by Anuppa Caleekal B.A. M.Sc.
The pre-natal world of the fetus while cradled in the mother’s womb is sustained in a well-protected environment, although not immune to the influences of its external environment. Fetal Alcohol Syndrome which was first observed by Lemoine et. al (1968) #1 and was later coined by Jones and Smith (1973) #2 in Seattle as the “fetal alcohol syndromeâ€? (FAS). In a broad sense FAS may be viewed as a repercussion of an external environmental influence on the internal physiological environment of the developing fetus. Alcohol acts as a teratogen (derived from the Greek word tera, meaning monster), an agent, which when prenatally exposed can cause serious risks to pre and post natal human development.
Fetal Alcohol Syndrome
(FAS) lies at the extreme end of the continuum of alcohol effects on the fetus with heavy persistent maternal alcohol consumption during pregnancy contributing most significantly to the full blown syndrome. Clinically, three areas are affected:
(1) prenatal and/or postnatal growth retardation (e.g. infants shorter in length and less in weight);
(2) Central Nervous System (CNS) damage such as permanent and irreversible brain damage, learning and behavioral disorders, deficits in memory and attention, hyperactivity, speech and language delays, poor coordination;
(3) head and facial abnormalities (e.g. small head circumference and abnormally small eyes). #3
Fetal Alcohol Effects
(FAE) diagnosed children have deficits in some or one of the above three areas of FAS and their mothers were found to drink smaller daily amounts of alcohol than mothers who had FAS offspring. #4 FAS were previously estimated, as the third most frequent cause of mental retardation after Down’s syndrome and certain neural tube defects. Current prevalence estimates FAS may be the leading most common, preventable cause of mental retardation in North America and Europe. In France, Sweden and North America, prevalence of FAS is 1 per 750 live births per year. #5 It is expected that FAS children will have some degree of mental impairment, ranging from minimal brain dysfunction to severe mental retardation. For every child identified with FAS, there are several others who are affected by alcohol exposure but who lack the full set of characteristics of FAS. FAE is more common than FAS and is estimated to be 3-10 times that of those diagnosed with full FAS. #6 Low birth is an example of FAE. It must be noted that although many other factors can also cause low birth weight, alcohol is said to account for 2% of the decreased birth weight associated with prenatal alcohol exposure. #7 Another example of FAE might be a case where there is some CNS damage, with signs of speech problems or attention deficit disorder, but no apparent facial and head abnormalities. The lack of specific criteria for FAE makes estimation of incidence statistics and diagnosis difficult.
Prenatal Alcohol Exposure
The terms FAS and FAE are not restricted to the fetal stage as the names denote. The fetal stage begins around days 46-48 when the first true bone cells replace cartillage. #8 The period beginning around the 8th week after conception to birth may be viewed as the fetal stage. The embryonic stage is the early period between weeks 2-8 after conception. This stage is marked by cell development or the structural stage in human development. These cells later differentiate to produce tissues and organs, which in turn serve bodily functions, marking the commencement of the fetal stage. After conception, between weeks 4-8, a transitory period from the embryonic to the fetal stage is important as that is a time of great vulnerability to the toxic effects of alcohol. Many of the clinical symptoms of FAS are structural (e.g. facial irregularities which occur in the embryonic stage). Alcohol also affects the pre-embryonic or blastocyst stage resulting in delayed implantation and structural changes. #9 Functional deficits such as damage to the CNS are usually produced at levels of alcohol exposure lower than those which would cause structural changes. Therefore although FAS is found at the adverse end of the continuum of alcohol effects, the progression of its symptoms can begin at any point in the course of prenatal development. Its effects linger postnatally and are for the most part, irreversible. #10
Alcohol and Women: Understanding the Risk
Women Tend to Metabolize Ethanol Faster than Men
Alcohol is soluble in both water and fat, thus it can penetrate all cell membranes and move throughout all body tissues. #11, #12 Passage of ethanol from mother to fetus occurs via the placenta to a point where fetal alcohol concentration is almost equal to maternal concentration. FAS/FAE is then not necessarily the result of only full-blown alcoholism but rather it can result from drinking any amount of alcohol in excess of the level to detoxify it thus placing the fetus at risk. This pattern of high-risk drinking behaviour is usually reflected among those who are considered heavy drinkers, but also may be seen among moderate drinkers who resort to binge-style drinking.
