Chapter

Alcohol Consumption and Prenatal Development

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Abstract

References to the association between alcohol and inferior offspring development and/or birth defects date back several hundred years in the scientific literature. For instance, during England’s gin epidemic of 1720–1750, considerable concern was expressed over alcohol’s adverse effects on unborn children; by the turn of the 20th century, epidemiological studies had actually documented alcohol’s risk to the developing fetus. During the early 1900s, a number of laboratory studies were also conducted to test alcohol’s effects on embryonic development in animals. However, these studies do not seem to have been prompted by a concern about alcohol’s role as a teratogen in humans but rather by practical considerations. Alcohol was considered representative of general anesthetic agents with the advantage of being readily available, soluble in water, and volatile.

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Chapter
Mental retardation is the most serious behavioral problem associated with fetal alcohol exposure, but other behavioral problems, e.g., “hyperactivity,” have also been connected with such exposure.
Chapter
The potential for developmental damage from alcohol exposure during gestation is now well established. Deleterious effects range from spontaneous abortion to a collective group of abnormalities called “fetal alcohol syndrome” (FAS) to subtle behavioral anomalies, such as attention deficits, that occur in the absence of observable physical abnormalities.
Article
Full-text available
Pregnant Sprague-Dawley dams were exposed to a liquid ethanol diet (35% ethanol-derived calories), an isocaloric pair-feeding regimen, restraint stress, or no treatment during the last week of pregnancy. Dams in each group received injections of testosterone propionate (TP) or the oil vehicle from days 15 through 20 of gestation. Birthweights of pups from dams administered TP and also exposed to alcohol, pair-feeding, or restraint stress were significantly depressed by as much as 40 percent compared to oil-injected counterparts. Prenatal exposure to alcohol, pair-feeding, or restraint stress in the absence of TP did not significantly depress birthweight, nor was birthweight depressed in animals from dams injected with TP but exposed to no other treatment. Results are discussed with respect to an inhibition of fetal growth produced by a possible synergism between activation of the hypothalamic-pituitary-adrenal axis and elevated androgen levels.
Article
Of the eleven children who were the first to be diagnosed as having the fetal alcohol syndrome ten years ago, two are now dead, one is lost to follow-up, and the remaining eight continue to be growth deficient and dysmorphic. With menarche, which occurred with normal timing, the female patients developed increased body fat. The mothers were all severe chronic alcoholics. Four of the eight known survivors are of borderline intelligence and have needed some remedial teaching. The other four are severely handicapped intellectually and need complete supervision outside the home. The degree of growth deficiency and intellectual handicap was directly related to the extent of craniofacial abnormalities. New features of the syndrome include dental malalignments, malocclusions, and eustachian tube dysfunction, which may relate embryologically to midface hypoplasia.
Article
The Research Institute on Alcoholism (RIA-Buffalo, New York) is a free-standing, state-supported institution for the conduct of biological, psychological, and social research on the etiology, prevention, and treatment of alcoholic disorders. With a total staff of about 80 persons, the Institute has stable state funding from its parent agency, the Division of Alcoholism and Alcohol Abuse, supplemented by external grant monies. Career development and training opportunities are supported through a variety of mechanisms and benefit from RIA's close association with the State University of New York at Buffalo. As a state agency, the RIA discharges a number of responsibilities of immediate relevance to the public welfare and relates to a variety of state and other organizations. The RIA is engaged in the conduct of several lines of inquiry and a central focus is upon the ontogeny of drinking careers and alcoholic disorders from adolescent through early adulthood.
Article
Three cases in one family—a girl and monozygotic girl twins, the offspring of a chronic alcoholic mother —are presented. They show a pattern of prenatal onset of growth deficiency and developmental delay, with microcephaly, small palpebral fissures, and multiple minor anomalies, recently described in a series of 11 unrelated cases by Jones et al. and named by them the "fetal alcohol syndrome." After considering alternative theories, we conclude, with them, that the cases demonstrate an association between the maternal alcohol intake and the abnormalities found in the offspring. We report these three cases in confirmation of their findings.
