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Women, Alcohol and Pregnancy

"I am an alcoholic woman and I am terribly afraid about what I have done to my baby."

Alcoholism is not well understood in the general population , let alone the differences in how alcoholism may differ in men and women. Over the past decade, however, research on alcoholism has increased, and although many questions remain, a better idea of the problem is coming to light. As more conclusions from numerous research studies are shared, it is apparent that:

1. The physiologic effects of alcohol use in women are more devastating than in men. Women are more susceptible the detrimental physiologic effects of alcohol with more rapid intoxication and more rapid development of liver disease.

2. There is a high correlation of co-morbidity with depression and abusive environments and alcohol use in women. Women are more likely to be "social victims" of another's alcohol problem. In one review of literature, alcohol abuse was involved in about half of the wife beating cases cited in the literature. Numerous studies have also reported that over half of women who abuse alcohol had a history of sexual abuse. It has been shown, too, that major depression is the most common primary diagnosis in women with secondary alcoholism.

3. The risk to the fetus associated with prenatal exposure has been well documented over the last twenty years. Fetal Alcohol Syndrome (FASD) results from the teratogenic effects of exposure to alcohol during fetal development. The risk varies for different women depending on many factors. Pattern of drinking, parity, the age of the woman, nutritional status, and genetic sensitivity are just a few of the risk factors that have been identified.

4. To further complicate the problem, limited resources are available to address the needs of women who abuse alcohol. Many cities and towns have drug abuse facilities that operate at capacity. However, for women who are pregnant in Alaska priority admission to State approved treatment programs is required. These women have prenatal care needs that can be managed by most drug treatment programs. Many women face obstacles including threat of legal action, absence of child-care, absence of insurance, and lack of transportation. These serve as barriers to women receiving appropriate treatment services.

Fetal Development & Maternal Drinking

T he following information was obtained from Ninth Special Report to the U.S. Congress on Alcohol and Health, June 1997(RP0973). Free copies of this report are available from National Clearinghouse for Alcohol and Drug Information, 1-800-729-6686.

E xperimental research has confirmed the teratogenic effects of alcohol ; however, studies have yet to reveal fully how the timing of a mother's drinking and the duration of a fetus' exposure disrupt particular stages of fetal development. In general, researchers theorize that because fetal development is sequenced throughout pregnancy, alcohol exposure at certain periods and doses during pregnancy will determine the defects observed in a child at birth and beyond. Determining the exact stage of exposure and specific dose that is associated with particular defects can be challenging in clinical studies because maternal consumption levels and timing of use are provided by the relatively inaccurate measure of a mother's self-report.

In animal studies, researchers can control for the numerous variables encountered in clinical studies (e.g., varying patterns and levels of drinking throughout pregnancy confounding factors such as smoking and nutrition), thus enabling more precise measures of the effects of alcohol at various levels and periods of exposure. Findings from these studies suggest that first-trimester exposure is associated with dysmorphic and neurological damage (Sulik and Johnston 1983). However, the central nervous system (CNS) is sensitive to alcohol exposure during a prolonged developmental period and, thus, can be affected even when exposure occurs only during the later part of pregnancy (Miller 1992; West and Goodlett 1990). The pattern of exposure also is an important factor. A recent animal study by Goodlett and Peterson (1995) demonstrated that binge-like exposure to alcohol during particular periods of gestation caused specific structural and behavioral deficits in the fetus.

As noted earlier, findings from several longitudinal clinical studies indicate that first-trimester exposure to alcohol is associated with craniofacial anomalies in children (Coles et al. 1985; Day et al. 1989; Ernhart et al. 1987; Graham et al. 1988). According to these studies, prenatal exposure also adversely affects growth. Findings from these studies, however, have been inconsistent in terms of periods of exposure that are critical to this outcome. Such inconsistencies may arise due to varying doses of exposure and postnatal stressors, including home environment and nutrition, in the different longitudinal studies. Day et al. (1989) reported that women in the Pittsburgh study who drank during the first or second trimester or both were at increased risk of having a low birth-weight infant. Deficits in length and head circumference measurements at birth also were associated with early first-trimester drinking. In the Atlanta study, neonatal growth deficits were observed in infants born to women to drank throughout pregnancy; however, children born to women who stopped drinking at the beginning of the second trimester approached the level of growth of non-alcohol-exposed infants (Coles et al. 1985). Coles (1994) suggests that, based on these findings, growth deficits at birth may occur when a mother drinks during the third trimester of pregnancy-a time when the fetus is growing rapidly. However, stopping alcohol used later in pregnancy may allow an adversely affected fetus to catch up on growth.

Some results indicate that timing of in utero exposure to alcohol also may affect postnatal growth. Findings from the Pittsburgh study suggest a relationship between alcohol exposure in later pregnancy and growth deficits in children examined at 8 months (Day et al. 1990), 18 month (Day et al. 1991a), 3 years (Day et al. 1991b), and 6 years (Day et al. 1994). The Detroit study, in a follow up examination of children at 6 months of age, reported similar findings (J.L. Jacobson et al. 1994b). Data from the Atlanta study showed that weight and stature of school-age children (5 to 7 years) exposed to alcohol throughout pregnancy were similar to measurements in non-alcohol-exposed children; however, deficits in head circumference observed at birth in the children exposed to alcohol persisted at the time of reexamination. This effect is consistent with findings from animal studies that noted deficits in head circumference of animals exposed to alcohol during the brain growth spurt (West and Goodlett 1990).

Results from longitudinal studies also have demonstrated critical periods of exposure for alcohol-induced neurobehavioral effects . In a longitudinal study of children born to women treated in Helsinki prenatal clinic, investigators found that during the 2-year follow up of the children, heavy alcohol exposure in the first trimester alone had no definite effect on mental or language development (Autti-Ramo et al. 1992). Exposure to heavy use during the first and second trimesters, however, increased the occurrence of delayed language development in the children . Similar observations were reported in the Atlanta study (Coles et al. 1991). School-age children (5 to 8 years) whose mothers had continued to drink throughout pregnancy had poorer sequential information processing and academic achievement than those whose mothers stopped drinking in the second trimester. Problems were noted in short-term memory, math skills, and decoding of letters and words. The lack of effects in the Pittsburgh sample as measured by the Bayley Scales (Richardson and Day 1991; Richardson et al. 1989) also suggests that neurobehavioral effects are more likely related to exposure to alcohol later in pregnancy. In this group, a high proportion of women reported moderate first-trimester drinking, yet very few drank at moderate or heavy levels during the second or third trimesters. Moderate first-trimester exposure also apparently was not sufficient to produce Bayley deficit.


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