Impact of fetal alcohol exposure on body systems: A systematic review

Caputo, Courtney; Wood, E. J.; Jabbour, Leila

doi:10.1002/bdrc.21129

Cited by 142 publications

(101 citation statements)

References 57 publications

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“…It is widely documented that prenatal alcohol (ethanol) exposure causes abnormalities in several organs and systems of the body, such as the heart, kidney, liver, gastrointestinal tract, and the endocrine and immune systems (Caputo, Wood, & Jabbour, 2016; Gauthier, 2015). However, the brain constitutes the most severely affected organ, exhibiting both structural and functional abnormalities in response to prenatal alcohol exposure (Caputo et al, 2016; Mattson, Schoenfeld, & Riley, 2001).…”

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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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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“…Interventions to reduce maternal alcohol consumption during pregnancy were associated with a 202.1 g (95% CI, 60.85-343.35) increase in offspring birth weight [Appendix in [107]]. Renal hypoplasia has been reported in association with fetal alcohol syndrome [113], and, in animals, acute prenatal alcohol exposure was associated with reduced nephron numbers and subsequently increased blood pressure levels [343]. The long-term consequences in humans require more study.…”

Section: Consensus Recommendationsmentioning

confidence: 99%

“…Supplementation of iron, micronutrients, balanced energy, calcium, zinc, and iodine in pregnant women have all been associated with reductions in LBW or preterm birth and, therefore, may have a positive impact on developmental programming in the kidney [103,107]. Maternal intake of alcohol, caffeine, as well as tobacco consumption are also known to be associated with an increased risk of LBW, preterm birth, as well as programming of childhood blood pressure, kidney size, and function [108,109,110,111,112,113,114,115]. Interventions to reduce smoking in pregnancy have been associated with reductions in the risk of LBW and preterm birth [107].…”

Section: Introduction To a Health Problemmentioning

confidence: 99%

The Impact of Kidney Development on the Life Course: A Consensus Document for Action

Brenner

Charlton

Luyckx

et al. 2017

Nephron

123

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Hypertension and chronic kidney disease (CKD) have a significant impact on global morbidity and mortality. The Low Birth Weight and Nephron Number Working Group has prepared a consensus document aimed to address the relatively neglected issue for the developmental programming of hypertension and CKD. It emerged from a workshop held on April 2, 2016, including eminent internationally recognized experts in the field of obstetrics, neonatology, and nephrology. Through multidisciplinary engagement, the goal of the workshop was to highlight the association between fetal and childhood development and an increased risk of adult diseases, focusing on hypertension and CKD, and to suggest possible practical solutions for the future. The recommendations for action of the consensus workshop are the results of combined clinical experience, shared research expertise, and a review of the literature. They highlight the need to act early to prevent CKD and other related noncommunicable diseases later in life by reducing low birth weight, small for gestational age, prematurity, and low nephron numbers at birth through coordinated interventions. Meeting the current unmet needs would help to define the most cost-effective strategies and to optimize interventions to limit or interrupt the developmental programming cycle of CKD later in life, especially in the poorest part of the world.

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“…Sindrome alkoholiko fetalaren frekuentzia 1-3/1.000 jaiotzekoa dela estimatzen da (Downen sindromearen antzera). Ikerketa batzuen arabera, haurdun dauden emakumeen %24a arrisku-kontsumitzailea da [13].…”

Section: Zergatik Egiten Digu Alkoholak Kalte?unclassified

Zergatik egiten digu alkoholak kalte?

Morera-Herreras

Fernández-Aedo

Miguélez

et al. 2017

EKAIA

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Laburpena: Gaur egun, alkohol-kontsumoa oso hedatua dago gure gizartean. Nahiz eta gizartearen aldetik oso onartua egon, iradoki izan da batetik efektu euforikoak eragiten dituela, eta bestetik asaldura fisiko zein psikiko kaltegarriak eragin diezazkiokeela organismoari. Alkoholaren zinetika nahiko aldakorra izan daiteke eta horrek nabarmen baldintzatzen ditu organismoan sortzen diren eragin akutuak. Bestalde, alkoholaren luzaroko kontsumoak ere efektu kaltegarriak ditu, esate baterako, menpekotasuna. Ondorioz, gizakiak alkoholdun edariak hartzeko behar handia sumatzen du. Horrekin lotuta, alkoholikoak tolerantzia garatuko du, eta gero eta alkohol kantitate handiagoak beharko ditu. Artikulu honetan, berrikusi egingo dira gorputzeko alkohol kontzentrazio handiagoak baldintzatzen dituzten prozesu zinetiko garrantzitsuenak, baita alkoholak eragindako efektu akutuak zein kronikoak ere.Hitz gakoak: Etanola, menpekotasuna, abstinentzia-sindromea, tolerantzia. Abstract:Alcohol consumption has widespread use and acceptance in today's society. Besides the euphoric effect, alcohol can also produce unpleasant psychological and physical side effects. The acute effects of alcohol depend on its kinetics which varies among the individuals. On the other hand, prolonged use can also produce severe unwanted effects, such as dependence. As a consequence, the person will have an urgent need to drink alcohol. At the same time, the alcoholic will develop tolerance and therefore higher amounts of alcohol will be required for obtaining the same effects. In this article, we will review the kinetic processes that have a higher impact in alcohol plasmatic concentrations. We will also analyze the acute and chronic effects induced by alcoholic beverages.

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Impact of fetal alcohol exposure on body systems: A systematic review

Cited by 142 publications

References 57 publications

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

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

The Impact of Kidney Development on the Life Course: A Consensus Document for Action

Zergatik egiten digu alkoholak kalte?

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