Article
The effects of prenatal alcohol on learning and retention of passive avoidance and discriminated shock escape were examined in offspring of rats who consumed isocaloric liquid diets containing either 35, 17.5 or 0% ethanol derived calories (EDC) or lab chow during pregnancy. Alcohol exposed progeny required more trials to reach criterion during passive avoidance acquisition and had shorter second trial latencies into the shock compartment than did controls. Both these measures were found to be direct functions of prenatal alcohol exposure. No differences between groups were evident during retention testing (1, 3, or 7 days later). During the 25 trial acquisition phase of T-maze escape, alcohol exposed progeny made more errors despite equivalent group performance by the end of training. During retention testing 24 hours later, these offspring again evidenced more errors regardless of whether or not the original contingencies were reversed. Both learning and retention deficits in the T-maze were directly related to the percent EDC consumed by the mother during pregnancy.
Article
The effects of prenatal exposure to three different types of alcoholic beverages (beer, wine, whiskey) and ethanol on postnatal growth and food and water consumption were studied in female rats. Dams were intubated with the equivalent of 3 g/kg of ethanol or alcohol twice daily throughout pregnancy. Control dams were intubated with isocaloric sucrose. All dams were pair-fed and pair-watered to ethanol-treated dams. At birth, all offspring were removed from their biological mothers and were placed with nondrug-treated surrogate dams. Body weights of females exposed to ethanol and wine remained significantly lower than pair-fed controls throughout the study (terminated at five months of age), whereas females exposed to beer and whiskey did not differ significantly from controls by eight and nine weeks of age, respectively. Feeding efficiencies, hydration, and osmotic regulation were not significantly affected by exposure to alcohol.
Article
The effects of alcohol intake on fetal brain development were examined during gestation. Pregnant rats were fed either laboratory chow, chow plus ethanol as 15% of the water, or chow sucrose to provide equal energy as rats consuming alcohol. Fetuses were removed on dat 18 of gestation and fetal brains were taken surgically. The number of fetuses, fetal weights and brain weights of the fetuses were lower in the ethanol-consuming group, although these differences were not statistically different from the control groups. RNA and DNA per fetal brain and brain cell number were significntly lower (P<0.05) in the ethanol group. The decreased parameters of brain development appear to be the result of alcohol intake and are not the result of a decreased energy intake.
Article
The fetal alcohol syndrome is characterized behaviorally by mental retardation, which is usually accompanied by growth retardation as well. Studies with rats were carried out to assess the effects of alcohol in utero on preweanling learning and memory, in the absence of growth and developmental deficiencies. In Experiment 1,4 g ethanol/kg was intubated in a liquid diet twice daily to rats on gestation days 6-21. When tested on day 12 on an appetitively-motivated straight alley task, ethanol treated pups did not differ from controls in rate of acquisition or extinction. In Experiment 2, ethanol was administered to dams via a high-protein liquid diet containing 30% ethanol derived calories between gestation day 6 to delivery. When tested on day 10 on an appetitively-motivated Y-maze discrimination task, ethanol treated pups required more trials to reach criterion during acquisition and reversal than controls. On day 12, the groups did not differ significantly on the performance of the previously acquired response. These results indicate that prenatal ethanol-induced impairments of learning (if sufficiently complex) are present in rat pups as early as 10 days of age.
Article
There are several methodological considerations associated with the administration of alcohol to pregnant animals that must be addressed before any unequivocal conclusions with respect to alcohol's behavioral teratogenicity can be made. Dose-response relations, blood alcohol levels, nutritional controls, etc., should be an integral part of studies in this area. Although some procedural problems have not yet been resolved, omission of basic controls seriously compromises the present status of many 'animal model' studies.
