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: 0.29). 01/2009; 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.


Available from: Rosa Louise Floyd, Jul 15, 2014
  • Source
    [Show abstract] [Hide abstract]
    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; 19(4). DOI:10.1007/s10995-014-1563-3 · 2.24 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: The behavioral consequences of fetal alcohol spectrum disorders (FASD) are serious and persist throughout life. The causative mechanisms underlying FASD are poorly understood. However, much has been learned about FASD from human structural and functional studies as well as from animal models, which have provided a greater understanding of the mechanisms underlying FASD. Using animal models of FASD, it has been recently discovered that ethanol induces neuroimmune activation in the developing brain. The resulting microglial activation, production of proinflammatory molecules, and alteration in expression of developmental genes are postulated to alter neuron survival and function and lead to long-term neuropathological and cognitive defects. It has also been discovered that microglial loss occurs, reducing microglia's ability to protect neurons and contribute to neuronal development. This is important, because emerging evidence demonstrates that microglial depletion during brain development leads to long-term neuropathological and cognitive defects. Interestingly, the behavioral consequences of microglial depletion and neuroimmune activation in the fetal brain are particularly relevant to FASD. This chapter reviews the neuropathological and behavioral abnormalities of FASD and delineates correlates in animal models. This serves as a foundation to discuss the role of the neuroimmune system in normal brain development, the consequences of microglial depletion and neuroinflammation, the evidence of ethanol induction of neuroinflammatory processes in animal models of FASD, and the development of anti-inflammatory therapies as a new strategy for prevention or treatment of FASD. Together, this knowledge provides a framework for discussion and further investigation of the role of neuroimmune processes in FASD.
    International Review of Neurobiology 01/2014; 118C:41-80. DOI:10.1016/B978-0-12-801284-0.00003-8 · 2.46 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Background Fetal alcohol spectrum disorders (FASD) result from fetal exposure to alcohol and are the leading cause of mental retardation in the United States. There is currently no effective treatment that targets the causes of these disorders. Thus, novel therapies are critically needed to limit the neurodevelopmental and neurodegenerative pathologies associated with FASD.MethodsA neonatal mouse FASD model was used to examine the role of the neuroimmune system in ethanol (EtOH)-induced neuropathology. Neonatal C57BL/6 mice were treated with EtOH, with or without pioglitazone, on postnatal days 4 through 9, and tissue was harvested 1 day post treatment. Pioglitazone is a peroxisome proliferator-activated receptor (PPAR)-γ agonist that exhibits anti-inflammatory activity and is neuroprotective. We compared the effects of EtOH with or without pioglitazone on cytokine and chemokine expression and microglial morphology in the hippocampus, cerebellum, and cerebral cortex.ResultsIn EtOH-treated animals compared with controls, cytokines interleukin-1β and tumor necrosis factor-α mRNA levels were increased significantly in the hippocampus, cerebellum, and cerebral cortex. Chemokine CCL2 mRNA was increased significantly in the hippocampus and cerebellum. Pioglitazone effectively blocked the EtOH-induced increase in the cytokines and chemokine in all tissues to the level expressed in handled-only and vehicle-treated control animals. EtOH also produced a change in microglial morphology in all brain regions that was indicative of microglial activation, and pioglitazone blocked this EtOH-induced morphological change.Conclusions These studies indicate that EtOH activates microglia to a pro-inflammatory stage and also increases the expression of neuroinflammatory cytokines and chemokines in diverse regions of the developing brain. Further, the anti-inflammatory and neuroprotective PPAR-γ agonist pioglitazone blocked these effects. It is proposed that microglial activation and inflammatory molecules expressed as a result of EtOH treatment during brain development contribute to the sequelae associated with FASD. Thus, pioglitazone and anti-inflammatory pharmaceuticals more broadly have potential as novel therapeutics for FASD.
    Alcoholism Clinical and Experimental Research 02/2015; 39(3). DOI:10.1111/acer.12639 · 3.31 Impact Factor