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Fetal Alcohol Syndrome

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Fetal Alcohol Syndrome

Fetal Alcohol Syndrome

Alcohol use and abuse during pregnancy is common among women in the United States. A national survey found that 59% of women ages 15 - 44 drank alcohol while pregnant. Sixty-six percent of these pregnant women reported alcohol use in their first trimester, 57 percent in the second trimester, and 54 percent in their third trimester (SAMHA, 1998). Prenatal alcohol exposure can have permanent adverse effects on a developing fetus. There are five classifications of prenatal alcohol exposure and the most severe outcome on the spectrum is fetal alcohol syndrome (FAS). FAS is a clinical diagnosis applied to children who have been exposed to alcohol during gestation and exhibit abnormalities in their physical and cognitive development. To meet the current diagnostic criteria a child must have symptoms in each of the following three areas: (1) growth deficiency (2) abnormalities in facial and skull structure; and (3) central nervous system (CNS) dysfunction (Stratton, Howe, & Battaglia, 1996; Larkby & Day, 1997).

Prevalence and Etiology of FAS


Over the years, researchers have used three different approaches in trying to measure the prevalence of FAS: passive surveillance systems, clinic based studies, and active case ascertainment in a segment of the general population. May and Gossage (2001) discussed the strengths and weakness of each approach and summarized the estimated prevalence of FAS produced by all three. Their findings estimated that the prevalence of FAS in the United States was 0.5 to 2.0 cases per 1,000 births during the 1980s and 1990s. It is significant to point out that not every woman who drinks alcohol during pregnancy will give birth to a child with FAS. Abel (1995) estimated that 4.3 percent of heavy drinkers give birth to an FAS child. Therefore it is important to define the factors that place certain women at risk to giving birth to a child with FAS.

Etiology and Risk Factors

Alcohol's effects on the developing fetus are complex. Clearly, no single mechanism or factor is responsible for the various alcohol-induced fetal damages. Epidemiological studies of FAS consistently point to several major risk factors that may place women at a greater chance of giving birth to an affected child. The most obvious factor to begin with is alcohol consumption and dosage. As stated above not every child whose mother drank alcohol during pregnancy develops FAS or other alcohol related effects. Maier and West (2001) discuss the risks associated with different patterns of alcohol exposure, such as binge-drinking versus continuous alcohol exposure. The human and animal studies they reviewed revealed two important findings: 1) a high blood alcohol concentration (BAC) is a critical factor in producing fetal brain injury and 2) it is not so much the total amount of alcohol that's consumed, but rather, the high number of drinks consumed at one occasion. When the total daily dose is the same, a binge drinking pattern produces a higher peak BAC which results in more severe brain injury than continuous alcohol exposure.

Maternal biological and health variables are among the most common and consistent risk factors for FAS. Studies in the United States and Canada have identified the following common risk factors associated with FAS: the mother is older than age 25 when FAS child is born; she already has three or more children when FAS child is born; and there is polydrug use; (NIAAA, 2000). In addition, some risk factors are merely associated or correlated with the mother's life style. Low socioeconomic status, unemployment, alcohol misuse in family or by partner, questionable martial status, loss of children to foster or adoptive placement and a local community tolerant of heavy drinking are social variables that have been found to be associated with FAS births both in the United States and in other parts of the world (Abel 1995; NIAAA, 2000).

Finally, developmental timing of the alcohol intake is a risk factor in determining the severity of FAS brain injuries. Fetal development is a sequential process and growth deficiencies, facial abnormalities, and CNS deficits occur at different points during gestation. From embryological studies, investigators know that facial abnormities occur when the midline of the face is formed during the first trimester. A significant correlation between first trimester alcohol exposure and the rate of these physical abnormalities was found in the Maternal Health Practices and Child Development Project (MHPCD), a longitudinal study of the long-term effects of prenatal alcohol exposure (Day et al., 1990). Whereas major facial and skull abnormities result from exposure in early pregnancy, growth is most affected by late exposure, and CNS deficits occur throughout gestation period. This means that offspring who are exposed to alcohol throughout pregnancy will not have the same outcome as offspring who are exposed only during early pregnancy or only at specific times during pregnancy (Larkby & Day, 1997). Korkman, Kettunen, and Autti-Ramo's research (2003) illustrated outcome differences due to timing of alcohol exposure. They conducted a study of early adolescents who were exposed to alcohol prenatally to find the relationship between duration of alcohol exposure and neuro-cognitive development. They found that children exposed to alcohol throughout pregnancy, performed well below the average on various neuro-cognitive tasks. In contrast, exposure during the first and second trimester only had mild restricted effects.

A recent study reports that a single exposure to high levels of alcohol can kill nerve cells in the developing brain. It looks at two risk factors: alcohol consumption and developmental timing. The researchers found that a rat brain is sensitive to high BAC during a brain development stage that corresponds to the brain growth stage in humans, called synaptogenesis. Synaptogenesis begins in about the sixth month of pregnancy and ends at about two years of age. In the study, the researchers intoxicated infant rats and maintained the BAC to twice the level that defines legal intoxication in humans. This single exposure caused brain cells to commit suicide by a process called apoptosis. In general, death of neurons by apoptosis occurs naturally. It helps the brain to get rid of unhealthy cells or cells that are not needed. However the apoptosis in the experiment exceeded the natural rate of cell death by almost 30 times in some parts of the brain. The alcohol also did not just cause cells that were going to die anyway to die more quickly, but it caused cells that



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