The Effect Of Exposure To Alcohol During Prenatal Development

2993 words - 12 pages

Exposure to alcohol during prenatal development is one of the leading causes of preventable birth defects and mental impairments (Bower, Szajer, Mattson, Riley, & Murphy, 2013; Nuñez, Roussotte, &Sowell, 2011; Sowell et al., 2008a). Fetal Alcohol Syndrome (FAS), the more severe form of PAE, affects two to seven out of every 1000 individuals in the United States (May et al., as cited in Simmons, Thomas, Levy & Riley, 2010). The term Fetal Alcohol Spectrum Disorder (FASD) describes an individual with varying levels of PAE. Sampson et al. (as cited in Simmons at al., 2010) estimated that one in every 100 individuals suffers from some form of FASD. With such a high prevalence in the population, numerous studies have been done showing the detrimental effects of PAE. The purpose of this paper is to review literature in brain development and structural changes in response to prenatal alcohol exposure (PAE).
PAE has several characteristic symptoms including brain and facial dsymorphology. Disruption of normal brain development due to prenatal alcohol exposure is linked to size reduction and/or damage in almost all parts of the brain (Lebel , Roussotte, & Sowell, 2011), decreased neuron generation rate, delayed and/or atypically migration of neurons during brain development, and decreased myelin and axon development (Guerri & Renau-Piqueras, 1997). PAE has also been linked to reduced motor coordination (Xie, Yang, Chappell, Li, & Waters, 2009), a lowered IQ and attention span, an increased tendency for hyperactivity, and a decreased ability in verbal learning and language skills (Yang et al., 2011). In addition, individuals exposed to high levels of alcohol in the womb have growth retardation (Lebel et al., 2011) and typical facial features such as a flattened midface, smoothed philtrum, a thin upper lip (Stratton et al., as cited in Roebuck-Spencer, Mattson, Deboard Marion, Brown, & Spencer, 2003), and a reduced palpebral fissure (Yang et al.).
Alcohol has been shown to alter normal brain development by interfering with normal cell processes responsible for cell division and gene expression. Guerri and Renau-Piqueras (1997) explained that alcohol affects cell division by inhibiting cytoskeleton activity. This increases the cells in the G0 and G1 phase, which reduces the number of mitotic cell undergoing cell division. A later study by Anthony, Zhou, Ogawa, Goodlett, and Ruiz (2008) found similar findings in the reduction of mitotic cells, but through induced apoptosis. They used mouse dorsal root ganglion stem cells to research the affect of PAE on the G1 and S phase of the cell cycle. Cell cultures were either exposure to 200 mg/dl or 400 mg/dl of alcohol, excluding the control group. These researchers found that alcohol exposure increased the levels of cyclin D1, cyclin D2, and E2F1, each of which play an important role in the regulation of the G1 and S phase of the cell cycle as well as subsequent cell division. Over expression of these...

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