Calcium homeostasis and bone metabolism during pregnancy, lactation, and postweaning: a longitudinal study (original) (raw)
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Bone, 2003
This longitudinal study evaluated bone turnover and the interrelationship between changes in bone biomarkers and habitual dietary calcium intake during pregnancy in a group of women ranging widely with regard to dietary calcium intake. Thirty-nine healthy pregnant and 30 nonpregnant women were studied. Calcium, phosphorus, 1␣,25-dihydroxyvitamin D (1,25diHOD), bone alkaline phosphatase (bALP), carboxyterminal propeptides of type I procollagen (PICP) and carboxyterminal telopeptides of type I collagen (CTX and ICTP) were measured in serum and calcium, and creatinine and aminoterminal telopeptide (NTX) were determined in urine. Serum calcium and phosphorus did not change but the urinary Ca/Creat ratio and 1,25diHOD increased throughout pregnancy (P Ͻ 0.001 and P Ͻ 0.0001, respectively). Serum b-ALP and PICP increased during the last two trimesters (P Ͻ 0.0001 and P Ͻ 0.001, respectively). All studied bone resorption markers increased compared to nonpregnant values throughout pregnancy. The highest increment was observed in the third trimester. The level of significance decreased as follows: CTX Ͼ NTX ϾICTP. Serum 1,25 diHOD versus calcium intake showed a positive and significant correlation (r ϭ 0.51, P Ͻ 0.02). A negative correlation between the absolute change in CTX, NTX, and b-ALP between the third and second trimester and calcium intake at the end of pregnancy was observed in pregnant women who did not cover adequately calcium intake requirements (r ϭ Ϫ0.47, P Ͻ 0.03; r ϭ Ϫ0.41, P Ͻ 0.05; and r ϭ Ϫ0.43, P Ͻ 0.05, respectively). These results suggest that skeletal response to pregnancy may not be entirely independent of maternal calcium intake, especially in women with usually low calcium intake. In summary, not only hormonal changes in calcium metabolism that occur during pregnancy but also other considerations, such as low dietary calcium intake, may lead to an increment in the biological activity of the skeleton. Additional studies must be conducted to confirm our findings and to gain a better understanding of skeletal response to a low calcium intake during pregnancy.
Calcium and Bone Metabolism During Pregnancy and Lactation
Journal of Mammary Gland Biology and Neoplasia, 2005
Pregnancy and lactation both place significant demands on the mother to provide sufficient calcium (among other minerals and nutrients) to the fetus and neonate. Despite facing similar demands for calcium during pregnancy and lactation, the maternal adaptations differ significantly between these two reproductive periods. Women lose 300 to 400 mg of calcium daily through breast milk, and this calcium demand is met by a 5-10% loss of skeletal mineral content during 6 months of exclusive lactation. Most importantly, the lost mineral is fully restored within a few months of weaning, such that women who have breastfed do not have a longterm deficit in skeletal mineral content. This article will review our present understanding of the adaptations in mineral metabolism that occur during pregnancy and lactation, and will focus on recent evidence that the breast itself plays a central role in regulating the adaptations during lactation.
Effect of prenatal calcium supplementation on bone during pregnancy and 1 y postpartum
The American Journal of Clinical Nutrition
Background Low calcium intake during pregnancy may cause maternal skeletal calcium mobilization to meet fetal needs. The Recommended Dietary Allowance (RDA) for calcium in nonpregnant, pregnant, or lactating women aged 19–50 y is 1000 mg/d; most women in the United States report consuming 60–80% of the calcium RDA. An insufficient calcium intake could increase maternal bone loss during pregnancy and reduce bone recovery postpartum. Objectives The aim of this study was to determine the effect of maternal calcium supplementation on peripheral cortical and trabecular bone loss during pregnancy and bone gain postpartum. Methods A total of 64 women were enrolled in the study at 16 wk of gestation and randomly assigned to receive 1000 mg Ca/d or placebo for the remainder of the pregnancy. Measurements were performed at 16, 26, and 36 wk of pregnancy and at 4 and 12 mo postpartum for serum 25-hydroxyvitamin D and markers of bone turnover. Trabecular and cortical bone mineral density (BMD) ...