Article
Pregnant Sprague-Dawley rats were intubated with 6 g/kg of ethanol (30% w/v) during different weeks of pregnancy or throughout pregnancy. Pair-fed vehicle-injected and ad lib fed dams served as controls. Alcohol exposure throughout pregnancy lengthened the gestation period and reduced litter size but did not affect maternal body weight changes to a greater extent compared with exposure during specific weeks of pregnancy. Exposure during the third week produced a depression of fetal weight (at birth) similar to that observed following ethanol exposure throughout pregnancy and greater to that observed following ethanol exposure during the first and second weeks of pregnancy. At 28 days of age, differences between groups prenatally exposed to alcohol during different weeks of gestation and pair-fed animals were variable: Although most groups weighed significantly less than pair-fed animals, male offspring exposed to alcohol throughout pregnancy did not differ significantly from pair-fed controls.
Article
Minimal Brain Dysfunction (MBD) is one of the most prevalent problems in present day pediatrics affecting an estimated 5-10% of the school age population. Recent evidence from several lines of investigation support the notion that brain catecholamines are involved in the basic pathophysiologic mechanisms of MBD. In order to explore these mechanisms in more detail, we have produced an experimental model of MBD in the developing rat pup that has many of the similarities of the clinical disorder found in children. The model is effected by the intracisternal administration of 6-hydroxydopamine (6-OHDA) In the 5 day old rat pup, resulting in a rapid and permanent reduction of brain dopamine to values less than 50% of controls. Treated rat pups develop hyper-activity which abates with maturity and persistent learning deficits. We now report the effects of methylphenidate (0.25-2.0mg/kg) on activity levels at 12,19 and 26 days and T-maze learning at 20 days of age. Methylphenidate significantly increased activity levels and had no effect on T-maze learning in normals. In contrast methylphenidate reduced activity and significantly improved T-maze performance in 6-OHDA treated animals. Our results suggest that the “paradoxical” response to methylphenidate found in 6-OHDA treated rat pups may result from central denervation supersensitivity.
Article
THE LITERATURE ON THE BEHAVIORAL EFFECTS OF HIPPOCAMPAL LESIONS IS REVIEWED AND IT IS CONCLUDED THAT A LESION PRODUCES A UNITARY DEFICIT. ON A PURELY DESCRIPTIVE LEVEL THIS DEFICIT CONSISTS OF AN ABILITY TO WITHHOLD A PREPOTENT RESPONSE, WHETHER LEARNED OR UNLEARNED. MANY HYPOTHESES ABOUT HIPPOCAMPAL FUNCTION ARE SHOWN TO BE INCONSISTENT WITH THE DATA OR OTHERWISE INADEQUATE. 4 IDEAS APPEAR TO BE GENERALLY SUPPORTED BY THE RESULTS IN THE LITERATURE, AND THESE ESSENTIALLY REPRESENT SLIGHTLY DIVERGENT VIEWS ABOUT POSSIBLE CAUSES FOR THE DEFICIT ABOVE. IN 3 OF THESE, THE HIPPOCAMPUS IS POSTULATED TO HAVE AN INHIBITORY FUNCTION, WHETHER PAVLOVIAN, STIMULUS-RESPONSE BOND SUPPRESSION, OR INHIBITION OF ATTENTION AND/OR STIMULUS INPUT. IN THE 4TH IDEA, THE HIPPOCAMPUS IS POSTULATED TO PLAY A CRUCIAL ROLE IN A WORKING MEMORY MECHANISM. (5 P. REF.) (PsycINFO Database Record (c) 2012 APA, all rights reserved)
Article
This article deals with the question of whether offspring of social drinkers would show, to a lesser degree, some of the behavioral characteristics of infants with fetal alcohol syndrome. Another question concerned individual differences in “temperament.”
Article
Abstract The influence of maternal ethanol drinking on the development of alcohol dehydrogenase and aldehyde dehydrogenases in the liver of the offspring was studied in Wistar rats. No statistically significant differences were found between the ethanol group and the control group.
Article
At delivery the newborn infant of a drunken mother had a bloodalcohol concentration of about 2.0‰. The elimination rate was calculated to be 0.08‰/h. The infant exhibited obvious features of an embryofetal alcohol syndrome. Several cases from literature are cited with ethanol given for therapeutic purpose in obstetrics and bloodalcohol concentration exceeding to 1‰–2‰. This means that values up to 2‰ in newborn infants without any other pathological findings should not solely be accepted as cause of death in forensic cases.
