Alcohol consumption during pregnancy among Southern city women

doi:10.1016/0376-8716(85)90078-X

Drug and Alcohol Dependence

Volume 16, Issue 1, September 1985, Pages 19-29

https://doi.org/10.1016/0376-8716(85)90078-X Get rights and content

Abstract

As national survey data on American drinking practices have suggested a higher rate of heavy drinking among Southern city women compared to women in other regions, this study sought to determine drinking patterns during pregnancy in this group. A consecutive sample of 428 prenatal patients, who were residents of a Southern metropolitan area, were interviewed during the fourth month prenatal clinic visit. Although close to 50% of this sample were abstainers, 11% of the drinkers were found to be heavy drinkers, averaging more than two drinks daily, while 18% were high-maximum drinkers, consuming at least five drinks on an occasion prior to pregnancy. Forty-eight percent of the drinkers had become abstainers during the first 4 months of pregnancy, which was significantly higher than the 35% found in a representative non-Southern population (P < 0.01). More frequent highmaximum drinking and increased drinking during pregnancy, both of which are potentially risky drinking practices for fetal outcome, were found primarily among blacks and those 14–19 years of age. The large proportion of both blacks (85%) and those 14–19 (33%) in this sample may put this population at high risk for adverse fetal outcomes related to alcohol consumption during pregnancy.

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Cited by (46)

