Prevention of fetal alcohol spectrum disorders.

Centers for Disease Control and Prevention, National Center on Birth Defects and Developmental Disabilities, Prevention Research Branch, Fetal Alcohol Syndrome Prevention Team, Atlanta, Georgia 30333, USA.
Developmental Disabilities Research Reviews (Impact Factor: 2.79). 02/2009; 15(3):193-9. DOI: 10.1002/ddrr.75
Source: PubMed

ABSTRACT Alcohol use among women of childbearing age is a leading, preventable cause of birth defects and developmental disabilities in the United States. Although most women reduce their alcohol use upon pregnancy recognition, some women report drinking during pregnancy and others may continue to drink prior to realizing they are pregnant. These findings emphasize the need for effective prevention strategies for both pregnant and nonpregnant women who might be at risk for an alcohol-exposed pregnancy (AEP). This report reviews evidence supporting alcohol screening and brief intervention as an effective approach to reducing problem drinking and AEPs that can lead to fetal alcohol spectrum disorders. In addition, this article highlights a recent report of the National Task Force on Fetal Alcohol Syndrome and Fetal Alcohol Effect that describes effective interventions to reduce alcohol use and AEPs, and outlines recommendations on promoting and improving these strategies. Utilizing evidence-based alcohol screening tools and brief counseling for women at risk for an AEP and other effective population-based strategies can help achieve future alcohol-free pregnancies.

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    ABSTRACT: Although the mechanism of ethanol toxicity during embryogenesis is unknown, our earlier studies on Japanese rice fish (Oryzias latipes) embryos indicated that the effects might be mediated through oxidative stress. In this study we have determined the oxidative stress and the mRNA content of four antioxidant enzymes (catalase, glutathione reductase, glutathione-S-transferase, and superoxide dismutase) during Japanese rice fish embryogenesis (from 0 day post-fertilization to hatching) and after exposing the embryos to ethanol (100 and 300 mM) for 48 h at three stages (0-2, 1-3 and 4-6 days post-fertilization, dpf) of organogenesis. We observed that oxidative stress was minimal in blastula, gastrula or neurula stages, increased gradually with the advancement of morphogenesis and reached its maximum level in hatchlings. The antioxidant enzyme mRNAs were constitutively expressed throughout development; however, the expression pattern was not identical among the enzymes. Catalase and superoxide dismutase (SOD) mRNAs were minimal in the fertilized eggs, but increased significantly in 1 dpf and then either sharply dropped (SOD) or maintained a steady-state (catalase). Glutathione-S-transferase (GST) was very high in fertilized eggs and sharply dropped 1 dpf and then gradually increased thereafter. Glutathione reductase (GR) maintained a steady-state throughout the development. Ethanol was able to attenuate oxidative stress in embryos exposed only to 300 mM 1-3 dpf; no significant difference with controls was observed in other ethanol-treated groups. The antioxidant enzyme mRNAs also remained unaltered after ethanol treatment. From these data we conclude that the attenuation of oxidative stress by ethanol is probably due to the inhibition of normal growth of the embryos rather than by inhibiting catalase, GST, GR or SOD-dependent activities.
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    ABSTRACT: Fetal alcohol exposure (FAE) can lead to a variety of behavioral and physiological disturbances later in life. Understanding how alcohol (ethanol, EtOH) affects fetal brain development is essential to guide the development of better therapeutics for FAE. One of EtOH's many pharmacological targets is the γ-aminobutyric acid type A receptor (GABAAR), which plays a prominent role in early brain development. Acute EtOH potentiates inhibitory currents carried by certain GABAAR subtypes, whereas chronic EtOH leads to persistent alterations in GABAAR subunit composition, localization and function. We recently introduced a flavonoid compound, dihydromyricetin (DHM), which selectively antagonizes EtOH's intoxicating effects in vivo and in vitro at enhancing GABAAR function as a candidate for alcohol abuse pharmacotherapy. Here, we studied the effect of FAE on physiology, behavior and GABAAR function of early adolescent rats and tested the utility of DHM as a preventative treatment for FAE-induced disturbances. Gavage administration of EtOH (1.5, 2.5, or 5.0 g/kg) to rat dams on day 5, 8, 10, 12, and 15 of pregnancy dose-dependently reduced female/male offspring ratios (largely through decreased numbers of female offspring) and offspring body weights. FAE (2.5 g/kg) rats tested on postnatal days (P) 25-32 also exhibited increased anxiety and reduced pentylenetetrazol (PTZ)-induced seizure threshold. Patch-clamp recordings from dentate gyrus granule cells (DGCs) in hippocampal slices from FAE (2.5 g/kg) rats at P25-35 revealed reduced sensitivity of GABAergic miniature inhibitory postsynaptic currents (mIPSCs) and tonic current (Itonic) to potentiation by zolpidem (0.3 μM). Interestingly, potentiation of mIPSCs by gaboxadol increased, while potentiation of Itonic decreased in DGCs from FAE rats. Co-administration of EtOH (1.5 or 2.5 g/kg) with DHM (1.0 mg/kg) in pregnant dams prevented all of the behavioral, physiological, and pharmacological alterations observed in FAE offspring. DHM administration alone in pregnant rats had no adverse effect on litter size, progeny weight, anxiety level, PTZ seizure threshold, or DGC GABAAR function. Our results indicate that FAE induces long-lasting alterations in physiology, behavior, and hippocampal GABAAR function and that these deficits are prevented by DHM co-treatment of EtOH-exposed dams. The absence of adverse side effects and the ability of DHM to prevent FAE consequences suggest that DHM is an attractive candidate for development as a treatment for prevention of fetal alcohol spectrum disorders.
    Neurochemical Research 03/2014; · 2.13 Impact Factor
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    ABSTRACT: Non-pregnant women can avoid alcohol-exposed pregnancies (AEPs) by modifying drinking and/or contraceptive practices. The purpose of this study was to estimate the number and characteristics of women in the United States who are at risk of AEPs. We analyzed data from in-person interviews obtained from a national probability sample (i.e., the National Survey of Family Growth) of reproductive-aged women conducted from January 2002 to March 2003. To be at risk of AEP, a woman had to have met the following criteria in the last month: (1) was drinking; (2) had vaginal intercourse with a man; and (3) did not use contraception. During a 1-month period, nearly 2 million U.S. women were at risk of an AEP (95 % confidence interval 1,760,079-2,288,104), including more than 600,000 who were binge drinking. Thus, 3.4 %, or 1 in 30, of all non-pregnant women were at risk of an AEP. Most demographic and behavioral characteristics were not clearly associated with AEP risk. However, pregnancy intention was strongly associated with AEP risk (prevalence ratio = 12.0, P < 0.001) because women often continued to drink even after they stopped using contraception. Nearly 2 million U.S. women are at AEP risk and therefore at risk of having children born with fetal alcohol spectrum disorders. For pregnant women and women intending a pregnancy, there is an urgent need for wider implementation of prevention programs and policy approaches that can reduce the risk for this serious public health problem.
    Maternal and child health journal. 07/2014;

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