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PubMed2004

Stone forming risk of calcium citrate supplementation in healthy postmenopausal women.

PURPOSE: We evaluated the effect of calcium citrate supplementation alone or in combination with potassium citrate on the stone forming propensity in healthy postmenopausal women. MATERIALS AND METHODS: A total of 18 postmenopausal women without stones underwent a randomized trial of 4 phases comprised of 2 weeks of treatment with placebo, calcium citrate (400 mg calcium twice daily), potassium citrate (20 mEq twice daily), and calcium citrate and potassium citrate (at same doses). During the last 2 days of each phase urine was collected in 24-hour pools for complete stone risk analysis. RESULTS: Compared to placebo, calcium citrate increased urinary calcium and citrate but decreased urinary oxalate and phosphate. Urinary saturation of calcium oxalate, brushite and undissociated uric acid did not change. Potassium citrate decreased urinary calcium, and increased urinary citrate and pH. It decreased urinary saturation of calcium oxalate and undissociated uric acid, and did not change the saturation of brushite. When calcium citrate was combined with potassium citrate, urinary calcium remained high, urinary citrate increased even further and urinary oxalate remained reduced from the calcium citrate alone, thereby marginally decreasing the urinary saturation of calcium oxalate. Urinary pH increased, decreasing urinary undissociated uric acid. The increase in pH increased the saturation of brushite despite the decrease in urinary phosphorus. CONCLUSIONS: Calcium citrate supplementation does not increase the risk of stone formation in healthy postmenopausal women. The co-administered potassium citrate may provide additional protection against formation of uric acid and calcium oxalate stones.

Aged↗
PubMed1994

Aluminum and lead absorption from dietary sources in women ingesting calcium citrate.

Animal models suggest that citrate-containing compounds augment absorption of aluminum from food and tap water, causing aluminum accumulation in bone and brain despite normal renal function. Citrate also enhances lead absorption in animals. We questioned whether use of calcium citrate by women as a calcium supplement causes an increase in aluminum or lead absorption from dietary sources. Changes in 24-hour urine aluminum and lead excretion, plasma aluminum level, and whole blood lead level were assessed in 30 healthy women before and during treatment with calcium citrate (800 mg of elemental calcium per day). During calcium citrate therapy, urinary aluminum excretion and plasma aluminum level increased significantly. In contrast, there were no changes in urine or whole blood lead levels. We conclude that treatment with calcium citrate significantly increases absorption of aluminum from dietary sources. Additional studies are needed to determine whether long-term use of calcium citrate leads to aluminum accumulation and toxicity.

Adult↗
PubMed1988

Calcium citrate, a nonaluminum-containing phosphate-binding agent for treatment of CRF.

Calcium citrate was evaluated as a dietary phosphate binder in 81 patients with end-stage renal disease. These patients were grouped as follows: Group 1, 43 patients who were treated with calcium citrate; and Group 2 (the control group), 38 patients who were treated with aluminum-containing compounds. Blood chemistries were measured monthly and medications adjusted to maintain the following levels: serum calcium, greater than 9 mg/dl; serum phosphorus, less than 5.5 mg/dl; and total CO2 content, greater than 22 mmol/liter. At the end of the treatment period, the following serum values were obtained in Groups 1 and 2, respectively: calcium, 9.6 +/- 1.2 mg/dl (mean +/- SD) versus 8.9 +/- 0.8 mg/dl (P less than 0.001); phosphorus 5.5 +/- 1.9 mg/dl versus 7.0 +/- 2.3 mg/dl (P less than 0.005); and calcium-phosphate product, 52 +/- 18 versus 61 +/- 21 (P less than 0.05). Differences in alkaline phosphatase, total CO2 content, and C-terminal parathyroid hormone (C-PTH) values were not statistically significant between the two groups. Fifteen patients in Group 1 were then switched to aluminum-containing compounds and chemistries were compared one month later. During calcium citrate therapy, serum calcium was significantly higher, while C-PTH and serum alkaline phosphatase were significantly reduced. No difference was noted in serum phosphorous and total CO2 content. A questionnaire completed by 17 patients in Group 1 documented excellent patient tolerance to calcium citrate. Hypercalcemia (greater than 10.5 mg/dl) was the only significant complication, but only one patient became symptomatic. We conclude that, as a phosphate binder, calcium citrate is at least as effective as aluminum-containing compounds.

Adult↗
PubMed1991

Calcium citrate markedly enhances aluminum absorption from aluminum hydroxide.

The effect of calcium citrate on intestinal aluminum absorption, assessed by the increment in urinary aluminum excretion, was evaluated in eight normal men. Baseline urinary aluminum excretion was determined for 2 days; thereafter, subjects ingested aluminum hydroxide for 3 days. In a cross-over study, subjects were given either calcium citrate, 950 mg four times a day, or placebo during the 3 days of aluminum hydroxide ingestion (2.4 g/d). Plasma aluminum levels were measured on the second control day and the third day of aluminum hydroxide ingestion. Baseline urinary aluminum excretion was 0.02 +/- 0.004 (6.5 +/- 1.1 micrograms/g creatinine) and 0.03 +/- 0.005 mumol/mmol creatinine (7.4 +/- 1.3 micrograms/g creatinine). These values increased during aluminum hydroxide therapy, but values were much greater when calcium citrate was ingested with aluminum hydroxide. On 3 consecutive days, urinary aluminum excretion levels were 11.1 +/- 3.23, 8.8 +/- 2.9, and 5.3 +/- 0.7 times greater during the administration of calcium citrate with aluminum hydroxide than with aluminum hydroxide alone. Plasma aluminum levels did not differ in the two treatment groups. Thus, calcium citrate markedly enhances the absorption of aluminum from aluminum hydroxide and the two must not be prescribed together in patients with renal failure.

