Term Paper: Effects of Alcohol Use on the Fetus

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FAS

Fetal Alcohol Syndrome was first discussed by Jones and Smith in 1973 as a pattern of abnormalities often seen in children born to mother's who consumed alcohol during pregnancy (Jones and Smith, 1973, p. 1000). The authors noted that while most mothers are careful about their actions during pregnancy, particularly in the first few months, those who chose to drink alcohol, particularly in large quantities, often bore children with severe facial abnormalities, central nervous system problems, and growth problems (Jones and Smith, 1972, p. 10001). This paper will discuss FAS, the causes of symptoms, the effects of alcohol on the developing fetus, and the long-term complications of the disease.

According to the Birth Defects Monitoring Program of the Center for Disease Control,.9 of every 10,000 births in the U.S. result in FAS, if excluding Native American FAS rates (Chavez, 1989, p. 207). However, other studies, such as those conducted by Sokol (1986, p. 902), showed the average for retrospective studies was 2.9 per 1,000 worldwide, compared with 1.1 per 1,000 for prospective studies worldwide, which is a much higher incidence. The difference is believed to be related to the populations used in the different studies. In Sokol's work, the participants were African-American or Native American and of lower socioeconomic status, whereas most CDC studies used predominantly white, middle class participants (Abel and Sokol, 1987, p. 68). In the first population, estimates show a prevalence of FAS of 2.6 per 1,000 births, whereas estimates of the second group show only a.6 per 1,000 births (Abel and Sokol, 1987, p. 66). Clearly, by including various ethnic and socioeconomic populations, study results can drastically differ.

According to the CDC, the rates of FAS by ethic group are as follows per 1,000 births: Asians 0.3, Hispanics 0.8, whites 0.9, blacks 6.0, and Native Americans 29.9 (Chavez, 1989, p. 206). Researchers of Native American populations and FAS note that although the rate is high overall, the specific incidence of FAS is highly varied between different cultures. May (1983, p. 377) notes the rate of FAS among Navajo and Pueblo tribes are similar to those of the general population, whereas the rates among Southwest Plains Indians are much higher. Factors such as culture, pattern of alcohol use, and socioeconomic status play a role in this difference in rates even among similar populations (Aase, 1981, 154).

However, many note that studies of FAS prevalence are complicated by methodological problems. Since defects are typically recorded only at birth, those whose complications develop later in life are difficult to study. Thus, catchments studies often vastly underestimate the incidence and severity of FAS. On the other hand, studies that follow FAS individuals over time tend to sample populations with a high incidence, and thus overestimate the prevalence of the disease (Abel, 1987, p. 62).

While the incidence rates of the disease vary between populations and over time, the cause of FAS remains clear. When a pregnant woman drinks, the alcohol he consumes is passed through the placenta to the fetus' circulatory system. Ethanol, the primary component of alcohol once in the blood stream, first impairs the blood flow of the placenta, causing hypoxia and malnutrition for the fetus. As the alcohol passes through the placenta to the fetus, it is rapidly distributed throughout the body (DEPH, 2003, online). Recent studies have shown that alcohol then interferes with L1 adhesion molecules, which assist in cell adhesion, and hinder the cell to cell attachments. Additionally, alcohol easily penetrates the active peptides from NAP and SAL, or brain proteins, as they work to protect nerve cells against alcohol (Wilkeymeyer, et al., 2002, p. 112). Other proposed mechanisms of action for ethanol include altered neural crest cell migration, increased cell death, mitochondrial cell dysfunction, effects on neurotransmitter systems, the inhibition of cell proliferation, and altered gene expression (DEPH, 2003, online). While these theories still need more research, it is clear the mechanisms of action of alcohol are directly linked to FAS.

In addition to the cell problems of the fetus with FAS, alcohol during pregnancy also can cause a host of other problems related to FAS. If the mother of the child is addicted to alcohol, the unborn fetus is dependant upon the drug as well. At birth, since the alcohol is no longer present, the central nervous system of the child is over stimulated, causing withdrawal that can last up to 18 months.

This can contribute to the teratogenic effects on FAS children, including deformities of the face, heart defects, and mental retardation (DEPH, 2003, online).

