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Results for “Fetal Alcohol Spectrum Disorders”

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PubMed1985

Ethanol and fetal nutrition: effect of chronic ethanol exposure on rat placental growth and membrane-associated folic acid receptor binding activity.

Rat placental composition and specific folate receptor activity were measured at 20 days gestation in dams exposed to chronic high doses of ethanol (6%, vol/vol) throughout gestation and in isocalorically pair-fed controls. Ethanol-exposed fetuses were smaller (ethanol = 3.28 +/- 0.08 vs. control = 4.01 +/- 0.10 g, p less than 0.001), but their placentae were larger (experimental = 0.534 +/- 0.02 vs. control = 0.399 +/- 0.01 g, p less than 0.001). The increased weight appears to be secondary to hyperplasia as total DNA was increased while the wet/dry, RNA/DNA, and protein/DNA ratios were not different. Despite larger placentae, specific folate receptor activity was significantly reduced in the ethanol-exposed tissue, whether expressed relative to membrane protein, placental weight, or total placental binding. These results confirm that ethanol exposure is placentotoxic and suggest an additional mechanism by which ethanol may lead to intrauterine growth retardation; namely, decreased folate receptor activity.

Animals↗
PubMed2004

Prenatal alcohol exposure causes long-term serotonin neuron deficit in mice.

BACKGROUND: Previous work from this laboratory showed that prenatal alcohol exposure at approximately 100 mg/dl from embryonic day (E)7 to early midgestation reduced the number and retarded the migration of serotonin (5-HT) neurons in the raphe nuclei in C57BL/6 mice. In this study, we report that the deficit of 5-HT neurons found in midgestation persisted on E18 and into young adulthood. METHODS: Pregnant dams were treated from E7 to E18 in three groups--(1) the alcohol group, fed with liquid diet with 25% ethanol-derived calories; (2) the isocaloric pair-fed group; and (3) the chow group for analysis of concentrations of active caspase-3--to study apoptosis at E18 in the brainstem and the number of 5-HT neurons at E18 and postnatal day 45. The concentrations of active caspase-3 were determined by using a colorimetric assay, and the 5-HT neurons were determined by immunocytochemistry. RESULTS: Prenatal alcohol exposure increased the concentration of active caspase-3 in the brainstem and caused reductions in brain weight by 20% and in the total number of 5-HT-immunostaining neurons in the dorsal and median raphe nuclei by 20% at E18 as compared with those of the pair-fed and chow controls. Continuous observation from prenatal to postnatal stages showed that the reduction of 5-HT-immunostaining neurons in the dorsal and median raphe nuclei persisted in the young adult stage. CONCLUSIONS: Upon prenatal alcohol exposure, an increased concentration of active caspase-3 and a decreased number of 5-HT-immunostaining neurons in the brainstem were observed at E18. The decreased number of 5-HT neurons persisted to the young adult stage of postnatal day 45. This suggests that ethanol has a long-lasting effect on 5-HT deficit. A fetal alcohol exposure-rendered lasting deficit of 5-HT and other transmitter systems may underlie the neuropsychiatric deficits in fetal alcohol spectrum disorder.

Animals↗
PubMed2005

Moderate fetal alcohol exposure impairs the neurogenic response to an enriched environment in adult mice.

