A Revised Conservative Estimate of the Incidence of FAS and its Economic Impact

Abel, Ernest L.; Sokol, Robert J.

doi:10.1111/j.1530-0277.1991.tb00553.x

Cited by 217 publications

(80 citation statements)

References 47 publications

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“…Estimates place the incidence of FASD at 10 in 1000 births, which still might be an underestimate. [103][104][105][106] Given that (1) more than 50% of childbearing women report using ethanol, 10 (2) nearly 50% of pregnancies are unplanned, 107,108 and (3) embryos are sensitive to ethanol before a woman is typically aware of pregnancy, abstinence-based approaches are unlikely to eliminate FASD. Thus, a complete understanding of the underpinnings of FASD is critical to human health.…”

Section: Discussionmentioning

confidence: 99%

Fishing for Fetal Alcohol Spectrum Disorders: Zebrafish as a Model for Ethanol Teratogenesis

2016

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Fetal Alcohol Spectrum Disorders (FASD) describes a wide array of ethanol-induced developmental defects, including craniofacial dysmorphology and cognitive impairments. It affects *1 in 100 children born in the United States each year. Due to the pleiotropic effects of ethanol, animal models have proven critical in characterizing the mechanisms of ethanol teratogenesis. In this review, we focus on the utility of zebrafish in characterizing ethanolinduced developmental defects. A growing number of laboratories have focused on using zebrafish to examine ethanol-induced defects in craniofacial, cardiac, ocular, and neural development, as well as cognitive and behavioral impairments. Growing evidence supports that genetic predisposition plays a role in these ethanol-induced defects, yet little is understood about these gene-ethanol interactions. With a high degree of genetic amenability, zebrafish is at the forefront of identifying and characterizing the gene-ethanol interactions that underlie FASD.

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Section: Discussionmentioning

confidence: 99%

Fishing for Fetal Alcohol Spectrum Disorders: Zebrafish as a Model for Ethanol Teratogenesis

2016

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“…This is of special interest because children born of black women have been reported to be at greater risk for fetal alcohol effects, including FAS and ARNDs, than other groups. [48][49][50] Umbilical cord vessels from mothers who consumed alcohol during their pregnancy showed higher amounts of DHA and AA than cord vessels from abstainers. This increase is significantly associated with average alcohol amounts consumed per day around the time of conception.…”

Section: Discussionmentioning

confidence: 99%

Effects of Alcohol Intake During Pregnancy on Docosahexaenoic Acid and Arachidonic Acid in Umbilical Cord Vessels of Black Women

Beblo

Murthy

Janisse³

et al. 2005

Pediatrics

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ABSTRACT. Objective. Alcohol influences the intake and metabolism of several nutrients including longchain polyunsaturated fatty acids (LC-PUFAs). The LCPUFAs docosahexaenoic acid (DHA) and arachidonic acid (AA) are particularly crucial for intrauterine growth and brain development. We hypothesized that alcohol consumption adversely affects LC-PUFA levels in pregnant women and their newborn infants.Methods. Pregnant black women (N ‫؍‬ 208) presenting at a core city antenatal clinic were screened and recruited. Shortly before delivery, maternal plasma was collected. After delivery, umbilical arteries and veins were dissected from the cords, total lipids were extracted from the vessel tissues and maternal plasma, and fatty acid levels were assayed by gas chromatography. For statistical analysis, subjects were categorized according to absolute alcohol intake per day (AAD) and absolute alcohol intake per drinking day (AADD) around the time of conception, with smoking and other potential confounders included in the analyses.Results. Significant differences in fatty acid composition of total lipid extracts were detected in umbilical cord vessels among the AADD groups: abstainers (AADD ‫؍‬ 0), moderate drinkers (AADD < 130 g), and heavy drinkers (AADD > 130 g). DHA and AA content in the arterial umbilical vessel wall was ϳ14% and ϳ10% higher in the moderate (n ‫؍‬ 127) and heavy (n ‫؍‬ 32) alcohol groups, respectively, than in abstainers (n ‫؍‬ 49). A small, nonsignificant increase (ϳ3%) was seen in the umbilical vein for AA but not for DHA. Alcohol intake was positively correlated to both DHA and AA concentrations in the arterial vessel wall but to neither in the venous wall nor maternal plasma. Maternal plasma DHA was positively correlated with both umbilical arteries and vein DHA, but there were no significant correlations for AA between maternal plasma and either umbilical vessel.Conclusions. Our findings indicate that alcohol intake during pregnancy is associated with altered DHA and AA status in fetal tissues. Although differences may be due to either metabolism and/or distribution, it is most likely a result of a direct influence of alcohol on fetal metabolism. Pediatrics 2005;115:e194-e203. URL: www.pediatrics.org/cgi