Differential effects of ethanol on c-jun N-terminal kinase, 14-3-3 proteins, and Bax in postnatal day 4 and postnatal day 7 rat cerebellum
2012, Brain Research
Citation Excerpt :
Both ethanol and control exposure periods were 2 h, 45 min each day. This acute exposure protocol mimics a “binge” pattern of ethanol consumption, which is a common consumption pattern in women who drink during pregnancy (Stephens, 1985). Two hours after the completion of exposure to ethanol or control conditions, pups were sacrificed via rapid decapitation.
These studies investigated ethanol effects on upstream cellular elements and interactions which contribute to Bax-related apoptosis in neonatal rat cerebellum at ages of peak ethanol sensitivity (postnatal day 4 [P4]), compared to later ages of relative resistance (P7). Analyses were made of basal levels of the pro-apoptotic c-jun N-terminal kinase (JNK), Bax, and the 14-3-3 anchoring proteins, as well as the responsiveness of these substances to ethanol at P4 versus P7. Dimerization of Bax with 14-3-3 was also investigated at the two ages following ethanol treatment, a process which sequesters Bax in the cytosol, thus inhibiting its mitochondrial translocation and disruption of the mitochondrial membrane potential. Cultured cerebellar granule cells were used to examine the protective potential of JNK inhibition on ethanol-mediated cell death. Basal levels of JNK were significantly higher at P4 than P7, but no differences in the other proteins were found. Activated JNK, and cytosolic and mitochondrially-translocated Bax were increased in P4 but not P7 animals following ethanol exposure, while protective 14-3-3 proteins were increased only at P7. Ethanol treatment resulted in decreases in Bax:14-3-3 heterodimers at P4, but not at P7. Inhibition of JNK activity in vitro provided partial protection against ethanol neurotoxicity. Thus, differential temporal vulnerability to ethanol in this CNS region correlates with differences in both levels of apoptosis-related substances (e.g., JNK), and differential cellular responsiveness, favoring apoptosis at the most sensitive age and survival at the resistant age. The upstream elements contributing to this vulnerability can be targets for future therapeutic strategies.
A single exposure to alcohol during brain development induces microencephaly and neuronal losses in genetically susceptible mice, but not in wild type mice
2009, NeuroToxicology
Maternal alcohol abuse during pregnancy can damage the fetal brain and lead to fetal alcohol syndrome (FAS). Despite public warnings discouraging alcohol use during pregnancy, many pregnant women continue to drink intermittently because they do not believe that occasional exposures to alcohol can be harmful to a fetus. However, because of genetic differences, some fetuses are much more susceptible than others to alcohol-induced brain injury. Thus, a relatively low quantity of alcohol that may be innocuous to most fetuses could damage a genetically susceptible fetus. Neuronal nitric oxide synthase (nNOS) can protect developing mouse neurons against alcohol toxicity by synthesizing neuroprotective nitric oxide. This study examined whether a single exposure to alcohol, which causes no evident injury in wild type mice, can damage the brains of mice genetically deficient for nNOS (nNOS−/− mice). Wild type and nNOS−/− mice received intraperitoneal injections of alcohol (0.0, 2.2, or 4.4 mg/g body weight) either as a single dose on postnatal day (PD) 4 or as repeated daily doses over PD4–9. Brain volumes and neuronal numbers within the hippocampus and cerebral cortex were determined on PD10. Alcohol exposure on PD4–9 restricted brain growth and caused neuronal death in both strains of mice, but the severity of microencephaly and neuronal loss were more severe in the nNOS−/− mice than in wild type. The 4.4 mg/g alcohol dose administered on PD4 alone caused significant neuronal loss and microencephaly in the nNOS−/− mice, while this same dose caused no evident injury in the wild type mice. Thus, during development, a single exposure to alcohol can injure a genetically vulnerable brain, while it leaves a wild type brain unaffected. Since the genes that confer alcohol resistance and vulnerability in developing humans are unknown, any particular human fetus is potentially vulnerable. Thus, women should be counseled to consume no alcohol during pregnancy.
Ethanol effects on neonatal rat cortex: Comparative analyses of neurotrophic factors, apoptosis-related proteins, and oxidative processes during vulnerable and resistant periods
2003, Developmental Brain Research
The developing central nervous system (CNS) is highly susceptible to ethanol, with acute or chronic exposure producing an array of anomalies and cell loss. Certain periods of vulnerability have been defined for various CNS regions, and are often followed by periods of relative ethanol resistance. In the present study, neonatal rats were acutely exposed to ethanol during a time when peak cell death is found in developing cerebral cortex (postnatal day 7; P7), and during a later neonatal period of ethanol resistance (P21). Comparisons at the two ages were made of basal levels of neurotrophic factors (NTFs), and in addition, ethanol-mediated changes in NTFs, apoptosis-related proteins, antioxidant activities, and generation of reactive oxygen species (ROS) were quantified at 0, 2, and 12 h following termination of exposure. It was found that at P21, basal levels of NTF nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) were considerably higher than at P7, possibly affording protection against ethanol neurotoxicity at this age. Following ethanol treatment at P7, approximately equal numbers of pro-apoptotic and pro-survival changes were produced, although most of the pro-apoptotic alterations occurred rapidly following termination of treatment, a critical period for initiation of apoptosis. At P21, however, the large majority of ethanol-mediated changes were adaptive, favoring survival. We speculate that the capacity of the older CNS to upregulate a number of protective elements within the cellular milieu serves to greatly mitigate ethanol neurotoxicity, while in younger animals, such adjustments are minimal, thus enhancing ethanol vulnerability within this developing region.