BACKGROUND: Prenatal ethanol exposure results in a spectrum of cognitive and behavioral deficits and affects an estimated thirteen percent of children born in the United States. The basis of prenatal ethanol-induced impairment of brain function has been widely studied in animal models, where significant changes in the physiological and structural plasticity of hippocampal function have been documented. Here, we explored the possibility that exposure to moderate levels of alcohol in utero might also result in long-lasting impairment of adult hippocampal neurogenesis, a novel form of plasticity that occurs throughout adulthood. METHODS: Female mice were trained to voluntarily consume 10% EtOH throughout pregnancy using the two-bottle choice paradigm, which results in moderate blood alcohol levels of approximately 121 mg/dl, as previously described (Allan et al., 2003). Offspring were exposed to standard or enriched living conditions for 8-12 weeks post-weaning. BrdU was administered at 50 mg/kg for 12 consecutive days. Mice in each housing condition were sacrificed at either 24 hrs or four weeks following the final BrdU injection, and BrdU cells within the dentate gyrus were evaluated using immuno-histochemical methods. RESULTS: Neither fetal alcohol exposure (FAE) nor enriched environment affected the number of proliferating progenitors within the subgranular zone (SGZ) of the dentate gyrus. However, FAE severely impaired the neurogenic response to enriched environment. Control mice housed in enriched environment displayed a two-fold increase in hippocampal neurogenesis, whereas FAE mice responded to enriched environment with neither enhanced progenitor survival nor enhanced neuronal differentiation. CONCLUSIONS: These observations indicate that moderate FAE results in a long-term, persistent defect in neurogenic responses to behavioral challenge.

Animals↗
PubMed2005

Baseline measures of fatty acid ethyl esters in hair of neonates born to abstaining or mild social drinking mothers.

Elevated levels of fatty acid ethyl esters have been documented in the meconium of neonates born to heavily drinking mothers. Recently, accumulation of FAEE has been documented in the hair of drinking adults. To be able to use this test in the diagnosis of Fetal Alcohol Spectrum Disorder, one needs to establish baseline FAEE levels in infants born to nonalcoholic women because ethanol occurs in the baby naturally even without drinking. Scalp hair of 56 infants born to nonalcoholic women attending a well-baby clinic was obtained. Levels of FAEE were measured by GC-MS. FAEE were detected in almost all hair samples. Offspring of women admitting to mild, infrequent drinking did not differ in FAEE hair levels from infants of total abstainers. Baseline levels of FAEE in neonatal hair of nonalcoholic mothers have been established. Mild infrequent maternal drinking does not elevate these baseline levels. This may help avoid false-positive determinations when assessing infants born to problem drinking mothers.

Adult↗
PubMed2003

Fetal alcohol and drug effects.

BACKGROUND: Alcohol and drug use by pregnant women are harmful to the developing embryo and fetus. Teasing apart the specific contributions of each substance to adverse child outcome, however, proves difficult in practice. The risks to the neonate include intra-uterine growth retardation, birth defects, altered neurobehavior, and withdrawal symptoms. Subsequent behavior, development, and neurologic function may also be impaired. REVIEW SUMMARY: Maternal cigarette smoking carries the greatest risk of impaired fetal growth of any of the substances discussed herein and has been linked to subsequent externalizing behaviors. Alcohol is a well-established teratogen. Heavy exposure to alcohol in a subset of infants is associated with fetal alcohol syndrome (FAS). Mental retardation is one of the main sequelae of alcohol exposure in utero. Fetal marijuana exposure has no consistent effect on outcome. Prenatal cocaine exposure has not been shown to have any detrimental effect on cognition, except as mediated through cocaine effects on head size. Although fetal cocaine exposure has been linked to numerous abnormalities in arousal, attention, and neurologic and neurophysiological function, most such effects appear to be self-limited and restricted to early infancy and childhood. Opiate exposure elicits a well-described withdrawal syndrome affecting central nervous, autonomic, and gastrointestinal systems, which is most severe among methadone-exposed infants. CONCLUSION: Most adverse effects of prenatal drug exposure are self-limited, with catch-up growth and resolution of withdrawal and of prior neurobehavioral abnormalities noted over time. The exception is alcohol, which is linked to life-long impairments (i.e., mental retardation and microcephaly) and possibly cigarette-related behavioral effects. The absence of tangible evidence of detrimental long-term cocaine effects may reflect limitations in the methodology used to identify children at greatest risk for adverse outcome.

Cannabis↗
PubMed1986

The effect of maternal ethanol intoxication on fetal cardiotocography: a report of four cases.

Fetal cardiotocography revealed no or poor variability and no reactivity to fetal movements and or external stimuli in four drunken women. This was taken as a sign of fetal hypoxia in one patient and led to emergency caesarean section although, the infant was not hypoxic. In the other three patients, cardiotocography normalized within 11-14 h when the mothers became sober.