In order to be diagnosed with FAS, three criteria must be present in the child. These include teratogenic effects common in FAS children, such as a flattened midface, thin upper lip, absent philtrum, and shortened eye slits. Secondly, the child must display typical growth retardation, such as a low birth weight, disproportional weight, or height and weight below the 5th percentile. Finally, the child must show central nervous system abnormalities, such as impaired motor skills, learning disabilities, behavioral disorders, and mental handicaps. A less serious form of FAS, that of PFAS, or Partial Fetal Alcohol Syndrome, requires at least two of the criteria above, while ARND, or Alcohol Related Neurodevelopmental Disorder, requires only a central nervous system abnormality (CDC, 2005, p. 6).

While the physical deformations and growth retardation of FAS children can be detrimental, it is the effect of FAS on the central nervous system that causes the majority of severe issues with FAS children. The exposure to prenatal alcohol causes structural deviations in the brain, resulting in a disruption of proliferation and migration of brain cells. This disruption can also cause a concurrent disruption in the electrophysiology and neurochemical balance in the brain. As a result, messages are not transmitted throughout the brain and body as they are in non-FAS children (Streissguth, 1997, 205). Recent studies using MRI technology have examined the brain of those with FAS, and confirm this structural damage. Additionally, limited studies have shown the neurotransmission differences in these individuals as well (Streissguth, 1997, 226).

However, as many researchers point out, these indicators are likely only a few of several types of brain disturbances affecting FAS individuals. Studying the architecture of the brain is a complex task, and many brain functions are simply not observable. Additionally, measurements of how the brain communicates are often impossible to research. Thus, while MRI imaging can detect some of the abnormalities of the central nervous system in FAS individuals, several aspects of the disease are immeasurable (Streissguth, 1997, 269).

The central nervous system abnormalities of FAS individuals are the most debilitating aspects of the disease. Unfortunately, prenatal alcohol exposure is one of the leading known causes of mental retardation in the United States (Abel, 1986, p. 1222). The range of abnormalities is vast, and include, as mentioned, both structural damage and transmission problems. Structural damage includes microephaly, or a smaller brain size, malformations which cause tremors and seizures, and damage to areas of the brain controlling motor skills, learning, memory, and behavior (Streissguth, 1997, 169).

These damaged areas lead to a host of central nervous system malfunctions. FAS causes delayed development of motor skills, such as sitting up, crawling, and walking, delayed fine motor skills such as grasping objects, impaired language development, and memory problems (WebMD, 1999, online). Learning disabilities are also common. These can include an inability to generalize information, to use recently learned skills, to predict cause and effect, to distinguish reality from fantasy, and an inability to link behaviors with experience (FAS Support Network, 2004, online). In terms of behavioral issues, the structural and neurological damage can cause poor judgment, distractibility, and impulsive behavior (WebMD, 1999, online), as well as hyperactivity (FAS Support Network, 2004, online).

As devastating as these effects are alone, there is an additional concern in FAS individuals, in that the effects of the disease are permanent, and are not outgrown. In terms of physical abnormalities, these individuals will continue to be of short stature, small, thin, may develop hearing defects, organ imperfections, bone problems, and eating and sleeping disorders (Streissguth, 1989, p. 154). Further, the learning deficits also persist into adulthood, causing problems with problem solving, decision making, and overall learning capacity (Streissguth, 1989, p. 156).

In addition, the damage of the central nervous system controlling behavior can cause continued problems for the FAS individual. Many FAS adults have difficulty with employment, legal issues due to a lack of understanding of cause and effect, alcohol abuse, child care, and overall mental health issues (Streissguth, 1991, p. 1963). Teenagers with the disease often experience low self-esteem and depression, and may exhibit unsafe behaviors such as sexual promiscuity and risk taking (Streissguth, 1991, p. 1964). As adults, these individuals are often socially isolated, have difficulties with interpersonal relations, short-term memory failure, and a large difficulty distinguishing reality from fantasy (Streissguth, 1991, p. 1965). When combined with learning disorders and physical abnormalities, these individuals are highly at risk for criminal activity, drug and alcohol use, and other forms of deviant behaviors.… [END OF PREVIEW]

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