| The plausibility of maternal nutritional status being a contributing factor to the risk for fetal alcohol spectrum disorders: the potential influence of zinc status as an example. | |
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MedLine Citation:
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PMID: 20333752 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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There is increasing evidence that human pregnancy outcome can be significantly compromised by suboptimal maternal nutritional status. Poor diet results in a maternal-fetal environment in which the teratogenicity of other insults such as alcohol might be amplified. As an example, there is evidence that zinc (Zn) can interact with maternal alcohol exposure to influence the risk for fetal alcohol spectrum disorders (FASD). Studies with experimental animals have shown that the teratogenicity of alcohol is increased under conditions of Zn deficiency, whereas its teratogenicity is lessened when animals are given Zn-supplemented diets or Zn injections before the alcohol exposure. Alcohol can precipitate an acute-phase response, resulting in a subsequent increase in maternal liver metallothionein, which can sequester Zn and lead to decreased Zn transfer to the fetus. Importantly, the teratogenicity of acute alcohol exposure is reduced in metallothionein knockout mice, which can have improved Zn transfer to the conceptus relative to wild-type mice. Consistent with the above, Zn status has been reported to be low in alcoholic women at delivery. Preliminary data from two basic science and clinical nutritional studies that are ongoing as part of the international Collaborative Initiative on Fetal Alcohol Spectrum Disorders support the potential role of Zn, among other nutritional factors, relative to risk for FASD. Importantly, the nutrient levels being examined in these studies are relevant to general clinical populations and represent suboptimal levels rather than severe deficiencies. These data suggest that moderate deficiencies in single nutrients can act as permissive factors for FASD, and that adequate nutritional status or intervention through supplementation may provide protection from some of the adverse effects of prenatal alcohol exposure. |
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Authors:
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Carl L Keen; Janet Y Uriu-Adams; Anatoly Skalny; Andrei Grabeklis; Sevil Grabeklis; Kerri Green; Lyubov Yevtushok; Wladimir W Wertelecki; Christina D Chambers |
Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Review |
Journal Detail:
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Title: BioFactors (Oxford, England) Volume: 36 ISSN: 1872-8081 ISO Abbreviation: Biofactors Publication Date: 2010 Mar-Apr |
Date Detail:
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Created Date: 2010-04-14 Completed Date: 2010-06-28 Revised Date: 2011-09-26 |
Medline Journal Info:
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Nlm Unique ID: 8807441 Medline TA: Biofactors Country: Netherlands |
Other Details:
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Languages: eng Pagination: 125-35 Citation Subset: IM |
Affiliation:
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Department of Nutrition, University of California, Davis, Davis, CA 95616, USA. clkeen@ucdavis.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Acute-Phase Reaction
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metabolism Animals Ethanol / metabolism Female Fetal Alcohol Syndrome / metabolism* Humans Nutritional Status / physiology Pregnancy Zinc / metabolism*, physiology |
| Grant Support | |
ID/Acronym/Agency:
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HD 01743/HD/NICHD NIH HHS; HD 26777/HD/NICHD NIH HHS; R01 HD001743-40/HD/NICHD NIH HHS; R01 HD026777-12/HD/NICHD NIH HHS; U01 AA014835-06/AA/NIAAA NIH HHS; U01AA014835/AA/NIAAA NIH HHS; U24 AA014811-06/AA/NIAAA NIH HHS; U24AA014811/AA/NIAAA NIH HHS |
| Chemical | |
Reg. No./Substance:
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64-17-5/Ethanol; 7440-66-6/Zinc |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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