Zinc Status of Infants with Fetal Alcohol Syndrome

Assadi, Farahnak; Ziai, Mohsen

doi:10.1203/00006450-198606000-00014

Cited by 36 publications

(13 citation statements)

References 16 publications

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“…An increase in absorption with age has been noted by Dorner et al (15) using enriched stable isotopes in studies in preterm infants. The reasons for the considerably scattered data on urinary Zn excretion in infancy (5, 16,17) are still unknown. The decrease in Zn concentration in human milk may be the reason for the decrease in urinary Zn excretion in the breast-fed infants investigated (Fig.…”

Section: Discussionmentioning

confidence: 99%

Longitudinal zinc balances in breast‐fed and formula‐fed infants

Sievers

Dörner

et al. 1992

Acta Paediatrica

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Longitudinal zinc (Zn) balance studies were performed under domestic conditions in term breast-fed (n = 10), term formula-fed (n = 5; Zn concentration in the formula: 4 mg/l) and preterm formula-fed (n = 3) infants during the first 17 weeks of life. Samples of milk, urine and feces were analyzed by atomic absorption spectrometry. The median daily Zn intake in breast-fed infants decreased from 0.592 (0.457-0.829) mg Zn/kg body weight to 0.151 (0.095-0.304) mg Zn/kg body weight in the first 17 weeks of life; comparable values for bottle-fed term infants were 0.58 (0.511-0.701) and 0.674 (0.529-0.731) mg Zn/kg body weight. The median percent retention of Zn intake was 27 (-60 to 81.4)% in breast-fed infants and 21.5 (-42 to 64)% in formula-fed infants. In view of the urinary and fecal Zn losses measured, a daily intake of 0.3-0.5 mg Zn/kg body weight is considered to be sufficient to ensure a Zn retention equivalent to breast-fed infants. This requires a Zn concentration of 2-3 mg/l of Zn depending on milk volume intake.

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Section: Discussionmentioning

confidence: 99%

Longitudinal zinc balances in breast‐fed and formula‐fed infants

Sievers

Dörner

et al. 1992

Acta Paediatrica

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“…In addition to pregnant women who are exposed to alcohol, infants with FASD have been reported to have low plasma Zn concentrations and higher 24‐h urinary Zn excretions compared with normal controls, indicating altered Zn homeostasis [103]. Interestingly, Murillo‐Fuentes et al [104] reported that rat pups whose mothers were given alcohol during the period of lactation were also characterized by higher than normal levels of urinary Zn excretion.…”

Section: Alcohol–zn Interactionsmentioning

confidence: 99%

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

Keen

Uriu‐Adams

Skalny³

et al. 2010

BioFactors

100

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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, while its teratogenicity is lessened when animals are given Zn supplemented diets or Zn injections prior to 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 (CIFASD) 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 for some of the effects of prenatal alcohol exposure.

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“…The manifestation of fetal dysmorphogenesis in alcoholic women appears to be related to the low zinc status of mater nal plasma [12]. Lower plasma zinc levels are seen in infants with FAS, for which increased urinary zinc excretion appears to be responsible [13], As zinc metalloenzymes and zinc-related enzymes or substrates, alco hol dehydrogenases (EC 1.1.1.1), carbonic anhydrase (EC 4.2.1.1), 2',3'-cyclic nucleo tide 3'-phosphohydrolase (EC 3.1.4.37) and insulin are known. Furthermore, the hippo campus, in which ethanol accumulates to peak levels [14], is well known to be rich in zinc [15].…”

Section: Discussionmentioning

confidence: 99%

Fetal Alcohol Syndrome in Rats: Conditions for Improvement of Ethanol Effects on Fetal Cerebral Development with Supplementary Agents

Tanaka¹,

Iwasaki²,

Nakazawa³

et al. 1988

Neonatology

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As a possible preventative measure for brain dysfunction in the fetal alcohol syndrome, the effect of zinc or vitamin E supplementation together with ethanol on the fetal cerebrum was investigated in rats. Contrary to our previously published data showing the good effect of 0.01% zinc with 30% ethanol on fetuses, the administration of 0.01% zinc with 20% ethanol, 0.03% vitamin E with 20% ethanol or 0.02% vitamin E with 10% ethanol during pregnancy did not result in a good effect on the body and cerebral weights of fetuses on gestational day 21. The development of dendritic branches on frontal cerebral neurons in fetuses was decreased in the order of the control, zinc with ethanol and ethanol groups. The concentration and content of α-tocopherol were increased, but those of zinc were not, in the fetal cerebrum with the maternal administration of vitamin E or zinc together with ethanol, respectively. These results suggest that the improvement of the brain function might depend on the deficient agent induced by maternal ethanol ingestion.

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Zinc Status of Infants with Fetal Alcohol Syndrome

Cited by 36 publications

References 16 publications

Longitudinal zinc balances in breast‐fed and formula‐fed infants

Longitudinal zinc balances in breast‐fed and formula‐fed infants

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

Fetal Alcohol Syndrome in Rats: Conditions for Improvement of Ethanol Effects on Fetal Cerebral Development with Supplementary Agents

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