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“…Prenatal exposure to ethanol can cause behavioral changes, such as hyperactivity, and learning and memory deficits: Indeed, gestational exposure is a leading known cause of mental retardation (Abel & Hannigan, 1995;Abel & Sokol, 1992;Sampson et al, 1997;Stratton, Howe, & Battaglia, 1996).…”

Section: Nih-pa Author Manuscriptmentioning

confidence: 99%

The effect of gestational ethanol exposure on voluntary ethanol intake in early postnatal and adult rats.

Youngentob¹,

Molina²,

Spear³

et al. 2007

Behavioral Neuroscience

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Clinical and epidemiological studies provide strong data for a relationship between prenatal ethanol exposure and the risk for abuse in adolescent and young adult humans. However, drugacceptance results in response to fetal exposure have differed by study, age at evaluation, and experimental animal. In the present study, the authors tested whether voluntary ethanol intake was enhanced in both the infantile and adult rat (15 and 90 days of age, respectively), as a consequence of chronic fetal drug experience. Experimental rats were exposed in utero by administering ethanol to a pregnant dam in a liquid diet during gestational Days 6-20. Compared with those for isocaloric pair-fed and ad lib chow control animals, the results for experimental animals demonstrated that fetal exposure significantly increased infantile affinity for ethanol ingestion without affecting intake patterns of an alternative fluid (water). Heightened affinity for ethanol was absent in adulthood. Moreover, the results argue against malnutrition as a principal factor underlying the infantile phenomenon. These data add to a growing literature indicative of heightened early postnatal acceptance patterns resulting from maternal use or abuse of ethanol during pregnancy. Keywordsfetal ethanol exposure; postnatal ethanol affinity; ethanol abuse; ethanol drinking behavior; fetal learning It has been well established that prenatal exposure to ethanol can exert profound detrimental effects in the developing fetus. The effects can be widespread, severe, and generally permanent. Depending on timing of exposure, and its duration and dose, these include stereotypical craniofacial malformations, poor suckling reflexes, decreased birth weight NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript (Abel & Hannigan, 1995;Astley, Clarren, Little, Sampson, & Daling, 1992;Clareen & Smith, 1978;Jones, Smith, Ulleland, & Streissguth, 1973; Lemoine, Harousseau, Borteyru, & Meneut, 1968;Martin, Martin, Streissguth, & Lund, 1977;Osborn, Harris, & Weinberg, 1993;Oulette, Rosett, Rosman, & Weiner, 1977;Streissguth, Landesman-Dwyer, Martin, & Smith, 1980;Ulleland, Wennburg, Igo, & Smith, 1970;Van Dyke, MacKay, & Ziaylek, 1982), and other profound neurodevelopmental effects in the nervous system Miller, 1992b). Prenatal exposure to ethanol can cause behavioral changes, such as hyperactivity, and learning and memory deficits: Indeed, gestational exposure is a leading known cause of mental retardation (Abel & Hannigan, 1995;Abel & Sokol, 1992;Sampson et al., 1997;Stratton, Howe, & Battaglia, 1996).The above notwithstanding, there are subtler yet potentially just as detrimental long-term consequences. Recent clinical and epidemiological studies indicate that prenatal exposure to ethanol is strongly associated with the risk for ethanol abuse in adolescent and young adult humans (Alati et al., 2006;Baer, Bar, Bookstein, Sampson, & Streissguth, 1998;Streissguth, 1998;Yates, Cadoret, Troughton, Steward, & Giunta, 1998). In effect, gestational exposure...

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A Revised Conservative Estimate of the Incidence of FAS and its Economic Impact

Cited by 217 publications

References 47 publications

Fishing for Fetal Alcohol Spectrum Disorders: Zebrafish as a Model for Ethanol Teratogenesis

Fishing for Fetal Alcohol Spectrum Disorders: Zebrafish as a Model for Ethanol Teratogenesis

Effects of Alcohol Intake During Pregnancy on Docosahexaenoic Acid and Arachidonic Acid in Umbilical Cord Vessels of Black Women

The effect of gestational ethanol exposure on voluntary ethanol intake in early postnatal and adult rats.

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