Article
Female rats received barbital or chlordiazepoxide (CDP) in their drinking water or ethanol in a liquid diet with drug administration beginning before breeding and continuing until the offspring were weaned. Control groups received either tap water and lab chow (untreated controls) or a liquid diet containing sucrose which was delivered in restricted amounts such that it was equicaloric to the diet consumed by the ethanol group. Both birth weight and weight at 1 week of age were reduced by barbital exposure but not by CDP exposure. Growth was reduced slightly in the ethanol group, as compared to the sucrose control group. At 21 days of age the offspring were trained to avoid footshock and retested at 28 days of age. In both sessions the barbital offspring displayed longer avoidance latencies than controls, while the CDP and ethanol groups displayed shorter latencies than controls only during the training session. When trained to respond for food presentation under a fixed-ratio 20 schedule, the response rates of the barbital and CDP groups were less than those of the untreated control group while the response rates of both the ethanol and sucrose groups were greater than those of the untreated control group. When injected with ethanol or pentobarbital, the duration of narcosis was less for the offspring of the CDP- and barbital-treated mothers than for the untreated controls. Ethanol and sucrose offspring were not different in this regard. These results demonstrate that chronic maternal ingestion of ethanol, barbital, or CDP during gestation and nursing can affect the growth, behavior, and drug sensitivity of the offspring.
Article
Thesis (M.S.)--Virginia Polytechnic Institute and State University, 1978.
Article
Current research on the effects on offspring of drinking during pregnancy has revived interest in an extremely old topic. Observations made during England's Gin Epidemic (1720-1750) were followed by warnings of 19th-century medical writers that parental drinking could damage the fetus. Many concurring studies were reported in the medical literature from 1865 to 1920. Research interest declined during Prohibition, and authorities later discounted the previous work. Recently a relationship between maternal drinking and abnormal morphogenesis has been again described.
Article
Liver abnormalities were found in three patients with fetal alcohol syndrome. The histological appearance was different in each case. Thick, sclerotic central veins were seen in two of the three cases. One patient had features typical of congenital hepatic fibrosis and cystic disease of the kidneys. Findings in these patients indicate that some cases of congenital hepatic fibrosis might be caused by high maternal alcohol ingestion in pregnancy.
Article
Offspring of mothers who consumed either 32, 19, 8, or 0% of their daily caloric intake in the form of ethanol during pregnancy were tested for passive avoidance. At 18 days of age, the number of trials to criterion and the within-group variability were direct functions of the amount of ethanol consumed by the mother during pregnancy. At 41--53 days of age, alcohol-treated pups still required more trials to criterion than controls and had faster speeds into the shock compartment on the first trial. When the progeny of mothers consuming either 35, 17, or 0% ethanol-derived calories during pregnancy were compared for conditioned taste aversion to a lithium chloride solution, a linear dose-response function was again evident. Animals in the alcohol-treated groups showed less suppression of drinking than controls. These investigations indicated that the effects of alcohol exposure in utero were manifested in behavioral outcomes involving response inhibition that were not correlated with the more familiar physical symptoms.
Article
Cardiovascular anomalies are a frequently reported feature of the fetal alcohol syndrome, but only rarely have such children been catheterized. This article fully described the cardiac anomaly in two infants with this syndrome. The malformations found in both cases include a ventricular septal defect, and the rather unusual finding of pulmonary artery dysplasia.
