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Alcohol, Chemistry and
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Ethyl Alcohol - Sources and Uses Distribution of Ethyl Alcohol in the Body Maternal Drinking and Child Development Effect of Alcohol on the Cardiovascular System Definitions of Substance Use, Abuse and Dependence Early Research about Alcohol and the Brain
Some estimate
the
average IQ of children with FAS is close to 70,
near the borderline range of mental
retardation. Hyperactivity is very prominent. Children with FAS have been described as "tremulous, hyperactive, and irritable", while children not manifesting the full signs of FAS behavior have sometimes been described as "fidgety" and "less compliant". The latter may be interpreted by parents and teachers as willful acts of defiance, rather than manifestations of the problem. Further, impairments in motor control are apparent. Attention deficits are common and have been called "nonalert state" in infants and an inability to organize, maintain attention, and focus in older children and adults. Attention deficits in FAS children appear to differ from those with Attention Deficit Hyperactivity Disorder (ADHD, 10th Special Report to Congress, 2000). FAS children are not able to shift attention as well as the ADHD children. This fact may provide diagnostic guidance and suggests the importance of preparing children with FAS for shifts or changes to come. One of the greatest problems for persons with FAS is the inability to communicate effectively (Streissguth, 1997). These deficits may involve verbal, gestural, and behavioral communication skills. Thus, the person’s ability to function in society and to form and maintain meaningful relationships is greatly diminished or lost. Children with FAS often choose peer groups of younger children so that they can feel secure and more comfortable. A difficulty arises when they approach puberty and tend to experiment sexually with their peers. It is important to recognize that the lack of communication skills may not be perceived as such, but rather as defiance. Thomas and colleagues were the first to show that the social deficits in children with FAS are more severe than what can be attributed to low IQ (Thomas et al., 1998). Lack of functional skills (i.e. adaptive living skills) is delineated by Streissguth (1997) as the greatest deficit in people with FAS. Their inability to generalize from one situation to another and to use appropriate judgement makes it extremely difficult to function favorably in everyday life. Therefore, these deficits must be recognized and specific educational programs designed to prepare the person as well as the family for present and future situations and environments that may be encountered. Sampson et al, (2000) reported that 94% of 415 participants with FAS or FAE had a history of mental health problems. Attention deficits were the most commonly reported in children and adolescents with FAS or FAE, while depression was most commonly mentioned in adults. Another study (25 participants, Famy et al, 1998) reported 74% with past psychiatric treatment with diagnoses of alcohol and substance abuse (60%), major depressive disorder (44%) and avoidant personality disorder (29%). Further assessment of children with the Child Behavior Checklist (Mattson and Riley, 1998) also showed they had deficits in attention. These mental health problems add an additional layer of complexity to all the issues related to dealing with the prenatal effects of alcohol. In summary, it is clear that the ability of ethanol to diffuse and mix with the body water and interact with a variety of biological processes both during and after development, has major implications for the maternal/infant relationship. Wrong choices by the mother can have severe consequences for both mother and child.
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Once distributed, alcohol has the opportunity to directly influence the growth and development of the child. Alterations by ethanol in the function of growth factors and other chemical mediators known to be important in guiding the development of the fetus have in fact been amply demonstrated. Ethanol can also influence fetal development indirectly by exerting effects on the mother, which in turn influence the fetus. These indirect effects can include altering the nutritional status of the mother so that the fetus gets less nutrition; altering the function of the placenta, so that fewer nutrients and/or oxygen gets to the fetus; producing metabolites of ethanol such as acetaldehyde, which is known to be toxic; and compounding the effects of other drugs (therapeutic and nontherapeutic) that mother might be taking. Each of these possibilities has been the focus of extensive investigation in both animal and human studies (10th Special Report to the U.S. Congress on Alcohol and Health, 2000). The degree of damage incurred by the fetus is influenced by several factors, including the period of gestation when alcohol exposure occurs, how much the mother drinks during pregnancy, the pattern and timing of her drinking, and the genetic makeup of both mother and child. Because of these factors and others, it is not possible to know what level of drinking is safe for each individual, and so abstinence is recommended to all women who are pregnant, nursing, or who may become pregnant. Recent studies have shown several risk factors for delivering alcohol-affected children. These include alcohol consumption during pregnancy (and specifically, binge drinking, maternal age > 25, low socioeconomic status, unemployment, living in a culture that is tolerant of heavy drinking, social transience, and being separated, divorced or never married (May, 1995).
