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CHAPTER

9

EFFECTS OF ALCOHOL ON FETAL AND POSTNATAL DEVELOPMENT

Introduction

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n 1968 in France (Lemoine et al. 1968) and in 1973 in the United States (Jones and Smith 1973; Jones et al. 1973), investigators first described in published reports the common pattern of birth defects observed in children born to alcoholic mothers. The distinct cluster of defects was labeled "fetal alcohol syndrome" (FAS) (Jones and Smith 1973). Since these reports, studies have established that alcohol is a physical and behavioral teratogen (an agent that produces defects in offspring in utero). It is generally agreed that in utero alcohol exposure can produce a spectrum of deleterious effects that exist along a continuum, ranging from gross morphological anomalies and mental impairment (including mental retardation) to more subtle cognitive and behavioral dysfunctions.

The minimal criteria for diagnosing FAS are (1) prenatal and postnatal growth retardation; (2) central nervous system (CNS) involvement, such as neurological abnormalities, developmental delays, behavioral dysfunction, intellectual impairment, and skull or brain malformations; and (3) 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 1989) (see figure 1). For those individuals who have only some of the attributes of FAS, the terms "fetal alcohol effects" (FAE) and "alcohol-related birth defects" (ARBD) are used (Clarren and Smith 1978; Sokol and Clarren 1989).

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Epidemiology of Fetal
Alcohol Syndrome

Efforts to obtain precise estimates of the incidence and prevalence of FAS are complicated by several factors. One problem stems from difficulties associated with diagnosing FAS (e.g., the facial features associated with the syndrome are difficult to recognize in the neonatal period, and CNS dysfunction may not be identified until several years after birth). Often only the most severely affected children are diagnosed readily at birth, and many FAS cases go undetected (Abel and Sokol 1987; Little et al. 1990; Sokol and Clarren 1989). A recent study by Little et al. (1990) provides evidence that underreporting of FAS may be significant. After studying the records of 40 infants born to 38 mothers known to have abused alcohol during pregnancy, the investigators found that medical personnel failed to identify alcohol-related injuries in any of the children who were subsequently identified as having FAS or FAE, even though maternal alcohol abuse was documented in the records. Because FAS is underreported in medical records, it is difficult to estimate its incidence reliably on the basis of this source of data. Similar concerns apply to registries of birth defects, which obtain most of their data from medical records.

Characteristics of the sample population can also affect estimates of FAS incidence rates. For example, if high-risk groups are overrepresented in the sample population, estimates based on these data may not be representative of the population at large.

On the basis of surveys of 19 published worldwide epidemiological studies on FAS frequency, Abel and Sokol (1987) estimated the incidence of FAS to be 1.9 cases per 1,000 live births. In a more recent analysis, however, these investigators revised their estimate to 0.33 FAS cases per 1,000 live births (Abel and Sokol 1991). The significant disparity in these rates may be due to methodologies employed in the more recent study, including the exclusion of data for some high-risk groups (e.g., Native Americans) and the use of medical records and registries of birth defects as a data source for various populations. In addition, because one of the primary objectives of the more recent study was to determine a conservative annual cost estimate for FAS in the United States, the estimated incidence rate from this study is a probable lower limit assessment of FAS frequency. Because of limitations in available data, current incidence estimates are only

approximate measurements of the magnitude of the problem.

Epidemiological studies suggest that some populations are at greater risk for this syndrome. Among African Americans, the risk for FAS is approximately seven times that of whites (Sokol et al. 1986). Rates as high as 10 per 1,000 (May et al. 1983) among some Native American populations and 120 per 1,000 (Robinson et al. 1987) among Canadian Indians have been reported in certain communities where alcohol abuse is rampant. However, prevalence varies considerably among different Indian communities.

Risk Factors for Fetal
Alcohol Syndrome

FAS has been identified only in children born to mothers who drank heavily while pregnant. Although such drinking increases the risk for FAS in offspring, not all women who drink excessively during pregnancy give birth to children. with FAS (Sokol et al. 1980).

