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

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 th...

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Published in:	BioFactors (Oxford) Vol. 36; no. 2; pp. 125 - 135
Main Authors:	Keen, Carl L., Uriu-Adams, Janet Y., Skalny, Anatoly, Grabeklis, Andrei, Grabeklis, Sevil, Green, Kerri, Yevtushok, Lyubov, Wertelecki, Wladimir W., Chambers, Christina D.
Format:	Journal Article
Language:	English
Published:	Hoboken Wiley Subscription Services, Inc., A Wiley Company 01-03-2010
Subjects:	Acute-Phase Reaction - metabolism alcohol Animals Ethanol - metabolism FAS FASD Female Fetal Alcohol Spectrum Disorders - metabolism Humans micronutrients Nutritional Status - physiology Pregnancy zinc Zinc - metabolism Zinc - physiology
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Summary:	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.
Bibliography:	ArticleID:BIOF89 NIAAA - No. U01AA014835; No. U24AA014811 NIH - No. 01743; No. HD 26777 ark:/67375/WNG-JWCQ62GZ-5 istex:BD0A401D7773265FF80CEE1C0353396E26B4E717 Tel.: +1‐530‐752‐6331; Fax: +1‐530‐752‐8966
ISSN:	0951-6433 1872-8081
DOI:	10.1002/biof.89