Adult↗
PubMed1982

Ethanol-associated selective fetal malnutrition: a contributing factor in the fetal alcohol syndrome.

The pathogenesis of the FAS, particularly the characteristic IUGR, may be due in part to ethanol-related placental injury. Ethanol and/ or acetaldehyde may impair placental transfer of nutrients essential for growth, e.g., amino acids. Such restriction could occur regardless of maternal nutritional status: selective fetal malnutrition. Impairment of placental nutrient transport at critical phases of fetal organogenesis could compound any direct fetotoxic effects of ethanol or acetaldehyde. The effect of ethanol upon human placental hormone synthesis and transport of vitamins, minerals, glucose, and nucleic acid precursors awaits further investigation. Similarly, potential interactions between ethanol and other xenobiotics commonly abused by alcoholics require clarification.

Amino Acids↗
PubMedDate not supplied

Prostaglandin synthesis inhibitors block alcohol-induced fetal hypoplasia.

Alcohol-induced growth retardation is a fetal effect consistently associated with maternal ethanol consumption. In humans, those infants whose mothers consume even a limited amount of ethanol during pregnancy have a significant incidence of growth inhibition. The molecular mechanism responsible for this growth deficiency is unknown, and prevention depends on maternal abstinence during pregnancy. The data reported here suggest that ethanol-mediated increases in tissue prostaglandin (PG) E levels (PGE1 plus PGE2) are correlated with the growth retardation. Further, simultaneous administration of PG synthesis inhibitors with the alcohol blocks the rise in tissue PG levels and protects against the alcohol-induced hypoplasia.

Animals↗
PubMedDate not supplied

Alcohol-related birth defects: syndromal anomalies, intrauterine growth retardation, and neonatal behavioral assessment.

Fetal alcohol effects in 359 infants born to disadvantaged women identified as having a history of alcohol abuse or as controls and who provided reports of alcohol use in pregnancy are being studied in a prospective design. Alcohol abuse was assessed with the Michigan Alcoholism Screening Test (MAST). Alcohol use (AA/day) was based on short-term recall covering 2-week periods prior to each antenatal visit. A tally of anomalies associated with fetal alcohol syndrome was obtained in a blinded examination of each infant. This tally was significantly related to the MAST classification and, for the MAST+ subjects, the tally was related to first trimester AA/day. Birth weight, length, and head circumference were negatively correlated with AA/day (entire pregnancy); however, the effect was attenuated and not statistically significant in models with covariate control. It is possible that these measures were near the threshold of effect. Scale scores of the Brazelton Neonatal Behavioral Assessment Scale and three scale scores of the Graham/Rosenblith Behavioral Examination of the Neonate were unrelated to the MAST classification and to AA/day.

Abnormalities, Drug-Induced↗
PubMedDate not supplied

Selective fetal malnutrition: effect of acute and chronic ethanol exposure upon rat placental Na,K-ATPase activity.

Intrauterine growth retardation (IUGR) is characteristic of the fetal alcohol syndrome (FAS). This IUGR is partly due to the toxic effect of ethanol upon placental function, including amino acid transport. Amino acid transport is dependent, in part, upon Na,K-ATPase; therefore, plasma membrane activity of Na,K-ATPase was measured in rat placentas following acute or chronic ethanol exposure. Acute (A) animals were chow fed and gavaged with ethanol on day 20 of gestation and killed 2 hr later; controls (A-C) received sucrose. Binge (B) animals were gavaged on gestation days 18 and 19; controls (B-C) received sucrose. Chronic animals were fed ethanol in a liquid diet containing 2% (CHR-2%) or 6% (CHR-6%) ethanol by volume and killed on day 20. Controls (CHR-2%-C or CHR-6%-C) were isocalorically pair fed. Maternal blood ethanol levels were 197.1 +/- 29.7 mg/dl (mean +/- SE) for A dams and 128.2 +/- 15.2 for B (drawn at time of death); 12.6 +/- 2.2 for CHR-2% and 195.0 +/- 26.0 for CHR-6% (drawn weekly and at time of death). Placental weight was increased and fetal weight decreased in the CHR-6% animals. A, B, and CHR-2% placental and fetal weights were unaffected. Na,K-ATPase specific activity was increased in B placentas: B = 134.7 +/- 16.5 versus B-C = 50.0 +/- 7.4 nmol of Pi/mg of protein/min (p less than 0.01). Conversely, CHR-6% treatment diminished enzyme activity: CHR-6% = 37.0 +/- 4.5 versus CHR-6%-C = 58.5 +/- 4.4 (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Perspectives on the pathophysiology of fetal alcohol syndrome.