Although the reasons for the apparent variability in risk are not fully understood, studies suggest that various biological and environmental factors, along with the amount and timing of prenatal alcohol intake, may govern vulnerability to FAS and FAE. Human and animal studies have shown that increasing age and parity of the mother may confer a heightened risk for alcoholinduced birth defects in offspring (Abel 1984; Abel and Dintcheff 1986; Abel and Greizerstein 1982). Individual differences in maternal metabolism of alcohol during pregnancy may also contribute to inconstant susceptibility to FAS and FAE (Brien et al. 1983). Finally, women who have been chronic heavy drinkers may pattern their drinking to maximize alcohol's intoxicating effects and may have a reduced capacity to metabolize alcohol (Frezza et al. 1990); both factors may increase the risk for fetal injury.

Genetic factors are also believed to influence vulnerability to FAS and FAE. Animal studies using various inbred rodent strains (Chernoff 1980; Goodlett et al. 1989) or selectively bred mice (Gilliam and Irtenkauf 1990) have demonstrated genetic differences in vulnerability to a given amount of alcohol exposure. In humans, differences in prenatal alcohol effects between dizygotic (fraternal) twins suggest that genotype may contribute to vulnerability for FAS (Chasnoff 1985; Christoffel and Salafsky 1975).

Researchers have used proxy measures, such as levels of alcohol consumption among pregnant women, to estimate the number of women who are at risk for having children with FAS. In a recent study, Serdula et al. (1991) examined trends in alcohol consumption in a large sample of American women. These investigators found that the prevalence of drinking among pregnant women declined over a 4-year period (1985–88) from 32 percent in 1985 to 20 percent in 1988. For those pregnant women who drank, however, the median number of drinks consumed per month did not change. Moreover, no decline in alcohol consumption was observed in populations of pregnant women who were less well educated, smokers, unmarried, or under the age of 25 years—a population that may already be at increased risk for poor pregnancy outcome.

Data on alcohol consumption among women of childbearing age, which can serve as an indicator of levels of drinking prior to recognition of pregnancy, may provide some measure of the number of women who may be at increased risk for having offspring with FAS or ARBD. Data from the 1988 Alcohol Supplement of the National Health Interview Survey indicate that of the 52 million women in the United States aged 18 to 44 years, 1.7 million drank two or more drinks per day (Alcohol Epidemiological Data System) and therefore were in the at-risk population.

Followup of Individuals
With Fetal Alcohol
Syndrome

Several investigators have followed the physical and developmental characteristics of individuals diagnosed with FAS. Their assessments have been limited largely to case series of children diagnosed with FAS at birth and therefore are based primarily on a selection of individuals who are severely impaired. In addition, because most of these clinical studies have not included control groups, it is difficult to assess whether the injuries observed resulted solely from alcohol or from alcohol combined with other risk factors.

Findings from followup assessments of case reports have shown that although many of the physical characteristics of FAS become less prominent with maturity, cognitive-behavioral deficits appear to endure with age (Spohr and Steinhausen 1987; Streissguth et al. 1985). Defi

cits include substantially reduced IQ and a multitude of behavioral disorders, as measured by neuropsychological assessment and psychological testing.

Children with FAS and FAE are frequently described as hyperactive, distractible, impulsive, and having short attention spans (Aronson et al. 1985; Streissguth et al. 1984, 1985)-behaviors that are similar to those observed in children with attention deficit disorder (ADD). Nanson and Hiscock (1990) compared activity level and attention in a group of children with FAS or FAE (ages 5 to 12 years) with the same features in both a group of children diagnosed with ADD and a control group. They found that the FAS or FAE children were more intellectually impaired (as measured by IQ score) than children in the ADD and control groups. However, laboratory measures of attention (performance on reaction time and vigilance tests) indicated that attentional problems in children with FAS or FAE were similar to those in children with ADD. The investigators proposed that treatment strategies designed to facilitate attention and learning in ADD children may benefit children with FAS or FAE.

Children with FAS and FAE are frequently described as hyperactive, distractible, impulsive, and having short attention spans-behaviors that are similar to those observed in children with attention deficit disorder (ADD).

Whereas most followup studies of clinical reports have focused primarily on preadolescent patients with FAS or FAE, Streissguth et al. (1989, 1991) reported on the manifestations of FAS and FAE in adolescents and adults. Included in this study were 43 adolescents (12 to 17 years old) and 18 adults (18 to 40 years old), of whom 74 percent were Native American, 21 percent were white, and 5 percent were African American. Seventy percent of the sample had been diagnosed in childhood with FAS and the remaining patients were described as having FAE. All of the mothers either were alcoholic or were known to have abused alcohol during pregnancy.

