The concept Fetal Alcohol Syndrome (FAS) refers to a set of birth defects that occur in children born to mothers who abused alcohol during pregnancy. The alcohol-induced defects include pre- and post-natal growth deficiencies, minor facial abnormalities, and damage to the developing central nervous system (CNS). FAS is the most serious condition physicians group under the heading of Fetal Alcohol Spectrum Disorders, which also includes Alcohol-Related Birth Defects, like alcohol-induced congenital cardiac defects that are unrelated to a diagnosis of FAS, and Alcohol-Related Neurodevelopmental Disorders, which occur in the absence of any facial birth defects or growth delays. The severity of birth defects associated with FAS can vary depending on the intensity, duration, and frequency of exposure to alcohol during gestation. In addition to these dose-related concerns, maternal factors such as the mother's genetics or how quickly she metabolizes alcohol, and the timing of exposure during prenatal development also impact alcohol-induced abnormalities. As birth defects and anomalies can arise when pregnant women consume alcohol, alcohol is a teratogen, an environmental agent that negatively impacts the course of normal embryonic or fetal development.

In the fifteen years between the discovery of fetal alcohol syndrome, or FAS, in 1973 and the passage of alcohol beverage warning labels in 1988, FAS transformed from a medical diagnosis between practitioner and pregnant women to a broader societal risk imbued with political and cultural meaning. In this dissertation, I examine how scientific, social, moral, and political narratives dynamically interacted to construct the risk of drinking during pregnancy and the public health response of health warning labels on alcohol.

Prenatal alcohol (ethanol) exposure can have dramatic effects on the development of the central nervous system (CNS), including morphological abnormalities and an overall reduction in white matter of the brain. The impact of ethanol on neural stem cells such as radial glia (RG) has proven to be a significant cause of these defects, interfering with the creation and migration of neurons and glial cells during development. The impact of ethanol on RG can occur as early as three weeks after fertilization and can persist through the third trimester of pregnancy, interfering with intrinsic mechanisms and signaling pathways to impede cellular proliferation, differentiation, and survival.

Prenatal exposure to alcohol (ethanol) results in a continuum of physical and neurological developmental abnormalities that vary depending on the timing, duration, and degree of alcohol exposure. Heavy exposure during development may lead to the condition Fetal Alcohol Syndrome (FAS), characterized by growth deficits, neurological deficiencies and minor facial abnormalities. Alcohol is a known teratogen, an agent that causes birth defects and acts upon developing embryos through mechanisms that are not yet fully understood. One of the better understood developmental effects of alcohol relates to the minor facial abnormalities associated with FAS, particularly the role that the gene sonic hedgehog (shh) plays in the regulation of craniofacial defects. In comparative animal studies, maternal exposure to alcohol results in the massive decrease of shh and shh transcription factors in affected cell populations. However, the exogenous application of shh to the developing embryo has shown limited success in reversing this expression, thereby restoring a normative pattern of craniofacial development in the affected embryo.

Maternal consumption of alcohol (ethanol) during pregnancy can result in a continuum of embryonic developmental abnormalities that vary depending on the severity, duration, and frequency of exposure of ethanol during gestation. Alcohol is a teratogen, an environmental agent that impacts the normal development of an embryo or fetus. In addition to dose-related concerns, factors such as maternal genetics and metabolism and the timing of alcohol exposure during prenatal development also impact alcohol-related birth defects.

Prenatal exposure to alcohol (ethanol) can result in a continuum of developmental abnormalities that are highly variable depending on the severity, duration, frequency, and timing of exposure during gestation. Defects of the corpus callosum (CC) have proven to be a reliable indicator of prenatal alcohol exposure as it affects the brain. Structural abnormalities of the CC occur along a continuum, like most alcohol-induced anomalies, whereby more severe prenatal exposure results in a greater expression of the abnormal trait. A variety of cognitive deficiencies are associated with defects of the fetal CC, the morphology of which can vary greatly between individuals and can be observed through neuroimaging over a broad transect of life stages.

A variety of developmental defects occur as a result of prenatal exposure to alcohol (ethanol) in utero. In humans, those defects are collectively classified as Fetal Alcohol Spectrum Disorders, with Fetal Alcohol Syndrome (FAS) representing the more severe defects. FAS is defined by pre- and post-natal growth retardation, minor facial abnormalities, and deficiencies in the central nervous system (CNS). In addition to those defects, prenatal exposure to alcohol impacts cardiogenesis, the developmental stage of heart formation.

Prenatal exposure to alcohol (ethanol) results in a continuum of physical, neurological, behavioral, and learning defects collectively grouped under the heading Fetal Alcohol Spectrum Disorder (FASD). Fetal Alcohol Syndrome (FAS) is part of this group and was first defined in 1973 as a condition characterized by pre- and postnatal growth deficiencies, facial abnormalities and defects of the central nervous system (CNS). The CNS is particularly vulnerable to the effects of ethanol during prenatal development. Severe exposure correlates with gross morphological abnormalities and an overall decrease in white matter. Mechanisms for how ethanol affects the development of the CNS are complicated, but damage to neural stem cell progenitor pools that give rise to neurons and glia is strongly suspected to be a major factor. Damage to this population of cells at any point during CNS development can result in abnormalities in the formation and maturation of these cells, from the initial differentiation through the maturation of neuronal networks. This damage can lead to a wide variety of cognitive deficiencies, functional impairments, and behavioral problems depending on the area of the brain impacted by prenatal ethanol exposure.

The term Fetal Alcohol Syndrome (FAS) was first published in 1973 in an article published in the British medical journal The Lancet. In that article, a group of pediatricians and psychiatrists at the University of Washington Medical School helped to define the morphological defects and developmental delays that can affect children born to alcoholic mothers. Those observations include pre- and post-natal growth deficiencies, minor facial abnormalities, and damage to the developing brain that can result in behavioral, learning, and cognitive abnormalities.

Maternal consumption of alcohol (ethanol) can result in a range of alcohol-induced developmental defects. In humans, those collective birth defects are called Fetal Alcohol Spectrum Disorders, with the most severe manifestation being Fetal Alcohol Syndrome (FAS). FAS is defined by pre- and post-natal growth retardation, minor facial abnormalities, and deficiencies in the central nervous system (CNS). The eye and ocular system development is particularly susceptible to the effects of prenatal alcohol exposure and can result in visual impairment or blindness.