Article
Infants of alcoholic mothers showed prominent EEG hypersynchrony in all three stages of sleep: in quiet sleep, indeterminate sleep and active-REM sleep. Spectral analysis of the EEG using fast Fourier transform revealed significant increase in power in most frequency bands in all three stages of sleep in infants born to alcoholic mothers when compared with normal healthy infants matched for gestational age. In quiet sleep "alcoholic" infants differed from healthy babies by significantly higher power in a wide range of frequency bands (1.5--17.5 Hz) with an average 143% increase of the integrated EEG (1.5--25 Hz). In indeterminate sleep "alcoholic" infants showed significantly higher power in all analyzed frequency bands (0.1--25 Hz) with an average 196% increase of the integrated EEG (1.5--25 Hz). In active-REM sleep infants of alcoholic mothers showed significantly higher power in the frequency range from 0.1 to 17.5 Hz in comparison with healthy controls. The average increase of the integrated EEG (1.5--25 Hz) was 200%. All healthy term infants showed significantly higher power in most frequency bands during quiet sleep in comparison with active-REM sleep. In infants born to alcoholic mothers this quiet sleep--REM sleep frequency spectrum difference in the majority of cases was nonsignificant mainly due to high values of the EEG power during REM sleep. It is unlikely that the EEG hypersynchrony in infants of alcoholic mothers represents one of the symptoms of the neonatal alcohol-withdrawal syndrome since hypersynchrony has been detected as long as 6 weeks after birth. During this time any withdrawal symptoms would have been dissipated.
Retrospective and prospective investigations of children to alcoholic women gave an incidence of fetal alcohol lesion of one per 300 deliveries of whom half had the complete fetal alcohol syndrome. Perinatal and infant mortalities were increased seven to tenfold and low birth weight (less than or equal to 2 500 g), preterm deliveries (less than 37 weeks) and smallness for gestational age (less than -2 S.D.) were increased eightfold, threefold and twelvefold, respectively. Small size at birth correlated with reduced mental performance later in life, 58% had IQ below 85 and 19% below 70.8% had cerebral palsy. The incidence of cerebral palsy associated with maternal inebriety was 1/5 000 deliveries, i.e. every sixth case of cerebral palsy. Tracing of alcoholic women during pregnancy and treatment gave favourable effect on intrauterine growth when sobriety could be induced early in pregnancy but could not protect from functional brain disturbance measured by neurological performance and be evoked response electroencephalography. Damage to the fetus by alcohol is now the largest known health hazard by a noxious agent that is preventable.
Article
The potential teratogenic effects of alcohol have been suspected for centuries, but it was not until the work of Lemoine in 1968 and the independent observations of Jones and Smith in 1973 that a distinct, dysmorphic condition associated with maternal, gestational alcoholism was described in medical literature. Yet in spite of the growing awareness of the clinical manifestations of the fetal alcohol syndrome, recognition has been minimal in many areas where alcoholism rates might suggest a sizable number of affected offspring. Consequently, the purpose of this article is to summarize the clinical features of ethyl alcohol teratogenesis to aid in the early recognition of those affected and to facilitate appropriate family preventive counseling and patient management.
Article
A clinical sample of 17 patients with fetal alcohol syndrome was given follow-up IQ testing 1-4 yr after an initial evaluation. Although 77% of the patients had a retest IQ that was within 1 SD of their initial IQ, some individual children did manifest considerable change in scores on retest. Repeated psychologic evaluation at regular intervals is recommended for children with fetal alcohol syndrome so that appropriate educational programming can be maintained in order to promote maximum development in each child.
Article
The effects of chronic alcohol administration and acute maternal oral alcohol intake on fetal development in rats were investigated, both regimens causing substantial increase in fetal mortality. Decrease body, brain, heart, kidney, and liver weight did not appear to be due to zinc deficiency.
Article
Throughout gestation pregnant Wistar rats consumed a nutritious liquid diet containing 35% ethanol-derived calories. Control mothers were fed lab-chow. Subsequently, the offspring of the ethanol-fed mothers displayed significantly greater activity (ambulation) in an open-field test at 28 and at 56 days of age, but not at 112 days of age. No differences in defecation were observed at any age.
Article
Maternal chronic ethanol abuse during pregnancy causes malformations of the offspring. Three children (aged 6 months, 9 months, 4 1/2 years) and 3 fetuses (17th, 18th, and 20th gestational week) showed a wide spectrum of disorders ranging from severe dysraphic state, arhinencephaly, porencephaly, agenesis of corpus callosum, a range from hydranencephaly to microdysplasias (p.e. reduced gyration of dentate nucleus and inferior olives), and a range from gastrochisis or congenital heart defects to craniofacial dysmorphogenesis and palmar crease anomalies. The patterns of the cerebral malformations were not as uniform as the clinical phenotype of the alcohol embryopathy. The observations did not support the assumption that there exists a specific period for alcohol teratogenicity.
