Fetal alcohol spectrum disorders: Prevalence rates in South Africa

Olivier, Leana; Curfs, Leopold; Viljoen, Denis

doi:10.7196/samj.2016.v106i6.11009

Cited by 72 publications

(78 citation statements)

References 20 publications

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“…The Western Cape Province (WCP) of South Africa has one of the highest documented rates of FASD in the world - recently estimated in one particular setting at 18.3---25.9% (May et al, 2016), compared to estimates of 2---5% in the United States (May et al, 2009). Estimates typically made at a community level are likely underestimates, as FASD remains largely under---diagnosed, and the surveillance systems, clinical---based studies, and referral clinics typically used to gather data have proven to be inadequate methods for determining the prevalence of this disease Olivier, Curfs, & Viljoen, 2016). Current meta---analytic data estimate the prevalence of FAS in South Africa at 10 to 15 per 10 000 people, meaning that according to these estimates, the prevalence of FASD could range from 9 to 15 per 1000 people (Popova et al, 2017).…”

Section: Fasd In Western Cape Province South Africamentioning

confidence: 99%

Attitudes toward alcohol use during pregnancy among women recruited from alcohol-serving venues in Cape Town, South Africa: A mixed-methods study

Fletcher

May

Seedat

et al. 2018

Social Science & Medicine

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Section: Fasd In Western Cape Province South Africamentioning

confidence: 99%

Attitudes toward alcohol use during pregnancy among women recruited from alcohol-serving venues in Cape Town, South Africa: A mixed-methods study

Fletcher

May

Seedat

et al. 2018

Social Science & Medicine

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“…FASD is estimated to affect 2–5% of children in the U.S. and Western European countries (www.cdc.gov; May & Gossage, 2001; 2011; May et al, 2009). In some regions of the world, however, FAS/FASD affects up to 29% of live births (Olivier, Curfs, & Viljoen, 2016). …”

Section: Introductionmentioning

confidence: 99%

Maternal alcohol exposure during mid-pregnancy dilates fetal cerebral arteries via endocannabinoid receptors

Seleverstov

Tobiasz

Jackson

et al. 2017

Alcohol

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Prenatal alcohol exposure often results in fetal alcohol syndrome and fetal alcohol spectrum disorders. Mechanisms of fetal brain damage by alcohol remain unclear. We used baboons (Papio spp.) to study alcohol-driven changes in the fetal cerebral artery endocannabinoid system. Pregnant baboons were subjected to binge alcohol exposure via gastric infusion three times during a period equivalent to the second trimester of human pregnancy. A control group was infused with orange-flavored drink that was isocaloric to the alcohol-containing solution. Cesarean sections were performed at a time equivalent to the end of the second trimester of human pregnancy. Fetal cerebral arteries were harvested and subjected to in vitro pressurization followed by pharmacological profiling. During each alcohol-infusion episode, maternal blood alcohol concentrations (BAC) reached 80 mg/dL, that is, equivalent to the BAC considered legal intoxication in humans. Circulating anandamide (AEA) and 2-arachidonoylglycerol (2-AG) remained unchanged. Ultrasound studies on pregnant mothers revealed that fetal alcohol exposure decreased peak systolic blood velocity in middle cerebral arteries when compared to pre-alcohol levels. Moreover, ethanol-induced dilation was observed in fetal cerebral arteries pressurized in vitro. This dilation was abolished by the mixture of AM251 and AM630, which block cannabinoid receptors 1 and 2, respectively. In the presence of AM251, the cannabinoid receptor agonist AEA evoked a higher, concentration-dependent dilation of cerebral arteries from alcohol-exposed fetuses. The difference in AEA-induced cerebral artery dilation vanished in the presence of AM630. CB1 and CB2 receptor mRNA and protein levels were similar in cerebral arteries from alcohol-exposed and control-exposed fetuses. In summary, alcohol exposure dilates fetal cerebral arteries via endocannabinoid receptors and results in an increased function of CB2.

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“…As a result, prenatal alcohol exposure (PAE) can lead to a wide range of cognitive and morphological abnormalities, including fetal alcohol spectrum disorders (FASD), with the most severe cases conforming to what has been defined as fetal alcohol syndrome (FAS) (20 -21). In countries with the highest percentage of alcohol consumption during pregnancy, FAS/FASD prevalence reaches 6%, with the global prevalence of FASD among children and youth being estimated at 0.77% (22)(23)(24)(25)(26).…”

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confidence: 99%

Proteomic Analysis of Baboon Cerebral Artery Reveals Potential Pathways of Damage by Prenatal Alcohol Exposure*

Bisen¹,

Kakhniashvili²,

Johnson³

et al. 2019

Molecular & Cellular Proteomics

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In BriefProteome analysis was performed to determine whether fetal alcohol exposure during mid-pregnancy would evoke changes in protein profile of fetal cerebral artery in baboons. We detected that levels of 238 proteins differed significantly between control and alcoholexposed fetuses. Proteins of metabolic pathways represented one of the major targets of alcohol. The differences were detected near term, long after alcohol exposure took place. Our findings point at novel targets of alcohol within developing brain vessels. Graphical Abstract Highlights• We studied mid-pregnancy alcohol exposure and baboon fetal cerebral artery.• 238 proteins differed between control and alcohol-exposed fetuses near-term.• Proteins of metabolic pathways represented one of the major targets of alcohol.• Alcohol effect on the development of fetal brain vessels is persistent.Alcohol is one of the most widely misused substances in the world. Alcohol consumption by pregnant women often results in an array of fetal developmental abnormalities, but the damage to the fetus by alcohol remains poorly understood. The limited knowledge regarding the molecular targets of alcohol in the developing fetus constitutes one of the major obstacles in developing effective pharmacological interventions that could prevent fetal damage after alcohol consumption by pregnant women. The fetal cerebral artery is emerging as an important mediator of fetal cerebral damage by maternal alcohol drinking. In the present work, we conduct proteomics analysis of cerebral (basilar) artery lysates of near-term fetal baboons to search for protein targets of fetal alcohol exposure. Our study demonstrates that 3 episodes of binge alcohol exposure during the second trimester-equivalent of human pregnancy are sufficient to render profound changes in fetal cerebral artery proteome. These changes persisted, as they were detected in near-term fetuses. In particular, the relative abundance of 238 proteins differed significantly between control and alcohol-exposed fetuses. Enrichment analysis pointed at the group of metabolic activity proteins as a major class targeted by alcohol. Western blotting confirmed upregulation of the aldehyde dehydrogenase 6 family member A1 (ALDH6A1) in cerebral artery lysates from alcohol-exposed fetuses. This upregulation translated to greater ALDH activity of cerebral artery lysate of near-term fetuses following prenatal alcohol exposure when compared with controls. Molecular

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Fetal alcohol spectrum disorders: Prevalence rates in South Africa

Cited by 72 publications

References 20 publications

Attitudes toward alcohol use during pregnancy among women recruited from alcohol-serving venues in Cape Town, South Africa: A mixed-methods study

Attitudes toward alcohol use during pregnancy among women recruited from alcohol-serving venues in Cape Town, South Africa: A mixed-methods study

Maternal alcohol exposure during mid-pregnancy dilates fetal cerebral arteries via endocannabinoid receptors

Proteomic Analysis of Baboon Cerebral Artery Reveals Potential Pathways of Damage by Prenatal Alcohol Exposure*

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