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 ?
A longitudinal study of pyridoxine and zinc supplementation of lactating women.
Forty lactating women were r and omly assigned to four treatment groups . Beginning at 1-d postpartum the women in each group received a daily vitamin-mineral supplement for 9 mo . The treatments differed only in the amount of vitamin B-6 ( 0.5 or 4.0 mg pyridoxine ) and zinc ( 0 or 25 mg ) included in the supplements . The 4.0-mg pyridoxine supplements significantly increased plasma total vitamin B-6 , plasma pyridoxal phosphate ( PLP ) , and milk total vitamin B-6 , thus showing that maternal intake exerts a significant effect on vitamin B-6 concentration in milk . There was no effect of vitamin B-6 intake on plasma , erythrocyte , or milk zinc concentration . The 25-mg zinc supplement also had no effect on plasma , erythrocyte , or milk zinc concentration , suggesting that maternal zinc intake is not a major regulator of milk zinc concentration
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 ?