The current observations confirm and extend earlier data demonstrating the deleterious effects of ethanol in the C57BL/6J mouse. Ethanol given to pregnant mice from gestation-day 5 to gestation-day 11 reduced the number of mice going to full term, decreased the number of pups per litter, and lowered the birthweight of the live pups. Prenatal exposure to ethanol also produced a high incidence of hydronephrosis in the offspring.
Article
Pregnant female rats consumed liquid diets containing either 35, 17, or 0% of the total calories as ethanol. Offspring of these females were tested for spontaneous alternation at 21 days of age and for reversal learning in a T-maze shock-escape paradigm at 20--21 days of age. In the spontaneous alternation test, rats exposed to alcohol prenatally took more trials than controls to enter the goal compartment opposite to that initially entered. In the T-maze escape study, alcohol-exposed offspring made more mistakes prior to criteron and more mistakes per trial than controls when the previously incorrect goal was made safe during reversal learning. In both studies linear dose-response functions were found. Furthermore, there was a significant tendency for the within-group variabitliy to increase as the level of prenatal exposure increased, perhaps indicating that the incidence as well as the severity of behavioral dysfunction was dose dependent. The results are interpreted in terms of a delay in the development of a central inhibitory system.
Article
In an initial study, the rate of blood alcohol disappearance was not significantly different in pregnant compared to nonpregnant rats, but blood alcohol levels were significantly different depending on dose. In a second study, pregnant rats received daily administrations (p.o.) of ethanol (30% w/v) in single doses throughout gestation. Pair-fed vehicle-treated, and nondrug-treated rats fed ad lib served as controls. All pups were removed from their biological mothers at birth and were raised by nondrug-treated surrogate mothers. At five months of age, both male and female offspring prenatally exposed to ethanol weighed less than controls and female offspring performed significantly worse than the offspring of vehicle-injected pair-fed control mothers, on a two-way shock-avoidance task. There were no significant group differences, however, for either sex in water-escape maze learning.
Article
Long-Evans hooded rats prenatally exposed to alcohol (4 or 6 g/kg) reared less in an open field and had longer step-down latencies when tested as adults than pair-fed controls. There were no differences between alcohol-treated animals and controls in spontaneous alternation or their response to a challenge dose of alcohol.
Article
Lower peak blood ethanol concentrations after 1 and 2 g of ethanol per kg were found in pregnant rats than in virgin females. No significant differences in adult "emotionality" or ethanol consumption were found in rats exposed to prenatal alcohol and in pair-fed and untreated controls.
Article
Sleep-awake state distribution during inter-feed intervals over a 24-hour period on the third day of life was investigated by means of a continuous non-intrusive bassinet sleep monitor. 31 infants were studied: 14 born to mothers who drank heavily throughout pregnancy (group A), eight whose mothers modified their heavy drinking (group B) and nine whose mothers never were heavy drinkers (group C). Over the 24-hour period, group A infants slept less than those in group B. In comparison with group C, group A infants had a larger proportion of quiet sleep episodes interrupted by awake or unclassified epochs, and were more restless, with more frequent major body movements. These pilot observations suggest that heavy maternal consumption of alcohol, when continued throughout pregnancy, is associated with a disturbance of sleep-awake state distribution. Successful therapy of heavy drinking during pregnancy may improve the physiological competence of the newborn to regulate sleep-awake states and facilitate interaction between mother and infant.
Article
The disappearance of alcohol from blood following a single dose is a function of age, but by the time the animals are 90 days old the results are consistent from animal to animal. A single dose given to a pregnant female is distributed between fetus and maternal tissues and fluids, with a portion of the alcohol trapped in the amniotic fluid. Kittens born to mothers receiving alcohol during the last 2 weeks of pregnancy demonstrate hyperactivity, small size with unimpaired growth rate, and slow maturation of the righting reflex. It would require more experimentation to decide whether these changes are due to alcohol withdrawal or to toxic effects of the alcohol per se.