Document Detail


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.
MedLine Citation:
PMID:  20333752     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
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:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review    
Journal Detail:
Title:  BioFactors (Oxford, England)     Volume:  36     ISSN:  1872-8081     ISO Abbreviation:  Biofactors     Publication Date:    2010 Mar-Apr
Date Detail:
Created Date:  2010-04-14     Completed Date:  2010-06-28     Revised Date:  2014-09-24    
Medline Journal Info:
Nlm Unique ID:  8807441     Medline TA:  Biofactors     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  125-35     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Acute-Phase Reaction / metabolism
Animals
Ethanol / metabolism
Female
Fetal Alcohol Spectrum Disorders / metabolism*
Humans
Nutritional Status / physiology
Pregnancy
Zinc / metabolism*,  physiology
Grant Support
ID/Acronym/Agency:
HD 01743/HD/NICHD NIH HHS; HD 26777/HD/NICHD NIH HHS; R01 AA021551/AA/NIAAA NIH HHS; R01 HD001743/HD/NICHD NIH HHS; R01 HD001743-40/HD/NICHD NIH HHS; R01 HD026777/HD/NICHD NIH HHS; R01 HD026777-12/HD/NICHD NIH HHS; U01 AA014835/AA/NIAAA NIH HHS; U01 AA014835-06/AA/NIAAA NIH HHS; U01AA014835/AA/NIAAA NIH HHS; U24 AA014811/AA/NIAAA NIH HHS; U24 AA014811-06/AA/NIAAA NIH HHS; U24AA014811/AA/NIAAA NIH HHS
Chemical
Reg. No./Substance:
3K9958V90M/Ethanol; J41CSQ7QDS/Zinc
Comments/Corrections

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