Effect of prenatal calcium supplementation on bone during pregnancy and 1 y postpartum

ABSTRACT 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) and content were assessed at the tibia and radius by peripheral quantitative computed tomography. Results Mean ± SD daily calcium intake at baseline was 733 ± 350 mg; only 25% of the women met the RDA. Thirty women (47% of those enrolled) remained in the study at 12 mo postpartum. After controlling for baseline bone value, serum 25-hydroxyvitamin D concentrations, length of breastfeeding, and body mass index, the calcium group had significantly greater increases in radial total BMD (P = 0.02) and tibial cortical BMD (P = 0.03) at 12 mo postpartum than the placebo group. Trabecular and total BMD at the tibia trended toward higher values (P < 0.06) in the calcium group than in the placebo group in the same models. Conclusions These data show that supplemental calcium provided during pregnancy may improve bone recovery postpartum in women consuming a typical US diet. A larger study is warranted to solidify the conclusions. This trial was registered at clinicaltrials.gov as NCT01145573.

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Serum 25-hydroxyvitamin D, parathyroid hormone, calcium intake, and bone mineral density in Spanish adults

Osteoporosis International ◽

10.1007/s00198-015-3219-6 ◽

2015 ◽

Vol 27 (1) ◽

pp. 105-113 ◽

Cited By ~ 30

Author(s):

J. M. Olmos ◽

J. L. Hernández ◽

P. García-Velasco ◽

J. Martínez ◽

J. Llorca ◽

...

Keyword(s):

Bone Mineral Density ◽

Parathyroid Hormone ◽

Bone Mineral ◽

Calcium Intake ◽

Mineral Density ◽

Hydroxyvitamin D ◽

25 Hydroxyvitamin D

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Vitamin D deficiency: A threat to bone health in breast cancer patients during adjuvant treatment with aromatase inhibitors

Journal of Clinical Oncology ◽

10.1200/jco.2006.24.18_suppl.554 ◽

2006 ◽

Vol 24 (18_suppl) ◽

pp. 554-554 ◽

Cited By ~ 3

Author(s):

P. Lonning ◽

J. Geisler ◽

L. E. Krag ◽

E. Løkkevik ◽

T. Risberg ◽

...

Keyword(s):

Breast Cancer ◽

Vitamin D ◽

Placebo Group ◽

Bone Loss ◽

Femoral Neck ◽

Vitamin D Deficiency ◽

Postmenopausal Women ◽

Breast Cancer Patients ◽

Hydroxyvitamin D ◽

25 Hydroxyvitamin D

554 Background: To evaluate potential detrimental effects of the aromatase inactivator exemestane on bone, 147 postmenopausal women with early breast cancer were randomised to receive either exemestane for 2 years or placebo (J. Clin. Oncol. 23 [22], 5126–5137, 2005). Exemestane increased the annual bone loss from the femoral neck (2.72%) compared to placebo (1.48%; P = 0.024) with a non-significant increase in the lumbar spine (exemestane 2.17% versus placebo 1.84%). The annual bone loss was higher than expected in the placebo arm. Methods: Various biomarkers involved in bone metabolism (25-hydroxyvitamin D, parathormone, calcium, estrogens, androgens) were analysed to elucidate their influence on bone status at baseline and BMD loss during treatment with exemestane compared to placebo. Results: Using a cut-off value of 30 ng/ml for 25-hydroxyvitamin D (J. Clin. Endocrinol. Metab. 90 [6], 3800–3801, 2005), the majority of study participants suffered from vitamin D deficiency (56 of 62 patients in the placebo group and 52 of 59 in the exemestane group). The mean levels (95% confidence interval) of vitamin D were 22.6 ng/ml (21.2 - 24.1) in the placebo group and 21.6 ng/ml (20.0 - 23.3) in the treatment group, revealing no differences between these groups. Low serum calcium levels at baseline were found to be significantly correlated to low BMD in the femoral neck in the exemestane group. However, individual levels of vitamin D, parathormone and estradiol at baseline were not correlated significantly to BMD. Conclusions: Considering an annual bone loss of 0.5% to be representative for postmenopausal women (Osteoporos. Int. 15, 881–886, 2004), our data indicate that vitamin D deficiency could be the most important factor elevating bone loss among patients treated with exemestane as well as in the placebo group. These findings, together with the observation of a moderate additional effect of exemestane on bone loss, underlines the need for proper vitamin D substitution of postmenopausal women in general and in breast cancer patients during treatment with aromatase inhibitors in particular. [Table: see text]

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