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 urinary calcium, magnesium, and zinc excretion in lactating and nonlactating postpartum women.
Postpartum lactating ( n = 12 ) and nonlactating ( n = 11 ) women and never pregnant women ( n = 14 ) collected urine sample s and diet records 2 d each month for 6 mo to determine whether postpartum women conserved urinary calcium , magnesium , or zinc . Mean daily excretions were analyzed by repeated- measures analysis of variance and covariance to assess group and time effects . Lactating women excreted less urinary calcium ( 1 - 6 mo ) than never pregnant ( n = 8) and nonlactating ( n = 4 ) women who did not use oral contraceptives ( P < 0.01 ) ; however , excretion rose ( P < 0.05 ) by 3 mo postpartum . In the nonlactating and never pregnant groups , women using oral contraceptives excreted less urinary calcium than the other women ( P < 0.01 ) . Lactating women excreted less urinary zinc ( 1 - 6 mo ) than did control and non-lactating women ( P < 0.01 ) . Mechanisms may possibly be operating during lactation that depress urinary calcium for > or = 2 mo and urinary zinc < or = 6 mo postpartum
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 ?