[Osteoporosis in pregnancy and lactation]
Medicina, 2000
Normal pregnancy and lactation lead to a combination of adaptive metabolic responses, the end result of which is to assure adequate delivery of mineral to the fetus while affording protection to the maternal skeleton. Elevated circulating levels of 1.25-OH vitamin D lead to increased efficiency of maternal intestinal calcium absorption and possibly lead to hypersecretion of calcitonin. Although serum concentrations of parathyroid hormone do not change during pregnancy, increased levels of a related hormone, PTH-related peptide, seem to contribute to a state of maternal functional hyperparathyroidism and maintain the fetal-maternal calcium gradient necessary to provide calcium to the fetus. Bone turnover increases during lactation and diminishes urinary calcium loss mobilizing mineral for the milk. Elevated levels of ionized calcium and phosphorus possibly correlate with increased bone resorption and decreased urinary excretion of these minerals. Bone mass is not normally lost during...
2004
Background: Physiologic adjustments in calcium homeostasis during pregnancy and lactation in women with marginal calcium intakes have not been described. Objective: The objective was to examine longitudinal changes in various aspects of calcium homeostasis during pregnancy and lactation in 9 healthy Brazilian women who habitually consumed Ȃ500 mg Ca/d. Design: Calcium homeostasis was assessed at 3 time points: 10-12 (early pregnancy, EP) and 34-36 (late pregnancy, LP) wk of pregnancy and 7-8 wk postpartum (early lactation, EL). At each time point, the following variables were measured: dietary calcium intake with a 3-d weighed food record, 24-h urinary calcium excretion (UCa), intestinal calcium absorption (%CaAbs) via administration of stable calcium isotopes with a breakfast meal, serum 1,25dihydroxyvitamin D, parathyroid hormone (PTH), insulin-like growth factor I (IGF-I), and biochemical markers of bone turnover. Results: Dietary calcium did not change during the study. %CaAbs increased from 69.7 Ȁ 5.4% (x Ȁ SEM) during EP to 87.6 Ȁ 4.5% during LP (P 0.05) and returned to 65.1 Ȁ 6.2% during EL. Compared with EP, UCa decreased 22% during LP and 68% during EL (P 0.05). The net mean change in calcium retention was 212 mg/d during LP and 182 mg/d during EL. Several significant associations were found between the main outcome variables (%CaAbs, UCa, and markers of bone turnover) and serum hormones, especially IGF-I and PTH. Conclusions: Calcium homeostasis appears to be attained by a more efficient intestinal calcium absorption during pregnancy and by renal calcium conservation during both pregnancy and lactation. IGF-I and PTH seem to play major roles in the adjustment of calcium metabolism during pregnancy and lactation.
Background: Physiologic adjustments in calcium homeostasis during pregnancy and lactation in women with marginal calcium intakes have not been described. Objective: The objective was to examine longitudinal changes in various aspects of calcium homeostasis during pregnancy and lactation in 9 healthy Brazilian women who habitually consumed Ȃ500 mg Ca/d. Design: Calcium homeostasis was assessed at 3 time points: 10 -12 (early pregnancy, EP) and 34 -36 (late pregnancy, LP) wk of pregnancy and 7-8 wk postpartum (early lactation, EL). At each time point, the following variables were measured: dietary calcium intake with a 3-d weighed food record, 24-h urinary calcium excretion (UCa), intestinal calcium absorption (%CaAbs) via administration of stable calcium isotopes with a breakfast meal, serum 1,25dihydroxyvitamin D, parathyroid hormone (PTH), insulin-like growth factor I (IGF-I), and biochemical markers of bone turnover. Results: Dietary calcium did not change during the study. %CaAbs increased from 69.7 Ȁ 5.4% (x Ȁ SEM) during EP to 87.6 Ȁ 4.5% during LP (P 0.05) and returned to 65.1 Ȁ 6.2% during EL. Compared with EP, UCa decreased 22% during LP and 68% during EL (P 0.05). The net mean change in calcium retention was 212 mg/d during LP and 182 mg/d during EL. Several significant associations were found between the main outcome variables (%CaAbs, UCa, and markers of bone turnover) and serum hormones, especially IGF-I and PTH. Conclusions: Calcium homeostasis appears to be attained by a more efficient intestinal calcium absorption during pregnancy and by renal calcium conservation during both pregnancy and lactation. IGF-I and PTH seem to play major roles in the adjustment of calcium metabolism during pregnancy and lactation.
