Effects of calcium supplementation and lactation on iron status.

Calcium has been shown to inhibit iron absorption. The consequences of chronic calcium supplementation on iron status are unclear, however. As part of a randomized calcium-supplementation trial in lactating and nonlactating women in the postpartum period, we determined whether long-term calcium supplementation and lactation status affected iron stores as measured by serum ferritin concentrations. Subjects (95 lactating and 92 nonlactating) were enrolled at approximately 6 mo postpartum and then randomly assigned to receive either 500 mg Ca as calcium carbonate or a placebo twice daily with meals for 6 mo. Lactating women weaned their infants approximately 2 mo after enrollment (ie, approximately 8 mo postpartum). Calcium supplementation had no effect on serum ferritin concentrations. At the end of the study, geometric mean serum ferritin concentrations were 28.4 microg/L in the calcium-supplemented group and 27.5 microg/L in the placebo group (P > 0.5). Lactation status was significantly related to serum ferritin concentrations. At baseline, serum ferritin concentrations were higher in lactating women than in nonlactating women (47.7 compared with 31.5 microg/L, P < 0.001). In lactating women, serum ferritin concentrations decreased by a mean of 17 microg/L after weaning. By 12 mo postpartum, mean serum ferritin concentrations in women who were previously lactating were not significantly higher than those of nonlactating women (30.5 compared with 25.5 microg/L). These findings provide reassurance that long-term calcium supplementation does not impair iron stores. Furthermore, lactation status should be considered when assessing iron nutriture of women and determinants of iron status in populations.

Effects of gestational age, maternal diabetes, and intrauterine growth retardation on markers of fetal bone turnover in amniotic fluid.

Little is known about the dynamics of bone formation and bone resorption in utero, particularly the normal changes that occur throughout gestation and in clinical situations that result in low bone mass at birth. The objectives of this study were to describe the effects of gestational age on markers of fetal bone turnover, and to investigate whether the reported low bone mass at birth in small-for-gestational-age (SGA) infants and infants of diabetic mothers (IDMs) was associated with biochemical markers of decreased bone formation or increased bone resorption in utero. Bone formation and resorption were assessed by measurement of carboxyterminal propeptide of type I procollagen (PICP) and cross-linked carboxyterminal telopeptide of type I collagen (ICTP), respectively, in 201 amniotic fluid samples. These markers are by-products of type I collagen formation and degradation, respectively, and have been used in the assessment of bone metabolism ex utero. Both PICP and ICTP concentrations in amniotic fluid were inversely associated with gestational age (P < 0.0001). Amniotic fluid concentrations of PICP increased exponentially in relation to infant birthweight (P = 0.008), and SGA infants had lower amniotic fluid PICP concentrations than controls (P = 0.07). The presence of diabetes in the mother was not associated with alterations in amniotic fluid PICP or ICTP concentrations. Although maturational effects on clearance of bone markers from amniotic fluid cannot be excluded, these data are consistent with a high turnover of bone matrix early in fetal life, and a reduction in bone formation when fetal growth is compromised.