Fetal alcohol syndrome (FAS) is a major known cause of fetal malformations and mental retardation. Prevention/intervention of FAS can only be achieved with identification of the mechanisms by which alcohol induces birth defects. The purpose of this paper is to discuss the data on possible mechanisms of FAS, and to give a number of suggestions for future research areas.

Acetaldehyde↗
PubMed1990

Prenatal alcohol exposure and language development.

The effects of fetal alcohol exposure on language and speech acquisition were investigated in a cohort of socioeconomically disadvantaged urban children. Language development was assessed by instruments derived from the Expressive and Receptive Scales of the Sequenced Inventory of Communication Development (SICD) at 1, 2, and 3 years, and by indices constructed from a taped speech sample at age 2 years. Three indices of maternal drinking were supplemented with birth weight and a tally of craniofacial anomalies as early indicators of fetal alcohol damage. No statistically significant relationships were found between the alcohol and language indices after statistical control for confounding variables. The anomalies tally was marginally related to reduced language scores. The statistical significance of this relationship, depended, however, on a single child with the characteristics of fetal alcohol syndrome. The pattern of results suggested that the anomalies tally, and to a lesser extent birth weight, are more sensitive indicators of fetal alcohol exposure than subsequent language development.

Child, Preschool↗
PubMed1991

Prenatal alcohol exposure and preschool physical growth: a longitudinal analysis.

This report examines the effects of fetal alcohol exposure on size and growth in an urban cohort followed prospectively through early childhood. Indices of prenatal drinking were related to measurements of weight, stature (length), and head circumference obtained at birth and during five subsequent in-home assessments. Small but statistically significant relationships were detected between short-term recall estimates of drinking during pregnancy and weight and length at birth. The strength of these relationships diminished during the preschool assessments. However, estimates of catch-up growth associated with alcohol exposure were not statistically significant. With the exception of a single case with a profile of signs characteristic of fetal alcohol syndrome, an adverse effect of prenatal alcohol exposure on head circumference was not indicated.

Alcohol Drinking↗
PubMed1991

Postnatal growth deficits in prenatal ethanol-exposed mice: characteristics and critical periods.

We previously reported that offspring of C57BL/6 mice maintained on liquid diets containing 20% or 25% ethanol-derived calories throughout pregnancy had birth weights comparable with controls but had weight reductions that became manifest around 23 to 28 days postnatally. Since this pattern of weight reduction may represent an unrecognized condition for human ethanol exposure, we completed a number of experiments to more thoroughly characterize the altered growth of prenatal ethanol exposed C57BL/6 mice. The results of this study indicate that consumption of liquid diets containing either 17% or 25% ethanol-derived calories during pregnancy can reduce growth of male and female offspring. Although attenuated postnatal growth of prenatal ethanol-exposed rodents is not commonly reported, prospective studies in humans suggest that in addition to having lower birth weights, children prenatally exposed to ethanol are postnatally growth retarded. Mice exposed to the low ethanol doses used in the present study had normal birth weights; however, their growth was attenuated between 19 and 28 days of age (preadolescent growth spurt) resulting in a weight reduction for at least 35 days, and which according to our previous report could extend into adulthood. The latter stages of gestation appear to be more sensitive to the postnatal growth retarding effect of prenatal ethanol exposure than early gestation. Caloric deficiency and postnatal maternal factors were eliminated as possible mechanisms for the growth deficit.

Animals↗