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
, 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
1. The physiologic
effects of alcohol use in women
than in men. Women are more susceptible the detrimental physiologic
effects of alcohol with more rapid intoxication and more rapid development
of liver disease.
is a high correlation of co-morbidity with depression
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.
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.
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.
& Maternal Drinking
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.
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
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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