Calcium supplements  increased BMD by 0.7 - 1.8 % at all five skeletal sites at one , two , and over two and a half years , but the size of the increase in BMD at later time points was similar to the increase at one year .
Increasing calcium intake from dietary sources or by taking calcium supplements produces small non-progressive increases in BMD , which are unlikely to lead to a clinical ly significant reduction in risk of fracture
OBJECTIVE To determine whether increasing calcium intake from dietary sources affects  bone mineral density ( BMD ) and , if so , whether the effects are similar to those of calcium supplements .
Calcium supplementation prevents seasonal bone loss and changes in biochemical markers of bone turnover in elderly New England women: a randomized placebo-controlled trial.
Elderly women are at increased risk for bone loss and fractures . In previous cross-sectional and longitudinal studies of women residing in northern latitudes , bone loss was most pronounced during winter months and in those consuming less than 1 g calcium per day . In this study we sought to test the hypothesis that calcium supplementation by either calcium carbonate or dietary means would prevent seasonal bone loss and preserve bone mass . Sixty older postmenopausal women without osteoporosis were r and omized to one of three treatment arms : Dietary milk supplementation ( D-4 glasses of milk/day ) , Calcium carbonate ( CaCO3 - 1000 mg/day in two divided doses ) , or placebo ( P ) . After 2 yr , placebo-treated women consumed a mean of 683 mg/day of calcium and lost 3.0 % of their greater trochanteric ( GT ) bone mineral density ( BMD ) ( P < 0.03 vs. baseline ) ; Dietary supplemented women averaged a calcium intake of 1028 mg/day and sustained minimal loss from the GT ( -1.5 % ; P = 0.30 ) , whereas CaCO3-treated women ( total Ca intake , 1633 mg/day ) suffered no bone loss from the GT and showed a significant increase in spinal and femoral neck BMD ( P < 0.05 ) . Femoral bone loss occurred exclusively during the two winters of the study ( i.e. total loss , -3.2 % ; P < 0.02 in placebo-treated women ) with virtually no change in GT BMD during summer . Serum 25-OH vitamin D declined by more than 20 % ( P < 0.001 ) in all groups during the winter months but returned to baseline in summer ; PTH levels rose approximately 20 % ( P < 0.001 ) during winter but did not return to baseline during the summers . Urine N-telopeptide and osteocalcin levels increased significantly but only in the P-treated women and only during winter . Serum insulin growth factor binding protein 4 , an inhibitory insulin growth factor binding protein , rose 15 % ( P < 0.03 ) from summer to winter , but this increase was significant only in those women consuming < 1000 mg/day of calcium . By multivariate analysis , total calcium intake was the strongest predictor of bone loss from the hip . Urinary N-telopeptide also closely correlated with GT BMD but only during winter ( P = 0.003 ) . We conclude that calcium supplementation prevents bone loss  in elderly women by suppressing bone turnover during the winter when serum 25-OH vitamin D declines and serum PTH increases . The precise amount of calcium necessary to preserve BMD in elderly women requires further studies , although in this study , at least 1000 mg/day of supplemental calcium was adequate prophylaxis against femoral bone loss
Calcium supplements  increased BMD by 0.7 - 1.8 % at all five skeletal sites at one , two , and over two and a half years , but the size of the increase in BMD at later time points was similar to the increase at one year .
Increasing calcium intake from dietary sources or by taking calcium supplements produces small non-progressive increases in BMD , which are unlikely to lead to a clinical ly significant reduction in risk of fracture
OBJECTIVE To determine whether increasing calcium intake from dietary sources affects  bone mineral density ( BMD ) and , if so , whether the effects are similar to those of calcium supplements .