We hypothesize , therefore , that zinc homeostatic adjustments during pregnancy and lactation improve zinc utilization sufficiently to provide the increased zinc needs in these stages and , therefore , mitigate immediate detrimental effects due to a low zinc intake .
Zinc plays critical roles during embryogenesis , fetal growth , and milk secretion , which increase the zinc need for pregnancy and lactation .
Increased needs can be met by increasing the dietary zinc intake , along with making homeostatic adjustments in zinc utilization .
Potential homeostatic adjustments include changes in circulating zinc , increased zinc absorption , decreased zinc losses , and changes in whole body zinc kinetics .
Although severe zinc deficiency during pregnancy has devastating effects , systematic review s and meta- analysis of the effect of maternal zinc supplementation on pregnancy outcomes have consistently shown a limited benefit .
The specific questions addressed are the following : How is zinc utilization altered during pregnancy and lactation ?
Are those homeostatic adjustments influenced by maternal zinc status , dietary zinc , or zinc supplementation ?
Zinc nutritional status during pregnancy: a longitudinal study.
Dietary zinc ( Zn ) intake and selected biochemical indices of Zn status were studied longitudinally at monthly intervals in 46 pregnant middle-income women , 10 of whom received a daily supplement of 15 mg Zn .  Mean dietary Zn intake for the nonsupplemented subjects ( group A ) was 11.3 + /- 4.1 mg/day ( 56 % of the Recommended Dietary Allowances ) , and for the Zn-supplemented subjects ( group B ) was 21.7 mg/day ( 109 % of the Recommended Dietary Allowance ) , including an average intake of 11.1 mg/day as supplemental Zn . The mean plasma Zn concentration of group A at 2 months gestation , 71.4 + /- 9.8 micrograms/dl , was 17 % lower than that of nonpregnant control women , and continued to decline significantly ( p less than 0.01 ) between 2 and 10 months gestation . Plasma Zn of group B did not differ significantly from group A at any stage of gestation . Mean serum alkaline phosphatase activity of group B was higher than that of group A at 7 of 8 months studied ( p less than 0.05 ) . The level of prenatal iron supplementation  in group A was negatively correlated with alkaline phosphatase activity and plasma Zn in the 2nd and 3rd trimesters , respectively . It is concluded that an early and progressive decline in plasma Zn which is not influenced by Zn intake occurs during gestation . Tentative st and ards for lower limits of normal at monthly intervals have been suggested . The higher alkaline phosphatase activity of group B compared with group A suggested that the dietary Zn intake of the latter was suboptimal . Prenatal supplemental iron may adversely affect maternal Zn status
We hypothesize , therefore , that zinc homeostatic adjustments during pregnancy and lactation improve zinc utilization sufficiently to provide the increased zinc needs in these stages and , therefore , mitigate immediate detrimental effects due to a low zinc intake .
Zinc plays critical roles during embryogenesis , fetal growth , and milk secretion , which increase the zinc need for pregnancy and lactation .
Increased needs can be met by increasing the dietary zinc intake , along with making homeostatic adjustments in zinc utilization .
Potential homeostatic adjustments include changes in circulating zinc , increased zinc absorption , decreased zinc losses , and changes in whole body zinc kinetics .
Although severe zinc deficiency during pregnancy has devastating effects , systematic review s and meta- analysis of the effect of maternal zinc supplementation on pregnancy outcomes have consistently shown a limited benefit .
The specific questions addressed are the following : How is zinc utilization altered during pregnancy and lactation ?
Are those homeostatic adjustments influenced by maternal zinc status , dietary zinc , or zinc supplementation ?