The plausibility of maternal nutritional status being a contributingfactor to the risk for fetal alcohol spectrum disorders: The potential influence of zinc status as an example

摘要

There is increasing evidence that human pregnancy outcomecan be significantly compromised by suboptimal maternalnutritional status. Poor diet results in a maternal—fetalenvironment in which the teratogenicity of other insults suchas alcohol might be amplified. As an example, there isevidence that zinc (Zn) can interact with maternal alcoholexposure to influence the risk for fetal alcohol spectrumdisorders (FASD). Studies with experimental animals haveshown that the teratogenicity of alcohol is increased underconditions of Zn deficiency, whereas its teratogenicity islessened when animals are given Zn-supplemented diets orZn injections before the alcohol exposure. Alcohol canprecipitate an acute-phase response, resulting in asubsequent increase in maternal liver metallothionein, whichcan sequester Zn and lead to decreased Zn transfer to thefetus. Importantly, the teratogenicity of acute alcoholexposure is reduced in metallothionein knockout mice,which can have improved Zn transfer to the conceptusrelative to wild-type mice. Consistent with the above, Znstatus has been reported to be low in alcoholic women atdelivery. Preliminary data from two basic science and clinicalnutritional studies that are ongoing as part of the international Collaborative Initiative on Fetal AlcoholSpectrum Disorders support the potential role of Zn, amongother nutritional factors, relative to risk for FASD. Importantly, the nutrient levels being examined in thesestudies are relevant to general clinical populations andrepresent suboptimal levels rather than severe deficiencies.These data suggest that moderate deficiencies in singlenutrients can act as permissive factors for FASD, and thatadequate nutritional status or intervention throughsupplementation may provide protection from some of theadverse effects of prenatal alcohol exposure.