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Calcium citrate abs/cdResearch
Dose dependency of calcium absorption: a comparison of calcium carbonate Calcium supplementation is recommended as a prophylaxis against bone loss. This study was performed to determine thedose dependency of calcium absorption in an attempt to derive an optimum dose schedule. Using the well-described oralcalcium load technique, we measured the calcium absorption from three different calcium doses (0.5, 1.0, and 2.0 g) of bothcalcium carbonate and calcium citrate administered to 21 normal subjects (4 men and 17 women, 22-60 years). Ninesubjects underwent two additional loads with 0.2 g of elemental calcium as calcium carbonate and as calcium citrate. Theintestinal calcium absorption from calcium carbonate and calcium citrate was estimated from the rise in urinary calciumfollowing oral ingestion of the respective calcium salt. The increment in urinary calcium post-load, reflective of intestinalcalcium absorption, rose rapidly from 0 to 0.5 g calcium loads with only slight subsequent increases from the 0.5 g to 2.0 gcalcium doses. Thus, results indicate that 0.5 g of calcium is the optimum dose of either calcium salt. Moreover, theincrement in urinary calcium post-load was higher from calcium citrate than from calcium carbonate at all four dosagelevels. The increment in urinary calcium (during the second 2 hr) following calcium citrate load (0.5 g calcium) was 0.104 +/- 0.096 mg/dl glomerular filtrate (GF), which was higher than that of 0.091 +/- 0.068 mg/dl GF obtained from 2.0 g calciumas calcium carbonate. These results confirm the superior calcium bioavailability from calcium citrate as compared withcalcium carbonate. Harvey JA, Zobitz MM, Pak CY. J Bone Miner Res 1988 Jun;3(3):253-8.
Calcium citrate: reduced propensity for the crystallization of calcium oxalate in urine resulting from induced hypercalciuria of calcium supplementation The effect of calcium citrate (800 mg calcium/day in 4 divided doses) on urinary biochemistry and crystallization of calciumsalts was examined in 18 normal subjects. During treatment, urinary calcium increased significantly (from 150 +/- 65 (SD)to 248 +/- 77 mg/day). Urinary citrate rose from 611 +/- 208 to 730 +/- 225 mg/day, owing largely to the alkali load. Theurinary saturation of calcium oxalate rose by only 41% during calcium citrate treatment, due mainly to citrate complexationof calcium (rather than by 62% without such complexation). Moreover, the formation product of calcium oxalate rose duringtreatment, indicating that the enhanced citrate excretion augmented the inhibitor activity against calcium oxalate crystallization.
Thus, calcium citrate may not be attendant with the risk for stone formation usually associated with calcium supplementation.
Harvey JA, Zobitz MM, Pak CY. J Clin Endocrinol Metab 1985 Dec;61(6):1223-5.
Effect of calcium supplementation on bone loss in postmenopausal women BACKGROUND. The use of calcium supplements slows bone loss in the forearm and has a beneficial effect on the axialbone density of women in late menopause whose calcium intake is less than 400 mg per day. However, the effect of acalcium supplement of 1000 mg per day on the axial bone density of postmenopausal women with higher calcium intakesis not known. METHODS. We studied 122 normal women at least three years after they had reached menopause who hada mean dietary calcium intake of 750 mg per day. The women were randomly assigned to treatment with either calcium(1000 mg per day) or placebo for two years. The bone mineral density of the total body, lumbar spine, and proximal femurwas measured every six months by dual-energy x-ray absorptiometry. Serum and urine indexes of calcium metabolismwere measured at base line and after 3, 12, and 24 months. RESULTS. The mean (+/- SE) rate of loss of total-body bonemineral density was reduced by 43 percent in the calcium group (-0.0055 +/- 0.0010 g per square centimeter per year) ascompared with the placebo group (-0.0097 +/- 0.0010 g per square centimeter per year, P = 0.005). The rate of loss of bonemineral density was reduced by 35 percent in the legs (P = 0.02), and loss was eliminated in the trunk (P = 0.04). Calciumuse was of significant benefit in the lumbar spine (P = 0.04), and in Ward's triangle the rate of loss was reduced by 67percent (P = 0.04). Calcium supplementation had a similar effect whether dietary calcium intake was above or below themean value for the group. Serum parathyroid hormone concentrations tended to be lower in the calcium group, as wereurinary hydroxyproline excretion and serum alkaline phosphatase concentrations. CONCLUSIONS. Calcium supplementationsignificantly slowed axial and appendicular bone loss in normal post-menopausal women. Reid IR, et al. N Engl J Med1993 Feb 18;328(7):460-4.
