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Introduction
Loomans et. al. (2012) found that teratogens can cause behavior problems in the offspring.
The prenatal and parental alcohol exposures have been shown to cause Attention Deficit Hyperactivity Disorder in children (Ware, et al. 2012).
ADHD results in overactivity, impulsivity, and inability to maintain attention under stereotypical school settings (Getahun, et al. 2013).
ADHD can also cause low self-esteem, mood swings and anxiety, which can affect the academic performance of students.
The cause of ADHD in children is not alcohol exposure. There are also signs of neurologic etiology (Frodl and Skokauskas 2012).
The diagnosis of ADHD was mild brain dysfunction (MBD), at the time (Rubia and colleagues, 2014).
Because memory-related problems are often linked to neurological dysfunction, ADHD cases were mostly reported in infants at high-risk for pre- and perinatal problems, or mothers with high-risk pregnancies.
Recent literature suggests that ADHA can be found in children without any brain dysfunction, which is contrary to the neurological basis of the condition (Cubillo and al., 2012).
The root cause of ADHD can be confusing. It can vary between a chaotic or disorganized environment to a childhood psychiatric disorder.
ADHD is more common in families that have had prenatal alcohol exposure, children with Fetal Alcohol Syndrome (FAS), or children of alcoholic mothers (Graham and colleagues, 2013).
The attempt to link ADHD to prenatal alcohol was not successful. It is hard to conceptually distinguish the prenatal effects from other effects such as parental alcohol abuse.
It is not clear whether ADHD is caused by post-natal alcohol exposure or direct alcohol exposure after birth.
Brown et. al. conducted a study in 1991 to identify these two guiding factors that lead to ADHD.
The article is entitled Effects of prenatal alcohol consumption at school age.
ADHD affects school students who have been exposed to prenatal alcohol.
Methodology
The study involved 68 mothers and children from a large group (n = 228) to study the effects of prenatal alcohol on ADHD generation.
The children were aged between 10 months and 5 years.
Black people are chosen because they come from low socioeconomic backgrounds.
The research by Coles et al. in 1991 was the sole basis for the selection of the sample.
This pool of subjects was from the same high-risk group, which included women who reported drinking alcohol throughout pregnancy (n = 25, despite having received proper education intervention at the time of recruitment to the large university teaching hospital (1990-1983).
Randomly selected women were chosen who had never drank alcohol and their children were healthy.
The final group consisted of women who reported having consumed alcohol in the first trimester (statistically significant), but stopped drinking during the remainder of the tenure of their pregnancy (“stopped drinking” n= 22).
The study was conducted by a group consisting of master’s level psychology students. It was conducted with the aid of distributing questionnaires among mothers and children.
The children who participated in the study were not informed about their mothers’ drinking habits.
The Addiction Severity Indicator (ASI) was used in the questionnaire (McClelland Luborsky, O’Brien, 1983).
Child Behavior Checklist (CBL), which assessed the child’s internal and exterior behavior (table 2 and 3).
Source: Brown et. al. 1991
Source: Brown et. al. 1991
Computerized vigilance tasks (CPTs) were used to analyze the sustained attention.
To assess the degree of impulsivity, Matching Familiar Figures Test was used.
Videotaped observational procedures were used to examine the interaction styles and activity levels.
Researchers are studying the effects of alcohol consumption pre- and post-natally on ADHD development.
The independent variable can be called the alcohol intake, which can be altered to alter the dependent variable, which is ADHD development among schoolchildren.
Results
Results showed that children exposed to alcohol during their neonatal period (pregnancy tenure), have problems with their ability to pay attention and maintain their focus.
Teachers also reported that they had frequent attention and behavioral problems.
Their mothers’ reports are inconsistent with those of the teachers.
The children’s current alcohol intake was monitored and no change was seen in their behavior. This had no effect on their internal behavior.
Multivariate analysis was used to validate the statistical significance of test results.
The results supported the hypothesis. They showed that children exposed to alcohol in their neonatal years showed problems in keeping their attention. This is one of the main symptoms of ADHD.
Conclusion
Brown and colleagues (1991) found that ADHD symptoms are associated with parental alcoholism. This argument was supported both by postnatal environmental effects and teratogenic effects.
Results also revealed that children exposed to alcohol during pregnancy had significantly higher behavioral problems in the eternalizing or internalizing domains than those whose mothers have not consumed alcohol in their lives.
Results also revealed that internalizing effects such as withdrawal from depression and anxiety were reduced when alcohol consumption was stopped.
However, the externalizing behaviors are still problematic. These include cognitive performance and attention deficits.
The statistical analysis supported the hypothesis.
Research findings revealed that ADHD affects children who were born to an alcoholic mother in the prenatal stage.
The research supports the conclusion that linking dependent and independent variables can help to support.
These findings are also consistent with previous research.
Streissguth (1986) found that children with severe CPT impairments make more errors and react more slowly than those without.
Their behavioral responses did not change, except for the attention-related problems.
Borwn and colleagues’ results were not disputed.
The Boyd et al. (1991) findings were overruled by Borwn et al.
(1991), which did not show any evidence of prenatal alcohol on children from low-income countries.
The study’s main strengths lie in its statistical analysis, which uses a wide range of parameters to examine attention deficit problems among children.
There are some weaknesses in the study, such as the small number of respondents (68), which could have caused biasness.
The study’s main weakness is the inclusion of black people in the primary focus group, who live in the lowest socio-economic bracket. This again creates bias.
A large focus group can improve the structure and design of the study. It is also possible to study the neurological basis of ADHD-afflicted children in order to establish a link between alcohol exposure and neurological predispositions in ADHD development (Graham and al., 2013).
These research findings can be extremely helpful in determining the effects of alcohol exposure during prenatal tenure on ADHD on the behavior and psychopathology of the children (Ware and al., 2013).
Refer to
Prenatal alcohol exposure and sustained focus in preschool years.
Neurotoxicology and Teratology, 13(1): 49-55.
Prenatal alcohol exposure and school age effects.
Attention and behavior.
Prenatal alcohol exposure and school age effects.
I.
Neurotoxicology and Teratology, 13(4): 357-367.
A review of frontostriatal and frontocortical brain abnormalities among children and adults with Attention Deficit hyperactivity Disorder (ADHD), and new evidence for ADHD dysfunction during motivation and attention.
European journal of Pediatrics, 171(2): 271-280.
A meta-analysis of structural MRI studies on children and adults with attention deficit hyperactivity disorders shows treatment effects.
Alcoholism: Clinical and Experimental Research 37 (s1).
Risk of problem behavior among 5- to 6-year-olds if they consume caffeine during pregnancy.
A new validation instrument for substance abuse patients is the addiction severity index.
Attention, distraction, and reaction time at 7 years of age and prenatal alcohol exposure.
Neurobehavioral Toxicology and Teratology.
Alcoholism: Clinical Research and Experimental Research, 36(8) 1431-1441.
Clinical and Experimental Research in Alcoholism, 37(3): 507-516.