Effects of ethanol on neurotrophic factors, apoptosis-related proteins, endogenous antioxidants, and reactive oxygen species in neonatal striatum: Relationship to periods of vulnerability
2003, Developmental Brain Research
The developing central nervous system is extremely sensitive to ethanol, with well-defined temporal periods of vulnerability. Many brain regions are particularly susceptible to ethanol during the early neonatal period, corresponding to the human third trimester, which represents a dynamic period of growth and differentiation. For this study, neonatal rats were acutely exposed to ethanol or control conditions at a neonatal age when the developing striatum has been shown to be vulnerable to ethanol (postnatal day 3 [P3]), and at a later age (P14), when this developing region is relatively ethanol-resistant. We then analyzed basal levels of neurotrophic factors (NTFs), and ethanol-mediated changes in NTFs, apoptosis-related proteins, antioxidants, and reactive oxygen species (ROS) generation, which may underlie this differential temporal vulnerability. Sequential analyses were made following ethanol exposure on these two postnatal days, with assessments of NTFs nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and neurotrophin-4 (NT-4); apoptosis-related proteins Bcl-2, Bcl-xl, Bax, Akt and c-jun N-terminal kinase (JNK); antioxidants superoxide dismutase, glutathione reductase and catalase; and ROS. The results indicated that basal levels of BDNF, and to some degree NGF, were greater at the older age, and that ethanol exposure at the earlier age elicited considerably more pro-apoptotic and fewer pro-survival changes than those produced at the later age. Thus, differential temporal vulnerability to ethanol in this CNS region appears to be related to differences in both differential levels of protective substances (e.g. NTFs), and differential cellular responsiveness which favors apoptosis at the most sensitive age and survival at the resistant age.
Deficiency of neuronal nitric oxide synthase (nNOS) worsens alcohol-induced microencephaly and neuronal loss in developing mice
2002, Developmental Brain Research
Previous work conducted in vitro suggests that nitric oxide (NO) protects developing neurons against the toxic effects of alcohol. We tested the hypothesis that neonatal mice carrying a null mutation for neuronal nitric oxide synthase (nNOS), the enzyme which synthesizes NO in neurons, have increased vulnerability to alcohol-induced microencephaly and neuronal loss. Wild-type mice and mutant (nNOS^−/−) mice received a single intraperitoneal injection of ethanol (0.0, 2.2, 3.3, or 4.4 g/kg) daily over postnatal days (PD) 4–9 and were sacrificed on PD10. Peak blood alcohol concentrations were approximately 170, 280, and 385 mg/dl for the 2.2, 3.3 and 4.4 g/kg/day treatment groups, respectively, and did not differ significantly between wild-type and nNOS^−/− strains. Exposure to alcohol induced dose-dependent reductions in total brain weight, forebrain weight and cerebellum weight in both strains of mice. However, the reductions in brain weight were significantly more severe in the nNOS^−/− mice than in wild type. Quantification of cerebellar neurons revealed that alcohol-induced losses of Purkinje cells and granule cells were both significantly greater in the nNOS^−/− mice than in wild type. The increased vulnerability of nNOS-deficient neurons to alcohol-induced cell death was confirmed in vitro. Cerebellar granule cell cultures derived from nNOS^−/− and wild-type mice were exposed for 24 h to 0, 100, 200 or 400 mg/dl ethanol. At each alcohol concentration, the nNOS^−/− neurons had a significantly greater cell loss than did the wild-type neurons. The results demonstrate that deficiency of nNOS decreases the ability of developing neurons to survive the toxic effects of alcohol. Because NO upregulates intracellular cGMP, which can activate cGMP-dependent protein kinase (PKG), we hypothesize that the NO–cGMP–PKG pathway has a neuroprotective role against alcohol toxicity within the developing brain.
Neonatal binge ethanol exposure using intubation: Timing and dose effects on place learning
1997, Neurotoxicology and Teratology
Neonatal rats were given ethanol using an acute intubation procedure that resulted in daily binge-like exposure with minimal effects on somatic growth. Acquisition of place learning in the Morris water maze was evaluated on postnatal days (PD) 26–31. In Experiment 1, a total of 5.25 g/kg/day of ethanol was administered in two daily intubations on PD 4–6, PD 7–9, or PD 4–9, producing mean peak BACs of 265 mg/dl. Place learning acquisition deficits in a 114-cm-diameter tank were found for the PD 4–9 and PD 7–9 groups, but not the PD 4–6 group. In Experiment 2, either 4.5 or 5.25 g/kg/day of ethanol was administered on PD 7–9 and place learning was tested in a 171-cm-diameter tank. Significant acquisition deficits resulted from the higher dose, and probe trial search patterns for both ethanol groups were significantly less localized than controls. In Experiment 3, no significant effects of either PD 7–9 dose were found on a visible platform task. These findings reveal selective place learning deficits in this intubation model of neonatal binge exposure, and confirm a temporal window of vulnerability to spatial learning deficits during the second neonatal week.

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^☆: Prepared for presentation at the APHA 112th Annual Meeting in Anaheim, CA, November 11–15, 1984.

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Alcohol consumption during pregnancy among Southern city women☆

Abstract

Lancet

Lancet

Am. J. Obstet. Gynecol.

American Drinking Practices

Alcohol use and alcohol problems among U.S. adults; results of the 1979 survey

Obstet. Gynec.