Prenatal Alcohol and Nicotine Exposure and the Subsequent Cognitive and Behavioral Deficits Seen in Children

Prenatal alcohol and nicotine exposure have well known physiological effects on the fetus. However, it is the goal of this thesis to inform the reader of of the deleterious effects that these substances can have on cognitive and behavioral development in children. A literature review in relation to this topic was conducted through online databases using key words. Though some of the results were inconsistent, enough evidence exists for women to be educated on the increased risks for cognitive and behavioral deficits in children exposed to alcohol and nicotine in utero. PRENATAL EXPOSURE AND BEHAVIOR 4 Prenatal Alcohol and Nicotine Exposure and the Subsequent Cognitive and Behavioral Deficits Seen in Children Alcohol and tobacco smoke are known to have deleterious effects on birth outcomes in neonates born to women who have used these substances during pregnancy. However, research is indicating that the effects of these legal substances are manifold and persist throughout childhood, possibly even into adulthood. The aim of this thesis is to show that prenatal alcohol and nicotine exposure cause cognitive and behavioral deficits that can be seen throughout childhood. The following pages will describe the researched biological effects of alcohol and nicotine on the developing fetus. This will be followed by a literature review of studies researching the effects of prenatal alcohol and nicotine exposure on cognition and behavior in children. Biological Effects of Alcohol Alcohol exposure causes damage to the central nervous system (CNS) of the developing fetus. Depending on the timing and amount of exposure, there may be different effects. This results in the variation in symptoms that are present in fetal alcohol spectrum disorders (FASD). New magnetic resonance imaging (MRI) technologies are being used to track brain changes in people exposed to alcohol prenatally, which has enabled discoveries related to specific areas of the brain and how they respond to alcohol exposure (Warren, Hewitt, & Thomas, 2011). Up to this point, a few of the regions that have been noted to be especially vulnerable include the frontal cortex, regions of the cerebellum, the corpus callosum, and the hippocampus. A certain type of MRI, known as diffusion tensor imaging (dtMRI), is able to notice changes in white matter nerve tracts. These changes in children with prenatal alcohol exposure PRENATAL EXPOSURE AND BEHAVIOR 5 (PAE) are thought to be related to alterations in information processing (Warren et al., 2011). As stated in Warren et al. (2011), embryonic frog models exposed to alcohol experienced altered gene expression leading to microcephaly, growth retardation, and microphthalmia. In humans, the oxidative stress that is induced by prenatal alcohol exposure may cause altered timing of apoptosis which can interfere with neuronal development, possibly leading to the above symptoms. Abnormalities have been found in the size of the corpus callosum as a result of alcohol exposure, leading to difficulties in verbal learning in this population. In addition, alcohol may cause basal ganglia volume reduction. This effect may result in lower intelligence quotient (IQ) scores. Other research suggests teratogenic effects of alcohol on the cerebellum, resulting in fine and gross motor delays and therefore affecting balance and motor control in this population (Coles, 2011; Dorrie, Focker, Freunscht, &