Alcohol has been found to be acutely toxic to the fetus
independently of the effects of malnutrition. A safe level cannot be
defined—any alcohol during pregnancy is dangerous.
In 1973, Kenneth L. Jones and David W. Smith from the University of
Washington School of Medicine in Seattle, Washington reported a syndrome
associated with alcohol in pregnancy. They coined the term "fetal
alcohol syndrome" (FAS) to describe a pattern of abnormalities
observed in children born to alcoholic mothers.
Alcoholism the Major Cause
It was originally postulated that malnutrition might be responsible
for these defects. However, the pattern of malformation associated with
FAS is not seen in children born to malnourished women, and alcohol has
been found to be acutely toxic to the fetus independently of the effects
of malnutrition.
Criteria for defining FAS were standardized by the Fetal Alcohol
Study Group of the Research Society on Alcoholism in 1980. Ernest L.
Abel and Robert J. Sokol published an article in Drug and Alcohol
Dependence in 1987 entitled "Incidence of Fetal Alcohol Syndrome
and Economic Impact of FAS-Related Anomalies." This article was
a comprehensive review of the data as we know it up until the late 1980’s.
In 1989, modifications to the manifestations of FAS were proposed by
Sokol and Sterling K. Clarren. The proposed criteria were:
- Prenatal and/or postnatal growth retardation (weight and/or length
below the 10th percentile).
- Central nervous system involvement, including neurological
abnormalities, developmental delays, behavioral dysfunction,
intellectual impairment, and skull or brain malformations.
- A characteristic face with short palpebral fissures (eye
openings), a thin upper lip, and an elongated, flattened midface and
philtrum (the groove in the middle of the upper lip).
Sokol and Clarren suggested the term "alcohol-related birth
defects" (ARBD) to describe anatomic or functional abnormalities
attributed to prenatal alcohol exposure. The term "possible fetal
alcohol effect(s)" (FAE) indicates that alcohol is being considered
as one of the possible causes of a patient's birth defects. In the view
of Sokol and Clarren, the frequent use of this term to indicate a birth
defect judged milder than FAS is incorrect, although others continue to
use it that way.
Mental handicaps and hyperactivity are probably the most debilitating
aspects of FAS, and prenatal alcohol exposure is one of the leading
known causes of mental retardation in the Western World. Problems with
learning, attention, memory, and problem solving are common, along with
incoordination, impulsiveness, and speech and hearing impairment.
Deficits in learning skills persist even into adolescence and adulthood.
It is generally accepted that the adverse effects of prenatal alcohol
exposure exist along a continuum, with the complete FAS syndrome at one
end of the spectrum and incomplete features of FAS, including more
subtle cognitive-behavioral deficits, on the other. Thus, infants with
suboptimal neurobehavioral responses may later exhibit subtle deficits
in such aspects of daily life as judgment, problem solving, and memory.
Alcoholics and Alcoholism Cited in Study
Catchment data on the incidence of FAS are derived from the Birth
Defects Monitoring Program of the Centers for Disease Control (CDC).
Based on data from 1,500 hospitals, CDC reported the nationwide
incidence of FAS to be 0.3-0.9 per 10,000 births (excluding Native
Americans). In contrast, Abel and Sokol surveyed 19 published
epidemiologic studies worldwide. The overall rate from all studies was
1.9 cases per 1,000 live births. The average for retrospective studies
surveyed by Abel and Sokol was 2.9 per 1,000, compared with 1.1 per
1,000 for prospective studies. Most reported cases in the United States
came from study sites where the mothers were black or Native American
and of low socioeconomic status. The estimated rate at these sites was
2.6 per 1,000 compared with 0.6 per 1,000 from other study sites, where
the mothers were predominantly white and of middle socioeconomic status.
According to the CDC catchment study, incidences of FAS per 10,000
total births for different ethnic groups were as follows: Asians 0.3,
Hispanics 0.8, whites 0.9, blacks 6.0, and Native Americans 29.9.