Women generally weigh less and have less body water than men making the volume of distribution of alcohol lower. Consequently blood alcohol levels can be higher in women than men when both have consumed equal amounts of alcohol. Because they frequently experience the same effects as men with less alcohol, women need to be informed of the potential hazards of achieving drinking parity with male drinking companions. Women tend to metabolize ethanol faster than men. #13 Recently it was found that women become intoxicated at a faster rate than men do because their stomachs have less of the “protective stomach enzyme� which is said to breakdown much of the alcohol in the stomach. Because of this lower amount of protective enzyme, more of what they drink enters the bloodstream in the form of pure alcohol. It is said about 30% more alcohol is absorbed into the bloodstream than in men as a consequent of having less of this enzyme known as, alcohol dehydrogenase. Therefore, even when low doses of alcohol are ingested in men and women, due to this decreased stomach metabolism, there is more alcohol availability in women. Over time women are exposed to higher blood alcohol concentrations than men are even though similar quantities of alcohol were ingested. This difference is greater than that explained by body weight and fat content alone. #14
Metabolism and Susceptibility
Studies indicate differential susceptibility to FAS occurring on both a racial and genetic basis. We do not know whether certain ethnic groups have a genetic susceptibility to FAS even though we do know that there are ethnic differences in the metabolism of alcohol. We also know that there is genetic control over the inter – individual variability in the rate of alcohol metabolism. In comparison to Caucasians, the Chinese, Native Americans and Japanese have a higher rate of alcohol metabolism. #15 Animal studies have shown certain strains of mice achieve higher blood alcohol levels (BAL) even though they consume the same amount of alcohol. There is also evidence of racial differences in acute reactions to ethanol in terms of alcohol sensitivity symptoms such as dizziness and hangovers. These were found to be greater among Orientals of Mongoloid heritage and American Indians than in Caucasian subjects when exposed to a mild dose. #15
In this respect it is possible, that fetal susceptibility to alcohol may also be dependent upon maternal racial and genetic compositions interacting with consumption patterns. The basis of these differences remains to be determined.
Consumption and Risk
Occasional drinking patterns, which are not on a daily or continuous basis during pregnancy, is not likely to increase the risk of FAS in offspring. However caution is advised for daily, light to heavy drinkers, as a safe level of alcohol consumption during pregnancy has not yet been established. Research indicates that increases in the amount of alcohol consumed by a pregnant woman increased the severity of alcohol’s effects in the offspring.
Heavily drinking during pregnancy (5 drinks or more daily; average of 3oz. Of pure alcohol per day) places the fetus at high risk for FAS. Risk for cranofacial anomalies, a reliable indicator of FAS, was found to increase with an average intake of 3 drinks daily during the period following conception and before pregnancy is confirmed. #16
Occasional drinking during this period did not increase risk.
Consumption risk factors associated with full FAS include increased number of drinking days, increased daily intake, and positive MAST scores (Michigan Alcohol Screening Test, one of the earliest instruments to detect alcoholism) reflecting an abusive drinking history. In terms of levels of consumption and risk of FAS offspring, the literature indicates that risk for FAS increases as consumption increases over 1oz. absolute alcohol per day.
Increased postnatal risk of clinical abnormality in the child at 4 years of age occurs at an intake of about 2oz. or more of absolute alcohol daily during pregnancy. #17 Neurobehavioral deficits may occur later and may result from lower levels of maternal drinking, and they appear to be more damaging in the long run. Binge drinking (more than 5 drinks on any occasion) and drinking during the first two months of pregnancy is considered to be the two strongest maternal predictors of postnatal neurobehavioral deficits. #16 Deficits include hyperactivity, distractability, speech and language problems.