Lifetime calcium intake and physical activity habits: independent and combined effects on the radial bone of healthy premenopausal Caucasian women Lifetime calcium intake and lifetime physical activity (PA) habits of 181 healthy premenopausal Caucasian women (aged20-50) were studied. Nondominant arm was measured by single-photon absorptiometry at the distal (Dis) or 5-mm site andthe midshaft (Mid) or two-thirds site of the radius. Values of bone mineral content (BMC), bone width (BW), and bonemineral density (BMD) were obtained. An intermediate or high lifetime Ca (greater than 500 mg/d) was significantly associatedwith a greater DisBMC (p = 0.0031), DisBMD (p = 0.0031), MidBMC (p = 0.0015), and MidBMD (p = 0.0015) when adjustedfor PA. Similarly, with Ca adjusted for, a high lifetime PA (greater than or equal to 45 min of moderate to strenuous activityfour times a week) was significantly associated with greater DisBMC (p = 0.0032), DisBMD (p = 0.0022), MidBMC (p=0.0012), MidBW (p = 0.0173), and MidBMD (p = 0.0546). These findings suggest important roles for both adequate Caintake and PA habits in enhancing peak adult skeletal mass and a trade-off between these two variables, when each wasintermediate or higher. Halioua L, Anderson JJ. Am J Clin Nutr 1989 Mar;49(3):534-41.
Dietary Ca2+ prevents NaCl-sensitive hypertension in spontaneously hypertensive rats by a sympatholytic mechanism The current study tested the hypothesis that dietary Ca2+ supplementation reverses the NaCl-sensitive component ofhypertension and the associated neurochemical abnormalities in the NaCl-sensitive spontaneously hypertensive rat (SHR-S). Male SHR-S were begun on one of four diets at 8 weeks of age: control (0.75% NaCl/0.68% Ca2+); high NaCl (8.00%NaCl/0.68% Ca2+); high Ca2+ (0.75% NaCl/2.00% Ca2+); and high NaCl/high Ca2+ (8.00% NaCl/2.00% Ca2+). HighNaCl SHR-S (X2 weeks) had higher mean arterial pressure (MAP) (161 +/- 4 mm Hg) than controls (149 +/- 3 mm Hg; Pless than .05). Supplementation with Ca2+ prevented the rise in MAP in high NaCl rats, but did not alter MAP in controls.
The 8% NaCl diet elevated plasma norepinephrine and reduced anterior hypothalamic (AHA) norepinephrine stores andturnover; concomitant Ca2+ supplementation restored both plasma norepinephrine and AHA norepinephrine turnover tonormal. Clonidine was microinjected into the AHA of rats maintained on the four diets for 2 weeks to test the hypothesis thatdietary Ca2+ supplementation prevents the previously observed NaCl-induced upregulation of alpha 2-adrenoceptors inAHA. Clonidine caused dose-dependent decreases in MAP that were greater in high NaCl rats than in controls. The Ca2+supplementation prevented the exaggerated depressor response to clonidine in the high NaCl group, but not in the controls.
The Ca2+ supplementation had no effect on pretreatment MAP or on MAP responses to clonidine in control NaCl-resistantSHR (SHR-R) or Wistar-Kyoto (WKY) rats. Thus, dietary Ca2+ supplementation prevents the NaCl-induced exacerbationof hypertension and augmented depressor response to clonidine in SHR-S by increasing noradrenergic input to AHA,thereby preventing the upregulation of AHA alpha 2-adrenoceptors. Oparil S, Wyss JM, Yang RH, Jin HK, Chen YF. Am JHypertens 1990 Aug;3(8 Pt 2):179S-188S.
The preceding abstracts were obtained from the Medline service maintained by the National Institutes of Health.
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