Heavy prenatal alcohol exposure and risk of stillbirth and preterm delivery

Cornman‐Homonoff, Joshua; Kuehn, Devon; Aros, Sofía; Carter, Tonia C.; Conley, Mary; Troendle, James; Cassorla, Fernando; Mills, James L.

doi:10.3109/14767058.2011.587559

Cited by 25 publications

(18 citation statements)

References 10 publications

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“…Often these children are isolated within isolettes with limited tactile or abnormal tactile stimulation. Secondly, there are some reports that prenatal exposure to ethanol may be correlated with prematurity [72, 73], although other studies refute this [74]. Finally, there is evidence that somatosensory functional connectivity (i.e.…”

Section: Discussionmentioning

confidence: 99%

Unilateral whisker clipping exacerbates ethanol-induced social and somatosensory behavioral deficits in a sex- and age-dependent manner

Wellmann¹,

Mooney²

2015

Physiology & Behavior

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Prenatal exposure to ethanol results in sensory deficits and altered social interactions in animal and clinical populations. Sensory stimuli serve as important cues and shape sensory development; developmental exposure to ethanol or sensory impoverishment can impair somatosensory development, but their combined effects on behavioral outcomes are unknown. We hypothesized that 1) chronic prenatal ethanol exposure would disrupt social interaction and somatosensory performance during adolescence, 2) that a mild sensory impoverishment (neonatal unilateral whisker clipping; WC) would have a mildly impairing to sub-threshold effect on these behavioral outcomes, and 3) that the effect of ethanol would be exacerbated by WC. Long-Evans dams were fed a liquid diet containing ethanol or pair-fed with non-ethanol diet on gestational day (G) 6-G21. Chow-fed control animals were also included. One male and female pup per litter underwent WC on postnatal day (P)1, P3, and P5. Controls were unclipped. Offspring underwent social interaction on P28 or P42, and gap-crossing (GC) on P31 or P42. Ethanol-exposed pups played less and crossed shorter gaps than control pups regardless of age or sex. WC further exacerbated ethanol-induced play fighting and GC deficits in all males but only in 28-day-old females. WC alone reduced sniffing in all males and in younger females. Thus, prenatal ethanol exposure induced deficits in social interaction and somatosensory performance during adolescence. Sensory impoverishment exacerbates ethanol's effect in 28-day-old male and female animals and in 42-day-old males, suggesting sex-and age-dependent changes in outcomes in ethanol-exposed offspring.

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Section: Discussionmentioning

confidence: 99%

Unilateral whisker clipping exacerbates ethanol-induced social and somatosensory behavioral deficits in a sex- and age-dependent manner

Wellmann¹,

Mooney²

2015

Physiology & Behavior

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“…In many countries prenatal alcohol exposure (PAE) has also been found to be a risk marker for increased maternal mortality, fetal mortality, infant and child mortality, preterm birth, and morbidity (Abel, 1977;Kesmodel et al, 2002;Burd and Wilson, 2004;Burd et al, 2008;Li et al, 2011;Cornman-Homonoff et al, 2012). South Africa-which has the highest reported rates of PAE and binge drinking in Africa-also has some of the world's highest rates of fetal alcohol spectrum disorders (Croxford and Viljoen, 1999;May et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

Prenatal alcohol exposure in the Republic of the Congo: Prevalence and screening strategies

Williams

Nkombo

Nkodia

et al. 2013

Birth Defects Research

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23.3% of women attending prenatal care in Brazzaville reported alcohol use during pregnancy and 83% of them continued to drink after recognition of pregnancy. Prenatal alcohol exposure should be the focus of efforts to improve identification of alcohol use prior to and during pregnancy to improve maternal and child health. Birth Defects Research (Part A) 97:489-496, 2013. © 2013 Wiley Periodicals, Inc.

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“…8 The occurrence of stillbirth among pregnancies exposed to ethanol has been shown to increase sixfold compared with the rate of stillbirths within the population as a whole. 9 Although PAE is teratogenic to multiple organ systems, it is especially harmful to the central nervous system because of its extended developmental period. PAE is the most common identifiable and preventable cause of intellectual disability in the United States.…”

Section: Introductionmentioning

confidence: 99%

Prenatal alcohol exposure, blood alcohol concentrations and alcohol elimination rates for the mother, fetus and newborn

2012

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Fetal alcohol spectrum disorders (FASDs) are a common cause of intellectual impairment and birth defects. More recently, prenatal alcohol exposure (PAE) has been found to be a risk factor for fetal mortality, stillbirth and infant and child mortality. This has led to increased concern about detection and management of PAE. One to 2 h after maternal ingestion, fetal blood alcohol concentrations (BACs) reach levels nearly equivalent to maternal levels. Ethanol elimination by the fetus is impaired because of reduced metabolic capacity. Fetal exposure time is prolonged owing to the reuptake of amniotic-fluid containing ethanol by the fetus. Alcohol elimination from the fetus relies on the mother's metabolic capacity. Metabolic capacity among pregnant women varies eightfold (from 0.0025 to 0.02 g dl À1 h À1 ), which may help explain how similar amounts of ethanol consumption during pregnancy results in widely varying phenotypic presentations of FASD. At birth physiological changes alter the neonate's metabolic capacity and it rapidly rises to a mean value of 83.5% of the mother's capacity. FASDs are highly recurrent and younger siblings have increased risk. Detection of prenatal alcohol use offers an important opportunity for office-based interventions to decrease exposure for the remainder of pregnancy and identification of women who need substance abuse treatment. Mothers of children with FAS have been found to drink faster, get drunk quicker and to have higher BACs. A modest increase in the prevalence of a polymorphism of alcohol dehydrogenase, which increases susceptibility to adverse outcomes from PAE has been reported. Lastly, detection of alcohol use and appropriate management would decrease risk from PAE for subsequent pregnancies.

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Heavy prenatal alcohol exposure and risk of stillbirth and preterm delivery

Cited by 25 publications

References 10 publications

Unilateral whisker clipping exacerbates ethanol-induced social and somatosensory behavioral deficits in a sex- and age-dependent manner

Unilateral whisker clipping exacerbates ethanol-induced social and somatosensory behavioral deficits in a sex- and age-dependent manner

Prenatal alcohol exposure in the Republic of the Congo: Prevalence and screening strategies

Prenatal alcohol exposure, blood alcohol concentrations and alcohol elimination rates for the mother, fetus and newborn

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