Alcohol Consumption during Stages of Pregnancy & Severity of Effects
The Trimesters: Blood Alcohol Concentration (BAC), Duration of Exposure and Dose Level
Each trimester of pregnancy marks a stage of fetal development and our understanding of FAS risk needs to be discussed in light of how the timing of fetal development interacts with dosage, duration of alcohol exposure and BAC. In the embryonic stage: the third postconception week of human pregnancy is considered the critical period for teratogenic actions of alcohol to produce the most severe and characteristic features of FAS. Drinking an average of 3 drinks/daily during the period following conception and just before pregnancy is confirmed, increases the risk of having a FAS child. Occasional drinking during this period did not increase risk.
The nervous system develops in the first 8 weeks, making the most damaging effects result in this period. Although damage to the brain may occur in the last trimester as well, vulnerability to brain damage is highest at 15-25 days. #18 There are also two periods of rapid brain growth in the 3rd month and from the 6th month to after birth. The CNS, heart, eyes, legs, arms, teeth, ears, palate, external genitalia are vulnerable to alcohol in the first trimester.
Malformations common to these areas suggest that structural damage commence early.
Research indicates that among heavy drinkers who continued drinking throughout pregnancy had offspring with higher incidence of birth defects than those who reduced or abstained in the 3rd trimester. #19 Women who drink moderately throughout pregnancy have also been found delivering offspring with adverse outcomes such as an increase in neurobehavioral problems even in absence of physical facial anomalies of FAS. #20 Those who drank at moderate levels and discontinued alcohol use at mid pregnancy fared better than continuous drinkers. Research findings indicate the peak BAC increases likelihood of aberrant brain growth. A key factor in determining severity of FAS effects may be peak BAC during the third trimester when it is a critical period for brain development. Peak BAC can significantly affect the minimum dose necessary for producing FAE. #21 Conditions such as binge drinking which affect peak BAC should be curtailed during pregnancy. Clarren’s data on animal studies indicate binge type alcohol exposure can alter brain function without physical malformations and this occurs early in gestation. #9
Peak BAC and Breast Feeding
Reaching peak BAC has implications also for breast-feeding. Although the amount of alcohol ingested by infants through breast milk is low even when a mother consumes as many as 4 drinks daily, it is sufficient to cause slight motor delay. No effect on mental development of fetus was found at this dosage. Drinking regularly while breast feeding increases the child’s risk of impaired motor development. #22 Alcohol use during breast-feeding also inhibits prolactin hormone necessary to maintain lactation. Alcohol use during pregnancy at moderate levels may impair child’s sucking reflex at birth. Blood alcohol level threshold slightly below the legal human intoxication level in the mother results in problems in maintaining lactation. #23 These problems in feeding inevitably affect the growth of the infant.
Implications for Alcohol Education
The importance of understanding the metabolism of alcohol in women and how it differs in men, ethnic groups poses implications on what direction preventive alcohol education should take.
Alcohol education targeted to women needs to explain primary differences between female and male metabolic processes of alcohol consumption and its consequences on individual personal health. The next task in alcohol education is to disseminate to women of childbearing age, the potential of alcohol as a teratogen to the embryo and that FAS and FAE are preventable. As a safe level of alcohol consumption during pregnancy has not yet been established, abstinence from drinking while pregnant remains to be the best precaution, yet not an adequate one, especially for those women who do not know they are pregnant until weeks later. This ultimately asks for looking for common denominators in alcohol education when designing programs for women of the childbearing age.
