Background. The effectiveness of calcium in retarding bone loss in older postmenopausal women is unclear. Earlier work suggested that the women who were most likely to benefit from calcium supplementation were those with low calcium intakes. Methods. We undertook a double-blind, placebo-controlled, randomized trial to determine the effect of calcium on bone loss from the spine, femoral neck, and radius in 301 healthy postmenopausal women, half of whom had a calcium intake lower than 400 mg per day and half an intake of 400 to 650 mg per day. The women received placebo or either calcium carbonate or calcium citrate malate (500 mg of calcium per day) for two years. Results. In women who had undergone menopause five or fewer years earlier, bone loss from the spine was rapid and was not affected by supplementation with calcium. Among the women who had been postmenopausal for six years or more and who were given placebo, bone loss was less rapid in the group with the higher dietary calcium intake. In those with the lower calcium intake, calcium citrate malate prevented bone loss during the two years of the study; its effect was significantly different from that of placebo (P less than 0.05) at the femoral neck (mean change in bone density [+/- SE], 0.87 +/- 1.01 percent vs. -2.11 +/- 0.93 percent), radius (1.05 +/- 0.75 percent vs. -2.33 +/- 0.72 percent), and spine (-0.38 +/- 0.82 percent vs. -2.85 +/- 0.77 percent). Calcium carbonate maintained bone density at the femoral neck (mean change in bone density, 0.08 +/- 0.98 percent) and radius (0.24 +/- 0.70 percent) but not the spine (-2.54 +/- 0.85 percent). Among the women who had been postmenopausal for six years or more and who had the higher calcium intake, those in all three treatment groups maintained bone density at the hip and radius and lost bone from the spine. Conclusions. Healthy older postmenopausal women with a daily calcium intake of less than 400 mg can significantly reduce bone loss by increasing their calcium intake to 800 mg per day. At the dose we tested, supplementation with calcium citrate malate was more effective than supplementation with calcium carbonate.
Two hundred eighty-four female adults (aged 40-70 years) were longitudinally studied to investigate the relationship between dietary supplemental vitamin A and serum biochemical markers of vitamin A toxicity. Serum retinol, retinyl esters, and retinol-binding protein (RBP), alkaline phosphatase and aspartate aminotransferase activities and bile acids were measured at baseline, 1 and 2 years. Fasting serum retinol and retinyl ester concentrations were determined by high-performance liquid chromatography, and dietary and supplemental intake of vitamin A were assessed by 3-day food records. There was no difference in dietary vitamin A intake between supplement users and nonusers. In supplemental users, the mean +/- SEM supplemental vitamin A intake was 952 +/- 81 IU/day (range 250-5000 retinol equivalents/day). Serum retinol, retinyl esters, and RBP concentrations were not different between the two groups during the 2-year period. For each group, serum retinyl esters significantly increased over time (p < 0.03), but the magnitude of the increase was not different between the groups. Serum levels of retinol, retinyl esters, and RBP were not correlated with vitamin A intake or age in either group. Biochemical measures of liver damage (serum alkaline phosphatase and aspartate aminotransferase activities and serum bile acids) were not related to serum retinol, retinyl esters or RBP concentrations, nor were they different between nonusers and users of supplemental vitamin A. This study provides evidence that long-term supplemental vitamin A in doses commonly found in multivitamin supplements does not present a risk for hypervitaminosis A.
Dual photon absorptiometry measurements of the spine are subject to drift associated with source, source strength, and truncal thickness. This study was conducted to determine the extent to which this drift in bone mineral density (BMD) measurements can be improved by analysis of scans with a new software version, 08C, and by applying external standard or phantom corrections to scans analyzed with the older version, 08B. A phantom, consisting of human lumbar vertebrae embedded in acrylic, and five clear acrylic plates to simulate a soft-tissue thickness range of 15.2-27.9 cm, was measured on a Lunar Radiation Corp DP3 scanner over the life of a 153-gadolinium (Gd) source and scans analyzed with software versions 08B and 08C. Phantom BMD was lower with 08C at both high [0.012 +/- 0.002 (SEM) g/cm2, P less than 0.001] and low (0.027 +/- 0.003 g/cm2, P less than 0.001) count rates than with 08B. Phantom BMD of scans analyzed with 08B increased with increasing source age and the source strength-related increment increased significantly as acrylic thickness increased (P = 0.014). When the same scans were analyzed with 08C, the thickness-related effect was corrected whereas a small (0.011 g/cm2/year) source-strength effect persisted. The effects of source strength and truncal thickness on BMD were also evaluated in 40 humans scanned at two detector collimations to vary count rate. With 08B, mean BMD was 1% greater when measured with 8 than with 13 mm collimation (mean difference 0.011 +/- 0.003 g/cm2, P = 0.001), whereas the version 08C, mean BMD was the same at the two collimations.(ABSTRACT TRUNCATED AT 250 WORDS)
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