Manifestations of Prenatal Alcohol Exposure The detrimental effects of prenatal exposure to ethanol were long suspected (cf Judges 13:3-5), but only first documented by Lemoine et al (1968) in France and later by Jones and Smith (1973) and Jones et al (1973) in the United States. Early diagnoses and descriptions were based on "the highly distinctive appearance of children of alcoholic parents, particularly alcoholic mothers" and amplified to include not only characteristic facial features, but also growth deficiency and central nervous system dysfunction. Thus, the term, Fetal Alcohol Syndrome (FAS) was coined (Jones and Smith, 1973) and defined on the basis of these three criteria. FAS is now recognized as the most common cause of mental retardation in America, surpassing Down syndrome, cerebral palsy, and spina bifida. While FAS is the disorder that enjoys the most public awareness, other alcohol-related developmental disorders, which are more common than FAS (conservative estimates suggest a 10:1 ratio), go relatively unnoticed. Unfortunately, if a child does not exhibit all three criteria for an FAS diagnosis, the child may go unrecognized and/or untreated, even though (s)he has some of the same cognitive and behavioral problems due to the effects of alcohol on the brain and may often fall "through the cracks". When left untreated, these individuals are at risk to develop secondary disabilities, a term used by Streissguth and colleagues (Streissguth, 1997, Streissguth and Kanter, 1999) to describe the host of problems that often arise when individuals with prenatal alcohol exposure do not receive support or assistance. These include mental health problems, disrupted school experiences, trouble with the law, incarceration, alcohol and drug abuse, and sexual misconduct or victimization. The manifestations of Prenatal Exposure to Alcohol fall on a continuum from severely affected (including death) to near normalcy. The most severely affected show:
Within these categories are a multitude of more specific problems as capsulated below. Less severe impact may result in the individual manifesting only subsets of these (10th Special Report to Congress, 2000). The craniofacial features of children with FAS are fairly readily distinquished from those of normal children and include small eye slits (palpebral fissures), a flat nasal bridge, and absent philtrum.
Growth deficiencies include being small for gestational age and retarded postnatal growth both in body size, weight, and cranial size. Brain insults include:
In addition, the prefrontal cortex important in cognitive functioning, and the hippocampus, involved in learning and memory, also appear to be damaged. Also, there may be alterations in babies’ cry patterns (Zeskind et al, 1996) and brain electrical activity (Kaneko et al, 1996a,b), which also reflect brain damage and CNS dysfunction. The damage to the brain translates into a host of cognitive and behavioral deficits (Mattson & Riley, 1998) including mental retardation, apparent learning and memory deficits , lack of executive functioning, hyperactivity, attention deficits, loss of motor control, and inability to recognize and utilize visual/spatial relationships. References: Famy, C., Streissguth, A.P., and Unis, A.S. (1998) Mental illness in adults with fetal alcohol syndrome or fetal alcohol effects. American Journal of Psychiatry 155(4):522-554. Gordis, E. (1991) Alcohol Research: Promise for the Decade. Rockville, MD: National Institute on Alcohol Abuse and Alcoholism. Jones, K.L. and Smith, D.W. (1973). Recognition of the fetal alcohol syndrome in early infancy. Lancet 2:999-1001. Jones, K.L., Smith, D.W., Ulleland, C.N., and Streissguth, A.P. (1973) Pattern of malformations in offspring of chronic alcoholic mothers. Lancet 1 (815):1267-1271. Kaneko, W.M., Ehlers, C.L., Philips, E.L., and Riley, E.P. (1996a). Auditory event-related potentials in fetal alcohol syndrome and Down’s syndrome children. Alcohol Clinical and Experimental Research 20(1):35-42. Kaneko, W.M., Phillips, E.L., Riley, E.P., and Ehlers, C.L. (1996b). EEG findings in fetal alcohol syndrome and Down syndrome children. Electroencephalography and Clinical Neurophysiology 98(1):20-28. Lemoine, P., Harouseau, H., Borteryu, J.T., Menuet, J.C. (1968). Les enfants des parents alcooliques: Anomalies observees apropos de 127 cas. Ouest Medical 21:476 – 482. Mattson, S.N., Jernigan, T.L., and Riley, E.P. (1994) MRI and prenatal alcohol exposure: Images provide insight to FAS. Alcohol Health and Research World 18(1):49 – 52. Mattson, S.N. and Riley, E.P. (1998). A review of the neurobehavioral deficits in children with fetal alcohol syndrome or prenatal exposure to alcohol. Alcoholism: Clinical and Experimental Research 22:279-294. May, PA (1995). A multiple-level comprehensive approach to the prevention of fetal alcohol syndrome (FAS) and other alcohol-related birth defects (ARBD). International Journal of Addiction 30:1549-1602. Sampson, P.D., Streissguth, A.P., Bookstein, F.L., and Barr, H.M. (2000). On categorizations in analyses of alcohol teratogenesis, Environmental Health Perspectives, 108 (3):1-15. Streissguth, A.P. (1997). Fetal Alcohol Syndrome: A Guide for Families and Communities. Paul Brooks Publishing Co: Baltimore, MD. Streissguth, A.P. and Kanter, J. (1999) The Challenge of Fetal Alcohol Syndrome: Overcoming Secondary Disabilities. University of Washington Press, Seattle. Tenth Special Report to the US Congress on Alcohol and Health (2000). US Departmentof Health and Human Services (NIH publication number 00-1583). Washington, DC. Thomas, S.E., Kelly, S.J., Mattson, S.N., Riley, E.P. (1998). Comparison of social abilities of children with fetal alcohol syndrome to those of children with similar IQ scores and normal controls. Alcoholism: Clinical and Experimental Research 22:528-533. Zeskind, P.S., Platzman, K., Coles, C.D., and Schuetze, P.A. (1996). Cry analysis detects subclinical effects of prenatal alcohol exposure in newborn infants. Infant Behavior and Development 19(4):497-500.
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