Guidelines are needed to address sex and drinking as one variable when they occur as a combination of two variables acting as one independent variable in a social act or exchange between individuals similar to the act of drinking and driving. The trend towards increased consumption and early sexual activity and teenage pregnancies places teenage girls at a high-risk group for delivering offspring with FAS. The inclusion in alcohol education programs of the potential important role contraception plays in the prevention of FAS/FAE is central to targeting women of the child bearing age. As a depressant, alcohol can do away with inhibition, which can in turn be conducive to sexual activity without the use of contraceptives. A Scottish study which examined contraceptive use and drinking among teenage men and women, found a decline in contraceptive use when intercourse was preceded by alcohol consumption. #24
There is then the need to address possible outcomes: planned and unplanned pregnancies in the realm of preventing the risk of having FAS/FAE offspring, along with the importance of contraceptive use especially since research findings have not yet determined a safe level of alcohol consumption during preconception and pregnancy.
Among alcoholic women prevalence of FAS has been estimated at 21 to 29 per 1000 births. A woman who has had a FAS child may have a recurrence risk as high as 25% more than the normal population. This risk increases as she continues to reproduce, being 85 times more frequent in older siblings of FAS children (170 per 1000) and 350 times (771 per 1000) more frequent in younger siblings of FAS children than in the general population. #5
Alcohol drinking patterns and its interaction with socialization and sexual experimentation usually gets formalized in the teen years and progresses into the college and university settings. The inclusion of FAS in alcohol education programs at the high school and university/college level would be vital preventative education for both male and females. Although much attention in the research has been placed on maternal exposure to alcohol, there is some speculation that the vulnerability of faulty cell development in FAS may extend to the sperm and not just the female germ cells. #9 We know that semen of alcoholics have shown to have aberrant sperm forms resulting in low birthweight as it occurs in a significantly greater number of offspring of “regular drinking fathers�. #25, #26
The preventive goal of alcohol education with the inclusion of topics on FAS and FAE would best be served if integrated into relevant disciplines in the school and university curricula. Life skills learned in planning a family and in producing offspring integral to a nation’s development of qualitative future human resources would also enable individuals to take responsibility of their own well-being and of others.
copyright Anuppa Caleekal
References
1. Lemoine, P. et al Les enfants des Parents Alcoliques: Anomalites Observees�, Quest Med, 25; 476- 482, 1968 cited in Warner, R.W., and Rosett, H.L., The Effects of Drinking on Offspring: An historical survey of the American and British Literature�, Journal of Studies on Alcohol, 36; 1395-1420, 1975.
2. Jones, K.L. and Smith, D.W., Recognition of the Fetal Alcohol Syndrome in early Infancy�, Lancet, 2: 999 – 1001, 1973.
3. Ashley, M., “Drinking by Mothers to be: A Discussion for Public Health Professionals�. Information Review, ARF, Toronto, 1979
4. Clarren, S.K. “FAS: Diagnosis, Treatment and Mechanisms of Teratogenesis�, Transplacental Disorders: Perinatal Detection, Treatment and Management, Alan R. Liss Inc., 1990
5. Burd, L. and Martsolf, J.T. “ Fetal Alcohol Syndrome; Diagnosis and Syndromal Variability�, Physiology and Behaviour, 46: 39-43, 1989.
6. Smith, I.E. et al, “Identifying high Risk Pregnant Drinkers; Biological and Behavioural Correlates of Continuous Heavy Drinking During Pregnancy�, in Journal of Studies on Alcohol, 48; 4, p.304, 1987.
7. Abel, E.l. and Sokol, R.J. “ A Revised Conservative Estimate of the Incidence of FAS and its Economic Impact. “Alcoholism: Clinical and Experimental Research, Vol. 15, no.3.” May/June 1991, 514 – 524.
8. Tittmar, H.G. ed. Advanced Concepts in Alcoholism, Pergamon Press, P.6. N.Y., 1982
9. Cervantes, L. “ Not for women Only FAS�. Alcoholism, Nov/dec., 1984.
10. Nutrition Today Teaching Aid, “ The Fetal Alcohol Syndrome�, U.S.A.
11. Abel, E.L., “ Fetal Alcohol Syndrome and Fetal Alcohol Effects’. New York Plenum Press, p.37, 1984.
12. Marsland D., Principles of Modern Biology, Holt, Rinehart & Winston Publishers, N.Y., 1964.
13. Harding, S.C. and Wilson, J.R., “Ethanol Metabolism in Men and Women�, Journal of Studies in Alcohol, 48; 4, 1987.
14. ISI Press Digest, “ Alcohol in Men and Women Understanding the Difference�, 11: March 11, 1990. p.8,9.
15. Agarwal, D.P. and Goedde, H.W. “Ethanol Oxidation: Ethnic Variations in Metabolism and Response�. Ethnic Differences in Reactions to Drugs and Xenobiotics, Alan R. Liss. Inc, 1986, p.99-112.