Most of the characteristic facial anomalies of FAS had become less distinctive in older patients, yet abnormalities of the upper lip and

small eye openings (palpebral fissures) remained important discriminating features. Short stature and microcephaly (small head) persisted with age.

Cognitive-behavioral handicaps were also present in adulthood (Streissguth et al. 1991). The average IQ score for the combined FAS and FAE group was 68; IQ scores were lower for individuals with FAS than for those with FAE. Deficits were noted in reading and spelling; however, deficiencies in arithmetic skills were the most characteristic academic disability. Older patients did not function better academically than younger ones, and patients with FAE did not perform significantly better on academic achievement tests than those with FAS (Streissguth et al. 1989). Attention deficits and problems with judgment, comprehension, and abstraction were the most common behavioral problems (Streissguth et al. 1991).

Because a number of these individuals came from unstable family environments, the deficits observed may have resulted from prenatal exposure to alcohol combined with other factors in the rearing environment. It is important to note that many of the individuals included in this study were selected from clinical caseloads. Therefore, the continuing problems observed in these individuals do not necessarily represent the entire spectrum of outcome for persons with FAS or FAE. Nonetheless, the studies mentioned above indicate that the multitude of effects associated with FAS and FAE may extend well beyond the early developmental stages of life.

Prospective Longitudinal
Studies

Studies have confirmed that mothers who drink heavily during pregnancy have an increased risk for offspring with FAS. Yet FAS is a consequence that represents the severe end of a continuum of alcohol-related neonatal injuries. Children exposed prenatally to alcohol exhibit a wide spectrum of adverse outcomes that range from FAS to more subtle neurobehavioral and cognitive impairments. In contrast to the followup assessments described above, prospective longitudinal studies with large cohorts can assess the full range of alcohol-induced neonatal impairments. Longitudinal studies enable researchers to measure maternal drinking as well as other factors that may influence prenatal and postnatal devel

opment and to examine the effects of these factors on offspring.

A number of prospective longitudinal studies conducted in the United States and Canada have contributed to current knowledge of the relationship between prenatal alcohol exposure and fetal development (see reviews by Russell 1991 and Day in press). Among these studies are the Seattle Longitudinal Study on Alcohol and Pregnancy, the Buffalo Women's Health Study, the Ottawa Prenatal Prospective Study, the Cleveland Prospective Alcohol-In-Pregnancy Study, the Georgia Alcohol and Pregnancy Research Project (Atlanta), and the Pittsburgh Maternal Health Practices and Child Development Study. This section will focus primarily on findings from these six studies.

Each of these studies used various test batteries to examine physical and neurobehavioral characteristics of offspring at birth and at various stages of postnatal development. Although many similar findings have emerged from these studies, some findings have been inconsistent. Such disparity is not unexpected, given the diversity of approaches used to probe the effects of fetal alcohol exposure. Recruitment and followup procedures differ, maternal sociodemographic characteristics and drinking patterns vary among the cohorts, diverse techniques for measuring maternal drinking are used, the timing and number of these measurements vary, and analytical techniques, including the selection and treatment of potentially confounding variables, are dissimilar. (See table 1 for a summary of methodologies used in each study.) Factors such as alcohol dosage, potency, timing of exposure, and exposure to other drugs may influence pregnancy outcome (Little and Streissguth 1981).

Growth Deficits and Physical Anomalies

In general, most of the studies that assessed dysmorphology reported an increased rate of FAS-associated birth anomalies among children born to heavier-drinking mothers. Studies that examined older children for these anomalies found that the relationship of anomalies to prenatal alcohol exposure persisted. Most of the studies reported that prenatal alcohol exposure was related to growth deficits at birth.

In the Seattle study, the population examined consisted predominantly of white middle-class women who were recruited in their fifth month of pregnancy. Among drinking women, average

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* AA = Absolute alcohol per day in ounces; 1 ounce is equal to approximately two drinks.

+ One woman had an AAP value of 34.8; this was reduced to the next highest level, 10.8. Without this adjustment, mean AAP = 0.9 (SD 3.5, median 0.5).

SOURCE: Russell 1991. Reprinted by permission of the publisher.

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