craniofacial abnormalities comparable to those seen in humans with FAS. In regards to the critical dose, there is a linear relationship between the dose of prenatal alcohol exposure and the incidence of FAS-related craniofacial abnormalities, with no safe threshold. It was also found that a binge pattern of drinking was more significantly associated with the craniofacial abnormalities seen in FAS than a continuous or less condensed pattern of drinking, even if the binge pattern involved a smaller absolute dose of alcohol. These results regarding both dose and pattern on prenatal alcohol exposure, suggest that binge-drinking patterns are most significantly associated with craniofacial abnormalities if consumed before pregnancy or during late pregnancy, whereas absolute high doses of alcohol in a non-binge pattern were most significantly associated with craniofacial abnormalities in the first trimester. Further research is required for clarification of the critical time and dose relationships involved in the production of the characteristic craniofacial dysmorphisms seen in FAS. A definite conclusion will aid in the public education and prevention programs for FAS if solid information can be provided about the harms of alcohol consumption during pregnancy in regards to timing and dose.
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