16. Haase, T.B. ed., Alcohol, Tobacco, and other drugs may harm the Unborn. U.S. Dept. of Health and Human Services, 1990.
17. Streissguth, A.P., “ Psychological and Behavioural effects in Children Prenatally Exposed to Alcohol�, in Alcohol Health and Research World, Fall, 10: 1, 1985
18. Santrock, J.W., Life Span Development, Brown Publishers, 1986.
19. Royal College of Physicians: The Working Party on Alcohol (1987) cited in Oppenheimer, E., “ Alcohol and Drug Misuse Among Women: An Overview”, British Journal of Psychology, 158 (Suppl.10), 36-44, 1991.
20. Coles, C.D. et al “ Neonatal Neurobehavioural Characteristics as Correlates of Maternal Alcohol Use During Gestation”, Alcoholism Clinical Experimental Research 9: 454 – 460, 1985.
21. Pierce, D.R., West, J.R., “ Blood Alcohol Concentration. A Critical factor for Producing FAE’, Alcohol, 3: 269 – 272,1986.
22. Little, R.E., Anderson, K.W., “ Maternal Alcohol Use during Breast Feeding and Infant Mental and Motor development at One Year�, New England Journal of Medicine, 321; 425-430, Aug. 17, 1989.
23. Subramanian, M.G. et al “ Alcohol Inhibition of Suckling – Induced Prolactin Release in Lactating Rats: threshold evaluation�, Alcohol, 8: 203-206, 1991.
24. Robertson, J.A. and Plant, M.A., “ Alcohol, Sex and Risks of HIV Infection�, Drug and Alcohol Dependence, 22,p.75-78, 1988.
25. Gallant, D.M., “ Cytological Abnormalities in Sperm of Alcoholics�, in Alcoholism: Clinical and Experimental Research, 16: 5, Sept./Oct.1986.
26. Little, R.E., Sing, C.F., “ Association of Fathers Drinking and Infants birthweight�, Lancet, 1: 1644-1645, 1986.
Other Publications by Anuppa Caleekal
Other Research Publications and Reports in Alcohol Education by Anuppa Caleekal
1. Caleekal, Anuppa. 1991. Working Paper on Alcohol and Pregnancy : A Literature Review and Operational Guidelines for High School Teachers Teaching Aid “, Health Promotions Branch, Homewood Health Services, Canada.
2. Caleekal-John, Anuppa and Pletsch, D.H. 1984. ” An Interdisciplanary Cognitive Approach to Alcohol Education in The University Curriculum, Journal of Alcohol and Drug Education, Volume 30, No. 1
3. Goodstadt, M.S. and Caleekal-John, Anuppa. 1984.” Alcohol Education programs for University Students. A Review of their Effectiveness. International Journal of the Addictions, November, Volume 19 (7)
4. Caleekal-John, Anuppa and Goodstadt, M.S. 1982. ” Alcohol Use and Its Consequences Among Canadian University Students. Canadian Journal of Higher Education, Volume X11. No 2.
5. Caleekal-John, Anuppa. 1982. “Perceived Needs Regarding Alcohol Problems and Alcohol Education Programs on Ontario University Campuses”. Addiction Research Foundation Substudy, Education Research Section, Toronto.
6. Caleekal-John, Anuppa. 1982. An Approach to Alcohol Education in Universities. M.Sc Thesis, University of Guelph, Canada. (Supervisor Dr. D.H. Pletsch, Chairman, Department of Rural Extension Studies, University of Guelph, Canada
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