Because of differences in study design, the ratios among the various
ethnic groups derived from the CDC catchment data cannot be used to
estimate FAS incidence for different ethnic groups as obtained from
prospective and retrospective studies. Among Native Americans, the
incidence of FAS varies among different cultures. Health units serving
principally Navajo and Pueblo tribes report an FAS prevalence similar to
that for the overall U.S. population, while for Southwest Plains
Indians, a much higher prevalence was reported (1 case per 102 live
births). Several factors, such as cultural influences, patterns of
alcohol consumption, nutrition, and metabolic differences have been
suggested to play a role in this difference.
In the case of blacks, the risk of FAS remains about sevenfold higher
than for whites, even after adjustment for the frequency of maternal
alcohol intake, occurrence of chronic alcohol problems, and parity
(number of children borne). This raises the question of some kind of
genetic susceptibility, the nature of which is unknown.
Apart from epidemiology, the key questions in FAS research include,
How much alcohol is too much? and, When is the fetus at greatest risk?
The major problem in addressing these questions is the lack of a
specific physiological measure that accurately reflects alcohol
consumption. There is no biological marker currently available to
measure alcohol intake, and self-reports of alcohol consumption may be
unreliable, perhaps especially so during pregnancy. Morrow-Tlucak and
colleagues found that women with more-serious alcohol-related problems
are those more likely to underreport their alcohol consumption when
interviewed during pregnancy.
Alcoholism and Alcoholics Not the Only Causes
While it is apparent that children who meet the criteria for FAS are
born only to those mothers who consume large amounts of alcohol during
pregnancy, studies have reported neurobehavioral deficits and
intrauterine growth retardation in infants born to mothers who
reported themselves to be moderate alcohol consumers during pregnancy.
In a prospective study of 359 newborns, Ernhart and colleagues found a
trend toward increasing head and facial abnormalities with increasing
embryonic alcohol exposure. An effect occurred at even the lowest
reported levels of alcohol intake, so that a clear threshold (minimum
amount of alcohol to produce an effect) could not be defined.
Given the range of defects that result from prenatal alcohol
exposure, the search for an overall threshold for fetal risk may be
unreasonable. Instead, each abnormal outcome in brain structure and
function and growth might have its own dose-response relationship.
Animal research has shown that different profiles of alcohol-related
birth defects are related to critical periods for specific aspects of
fetal development. Thus, heavy alcohol consumption throughout pregnancy
results in a wide variety of effects characteristic of FAS, while
episodic binge drinking at high levels results in partial expression of
the syndrome, with the abnormalities being unique to the period of
exposure. Vulnerability of individual organ systems may be greatest at
the time of their most rapid cell division.
An important strategy for preventing alcohol-related birth defects is
the development of better screening techniques to identify women at high
risk for heavy alcohol consumption throughout their pregnancy. Currently
available laboratory tests for detecting biochemical markers of heavy
drinking are not as sensitive as self-report screening instruments,
whereas the latter are complicated by denial.
A possible way to overcome denial might be to inquire about past,
rather than present, drinking. This is suggested by the results of a
study showing that self-reports of first trimester drinking made at the
seventh month of pregnancy are often higher than those made at the
fourth month. The researchers suggested that women may feel safer
reporting higher levels of drinking farther away from the event.
Although this strategy may not reveal a drinking problem until
relatively late in pregnancy, intervention at this time is still useful.
While abstaining during the second trimester does not eliminate the risk
of fetal abnormalities, it does seem to mitigate some of the behavioral
effects that may occur shortly after birth.
Sokol and colleagues developed a simple and brief questionnaire to
help circumvent denial and underreporting of heavy drinking by pregnant
women. The test instrument, referred to as T-ACE, correctly identified
69 percent of the "risk drinkers" (defined as those consuming
1 ounce of absolute alcohol per day, equivalent to two standard drinks
per day) out of a cohort of 971 pregnant women. T-ACE was found to be
superior to other standard instruments used for detecting alcohol abuse,
such as MAST and CAGE. The test is brief, and may be administered easily
in prenatal clinics and obstetricians' offices. Its key feature is a
tolerance ("T") question, "How many drinks does it take
to make you feel 'high?' " (Tolerance is acquired by drinking.)
Clinical experience suggests that questions about tolerance are less apt
to be perceived by lay persons as an indication of drinking, and are
therefore less likely to trigger denial. A more reliable indicator of
heavy drinking awaits the development of objective biochemical markers.
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