Fetal alcohol syndrome: a prospective national surveillance study

Elliott, Elizabeth J; Payne, Jan; Morris, Anne; Haan, Eric; Bower, Carol

doi:10.1136/adc.2007.120220

Cited by 105 publications

(113 citation statements)

References 19 publications

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“…In the USA, the estimated prevalence is 2e7 cases per 1000 live births [23]. Studies from Europe [24], Africa [25e27], Israel [28], Australia [29,30], and Russia [31] show a much higher prevalence. The highest prevalence to date has been reported from high-alcohol-consuming regions of South Africa (90 per 1000 births) [32].…”

Section: Fetal Alcohol Syndromementioning

confidence: 99%

Urgent global opportunities to prevent birth defects

Kancherla

Oakley

Brent

2014

Seminars in Fetal and Neonatal Medicine

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Section: Fetal Alcohol Syndromementioning

confidence: 99%

Urgent global opportunities to prevent birth defects

Kancherla

Oakley

Brent

2014

Seminars in Fetal and Neonatal Medicine

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“…5 The terminology Fetal Alcohol Spectrum Disorders (FASD) has been coined to define any defect caused by embryonic or prenatal alcohol exposure. 1,[6][7][8][9] Due to the high prevalence of drinking, FASD is a widespread disease in many ''Westernized'' nations. 8 In the United States alone, amounts of ethanol consumption during pregnancy vary greatly.…”

mentioning

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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“…In a high-risk community in South Africa, the prevalence in first graders was as high as 65.2 -74.2 per 1000 children . In Australia, the prevalence of FAS in children under the age of 5 between 2001 and 2004 was estimated to be 0.037 per 1000 non-Indigenous children, or 1.46 per 1000 Indigenous children (Elliott et al, 2008). The authors of this study did indicate that these figures are likely to be underestimated due to difficulties associated with diagnosis.…”

Section: Evidence In Humansmentioning

confidence: 62%

“…A study on 92 Australian cases of Fetal Alcohol Syndrome (discussed in more detail in Section 1.3.1) between 2001 and 2004 found that 78.3% of affected children had also been exposed to a secondary drug (e.g., nicotine, marijuana, and heroin) during gestation (Elliott et al, 2008). Of these, nicotine was the most frequently identified as being used with alcohol, with 67.4% of affected children also being identified as exposed to nicotine during pregnancy (Elliott et al, 2008), despite only 17.3% of mothers who were surveyed Australia-wide, who gave birth in 2003, admitting to smoking cigarettes during their pregnancies (Laws et al, 2006).…”

Section: Gestational Alcohol and Tobacco Usage In Australiamentioning

confidence: 99%

“…Of these, nicotine was the most frequently identified as being used with alcohol, with 67.4% of affected children also being identified as exposed to nicotine during pregnancy (Elliott et al, 2008), despite only 17.3% of mothers who were surveyed Australia-wide, who gave birth in 2003, admitting to smoking cigarettes during their pregnancies (Laws et al, 2006). A recent study which enrolled pregnant women from north-east New South Wales and south-east Queensland from 2007 -2011 found that women who smoked during pregnancy were more likely to also consume alcohol both at any level, and in a highrisk manner during pregnancy (Cameron et al, 2013), with similar trends identified in a cohort of women in Michigan (USA) (Flynn et al, 2003).…”

Section: Gestational Alcohol and Tobacco Usage In Australiamentioning

confidence: 99%

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A study of the consequences of early gestational ethanol and/or nicotine exposure in the mouse

Yamada¹

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The in utero environment is a critical determinant of the immediate and future health of the developing fetus. In Australia, two of the most commonly used drugs during pregnancy are alcohol and nicotine. Prolonged periods of gestational exposure to alcohol and nicotine, separately, have been associated with a range of adverse outcomes in the offspring, in both humans and experimental animal models. The consequences of ethanol and nicotine exposure restricted to early gestation on resultant offspring are poorly characterised, and few animal models exist to build greater understanding. Moreover, the immediate molecular changes associated with exposures to ethanol and/or nicotine restricted to early gestation has yet to be described.This thesis utilised mouse models of early gestational ethanol and/or nicotine exposure to explore the impact of each of these exposures on offspring growth, as well as their associated transcriptional and epigenetic changes. In each model, pregnant C57BL/6 dams were provided with ad libitum access to solutions of 10% ethanol and/or 100 µg/ml nicotine from fertilisation (0.5 dpc) to midgestation (8.5 dpc). The exposure window utilised in each of the models is developmentally equivalent to the first three to four weeks of a human pregnancy.Previously, our laboratory identified reduced growth, microcephaly, and gene expression changes in the liver and hippocampus of the postnatal offspring of the model of prenatal ethanol exposure utilised in this thesis. In contrast, at mid-gestation (9.5 dpc), there was no evidence of developmental delay (somite number), reduced growth (crown-rump length), or microcephaly.Further, a genome-wide gene expression microarray (targeting 30 855 genes) and a screen of the expression of 641 microRNAs, identified only one gene (Bcl11b) as differentially expressed in male 9.5 dpc whole embryos following the ethanol exposure. These data suggest that there is a delay between the ethanol exposure and the onset of adverse phenotypes -arguing that the embryo is somehow able to form a memory of the ethanol exposure. The absence of widespread transcriptional changes suggests that changes in embryonic mRNA and microRNA expression are unlikely to be major contributors to the memory of the exposure.A early gestational model of nicotine exposure was newly established in this thesis. This nicotine exposure resulted in an average serum cotinine (metabolite of nicotine) concentration similar to that reported in humans who smoke 10 to 15 cigarettes per day. This exposure was sufficient to induce a reduction in body size both at mid-gestation and postnatally, but not at late gestation. Furthermore, the increased expression of Zscan10 in the whole male 9.5 dpc embryo was identified and validated across multiple cohorts. Zscan10 encodes for a transcription factor expressed throughout development, with a proposed role in the regulation of progenitor cells. The increased expression of Zscan10 in the nicotine-exposed embryos was associated with a reduction in DNA methylation ...

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Fetal alcohol syndrome: a prospective national surveillance study

Cited by 105 publications

References 19 publications

Urgent global opportunities to prevent birth defects

Urgent global opportunities to prevent birth defects

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

A study of the consequences of early gestational ethanol and/or nicotine exposure in the mouse

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