Journal of Bone and …, 1995
A randomized clinical intervention trial to determine effects of lactation and 1 g of calcium (Ca) on bone remodeling was conducted in 15 women (calcium = 7, placebo [PI = 8) consuming 13-2.4 g of Ca/day from diet + prenatal supplement. Study periods were baseline, 5 2 weeks postpartum; lactation, 3 months lactation; and postweaning, 3 months postweaning. Bone mineral density (BMD) corrected for body weight was determined by dual-energy X-ray absorptiometry (DXA). Indicators of calcium metabolism, bone turnover, and lactation were measured: calcium metabolism, parathyroid hormone (PTH), 25-hydroxyvitamin D (25 [OH] D), 1,25-dihydroxyvitamin D (1,25 [OH],D); bone turnover, formation, procollagen I carboxypeptides (PICP), osteocalcin, and bone alkaline phosphatase (B-ALP), resorption, tartrate resistant acid phosphatase (TRAP); and lactation, prolactin (PRL). Mean BMD changes differed by site: baseline to lactation-43% (P) (p < 0.04) and-63% (Ca) (p < 0.01) at the lumbar spine (L2-U) and 5.7% gains of the ultradistal (UD) radius (Ca) (p < 0.04); lactation to postweaning,-6% to-11% at all sites of the radius and ulna (Ca, P) (p < 0.04) +3% at L2-U (Ca) (p < 0.03); baseline to postweaning, (UD) radius-5.2% (P) (p < 0.03), UD radius + ulna-6% to-8% (Ca, P) (p < 0.04) but no significant loss of L2-L4 or total body. Bone turnover markers were higher at lactation than postweaning: PICP (+34%,p < 0.001), osteocalcin (+25%,p < 0.01), TRAP (+ll%,p < 0.005) as was PRL (+81%,p < 0.001). Indicators of calcium metabolism were higher postweaning than lactation for PTH (+4wo,p < 0.01) and 25(OH)D (+45%, p < 0.02) but not for 1,25(OH),D. There were no differences between P or Ca for indices of calcium metabolism, bone turnover, or PRL. An increase in markers of bone turnover and a loss of BMD of the spine during lactation appears to be part of the physiological changes of lactation and not preventable by increasing calcium intake above the recommended dietary allowance (RDA). A return of BMD toward baseline of the spine but not the arm, was associated with an increase in PTH without an increase in 1,25(OH),D postweaning. Loss of estrogen during lactation and a return postweaning may play an important role.
The American Journal of Clinical Nutrition, 2006
Background: Few data exist on longitudinal changes in bone calcium turnover rates across pregnancy and lactation. Objective: Our aim was to characterize calcium kinetic variables and predictors of these changes across pregnancy and early lactation in women with low calcium intakes. Design: Stable calcium isotopes were administered to 10 Brazilian women during early pregnancy (EP; weeks 10-12 of gestation), late pregnancy (LP; weeks 34-36 of gestation), and early lactation (EL; 7-8 wk postpartum). Multicompartmental modeling was used to assess the rates of bone calcium turnover in relation to calcium intakes and circulating concentrations of parathyroid hormone (PTH), insulin-like growth factor 1, and 1,25-dihydroxyvitamin D. Results: Rates of bone calcium deposition increased significantly from EP to LP (P ҃ 0.001) and were significantly associated with serum PTH during LP (P ͨ 0.01). Rates of bone calcium resorption were also higher during LP and EL than during EP (P ͨ 0.01) and were associated with both PTH (P ͨ 0.01) and IGF-1 (P ͨ 0.05) during LP but not during EL. Net balance in bone calcium turnover was positively associated with dietary calcium during EP (P ͨ 0.01), LP (P ͨ 0.01), and EL (P ͨ 0.01). The mean (ȀSD) calcium intake was 463 Ȁ 182 mg/d and, in combination with insulin-like growth factor 1, explained 68-94% of the variability in net bone calcium balance during pregnancy and lactation. Conclusions: Net deficits in bone calcium balance occurred during pregnancy and lactation. Increased dietary calcium intake was associated with improved calcium balance; therefore, greater calcium intakes may minimize bone loss across pregnancy and lactation in women with habitual intakes of 500 mg calcium/d.