Oral Vitamin D Supplements Increase Serum 25-Hydroxyvitamin D in Postmenopausal Women and Reduce Bone Calcium Flux Measured by 41Ca Skeletal Labeling.
J Nutr. 2015 Oct;145(10):2333-40. doi: 10.3945/jn.115.215004. Epub 2015 Sep 2.
Schild A1, Herter-Aeberli I2, Fattinger K1, Anderegg S2, Schulze-König T3, Vockenhuber C3, Synal HA3, Bischoff-Ferrari H4, Weber P5, von Eckardstein A6, Zimmermann MB7.
1 Department of General Internal Medicine, University Hospital Bern and University of Bern, Bern, Switzerland;
2 Laboratory of Human Nutrition, Institute of Food, Nutrition, and Health, and.
3 Laboratory of Ion Beam Physics, ETH Zurich, Zurich, Switzerland;
4 Centre on Aging and Mobility, University of Zurich and Waid City Hospital, Zurich, Switzerland; Geriatric Clinic and.
5 Human Nutrition and Health, DSM Nutritional Products, Kaiseraugst, Switzerland; and.
6 Institute of Clinical Chemistry, University Hospital Zurich, Zurich, Switzerland.
7 Laboratory of Human Nutrition, Institute of Food, Nutrition, and Health, and michael.zimmermann at hest.ethz.ch.
Reminder, the Institute of Medicine stated (incorrectly) that 20 nanograms was sufficient for bone health
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Ensuring adequate vitamin D status in older adults may reduce the risk of osteoporosis. The serum 25-hydroxyvitamin D 25(OH)D concentration is the recommended biomarker of vitamin D status, but the optimal serum 25(OH)D concentration for bone health in postmenopausal women remains unclear.
The aim of this study was to apply the highly sensitive (41)Ca skeletal labeling technique and the measurement of urinary (41)Ca:(40)Ca ratios to determine the serum 25(OH)D concentration that has greatest benefit on bone calcium flux in postmenopausal women.
We administered a mean intravenous (41)Ca dose of 870 pmol to healthy postmenopausal women n = 24, age (mean ± SD): 64 ± 6.0 y without osteoporosis. After 6 mo, at the nadir of their wintertime serum 25(OH)D status, each of the women sequentially consumed daily oral cholecalciferol supplements of 10, 25, and 50 μg/d (in this order), each for 3 mo. We assessed serum 25(OH)D concentrations monthly and urinary (41)Ca:(40)Ca ratios biweekly. (41)Ca:(40) Ca ratios were measured with low-energy accelerator mass spectrometry. With the use of pharmacokinetic analysis, we determined the effect of varying serum 25(OH)D concentrations on (41)Ca transfer rates.
At baseline, the mean (95% CI) serum 25(OH)D concentration was 16.2 (13.5, 18.8) μg/L. After the first, second, and third intervention periods, mean (95% CI) serum 25(OH)D increased to 29.8 (27.2, 32.4), 36.9 (34.2, 39.7), and 46.6 (41.2, 52.0) μg/L, respectively. Supplementation was associated with a downward shift in the urinary (41)Ca: (40)Ca ratio compared with the predicted (41)Ca: (40)Ca ratio without vitamin D supplementation. In the model, the most likely site of action of the increase in serum 25(OH)D was transfer from the central compartment to a fast exchanging compartment. At this transfer rate, predicted values were a concentration with half-maximal effect of 2.33 μg/L and an estimate of the maximal effect of 31.7%. After the first, second, and third intervention periods, the mean changes in this transfer rate were +18.0%, +25.7%, and +28.5%, respectively.
In healthy postmenopausal women, increasing serum 25(OH)D primarily affects calcium transfer from the central compartment to a fast exchanging compartment; it is possible that this represents transfer from the extracellular space to the surface of bone. A serum 25(OH)D concentration of ∼40 μg/L achieves ∼90% of the expected maximal effect on this transfer rate. This trial was registered at clinicaltrials.gov as NCT01053481.
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Report on this study
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