Adult↗
PubMedDate not supplied

[Effect of dietary calcium vs calcium citrate on conventional biochemical markers in perimenopausal women].

OBJECTIVE: To compare the effect of calcium citrate and a calcium enriched diet on conventional biochemical markers. MATERIAL AND METHODS: Eighty-two women aged 30 to 35 years were randomized to any of three groups:A control group of 23 women who remained intact in their dietary habits and physical activity; a second group of 28 women who received 1000 mg of dietary calcium plus physical activity 30 minutes three times per week; and a third group of 31 women who received 600 mg of calcium citrate plus 500 mg of dietary calcium and physical activity three times per week for seven months. Calcaneum bone densitometry was measured to classify women into normal and osteopenic groups. Biochemical markers were measured at baseline and at the end of the study, as follows: serum alkaline phosphatase, magnesium, calcium and phosphorus, as well as the calcium/creatinine ratio in urine. RESULTS: Thirty-four percent of women were osteopenic. These women showed a significant reduction in the final level of calcium in the third group, as compared to the second group (p < 0.05, 7.4 mg/dl vs 8.8 mg/dl). The final measurement showed significant hypermagnesemia in the second group, as compared to the third group (p < 0.05). Phosphorus levels decreased in the second group (3.5 to 3.2 mg/dl) (p > 0.05). The calcium/creatinine ratio was normal in all groups. CONCLUSIONS: The second group showed a higher bone production than the third group. No group showed bone resorption.

Adult↗
PubMed1998

Citrate, calcium, phosphate and magnesium in sows' milk at initiation of lactation.

Colostrum and milk were collected from ten sows at frequent intervals from before farrowing until 9 d after farrowing. Ionized calcium, pH, and total concentrations of citrate, calcium, phosphate and magnesium were measured in whole milk. The diffusible fraction of the mammary secretion was separated by ultrafiltration and was used for the measurement of diffusible citrate, calcium, phosphate and magnesium. The pH before farrowing was 5.7, and increased to 6.5 on day 4 as total calcium and phosphate also increased. Before farrowing, total and diffusible citrate were 7.8 and 7.3 mM respectively, while diffusible phosphate was 11.9 mM, and these concentrations all decreased during the study period. Total magnesium ranged between 3.3 and 4.1 mM, while diffusible magnesium ranged between 2.0 and 3.1 mM. While these concentrations and patterns of change of diffusible calcium and citrate are quite different from those of women's milk during the first week after birth, theoretical physicochemical relationships between diffusible calcium and citrate, and ionized calcium and HPO4(2-) were corroborated by these results. We conclude that diffusible citrate plays an important role in the determination of the concentration of diffusible calcium. However, while citrate may be the major determinant of the total concentration of calcium in women's milk, this is not the case in sows' milk.

Animals↗
PubMed1993

Calcium citrate without aluminum antacids does not cause aluminum retention in patients with functioning kidneys.

It has been suggested that calcium citrate might enhance aluminum absorption from food, posing a threat of aluminum toxicity even in patients with normal renal function. We therefore measured serum and urinary aluminum before and following calcium citrate therapy in patients with moderate renal failure and in normal subjects maintained on constant metabolic diets with known aluminum content (967-1034 mumol/day, or 26.1-27.9 mg/day, in patients and either 834 or 1579 mumol/day, or 22.5 and 42.6 mg/day, in normal subjects). Seven patients with moderate renal failure (endogenous creatinine clearance of 43 ml/min) took 50 mmol (2 g) calcium/day as effervescent calcium citrate with meals for 17 days. Eight normal women received 25 mmol (1 g) calcium/day as tricalcium dicitrate tablets with meals for 7 days. In patients with moderate renal failure, serum and urinary aluminum were normal before treatment at 489 +/- 293 SD nmol/l (13.2 +/- 7.9 micrograms/l) and 767 +/- 497 nmol/day (20.7 +/- 13.4 micrograms/day), respectively. They remained within normal limits and did not change significantly during calcium citrate treatment (400 +/- 148 nmol/l and 600 +/- 441 nmol/day, respectively). Similarly, no significant change in serum and urinary aluminum was detected in normal women during calcium citrate administration (271 +/- 59 vs 293 +/- 85 nmol/l and 515 +/- 138 vs 615 +/- 170 nmol/day, respectively). In addition, skeletal bone aluminum content did not change significantly in 14 osteoporotic patients (endogenous creatinine clearance of 68.5 ml/min) treated for 24 months with calcium citrate, 10 mmol calcium twice/day separately from meals (29.3 +/- 13.9 ng/mg ash bone to 27.9 +/0- 10.4, P = 0.727). In them, histomorphometric examination did not show any evidence of mineralization defect. Thus, calcium citrate given alone without aluminum-containing drugs does not pose a risk of aluminum toxicity in subjects with normal or functioning kidneys, when it is administered on an empty stomach at a recommended dose of 20 mmol calcium/day.

Absorption↗
PubMed1999

The effect of calcium citrate on bone density in the early and mid-postmenopausal period: a randomized placebo-controlled study.

This placebo-controlled randomized trial was conducted to ascertain the value of calcium citrate supplementation in averting bone loss in 63 postmenopausal women, 57 of whom were early postmenopausal (five years after menopause) and six of whom were mid-postmenopausal (five to ten years after menopause). Bone density data were available for 25 women who took 800 mg of calcium citrate daily and 31 women who received placebo for one to two years. The two groups were similar in baseline age, years postmenopause (3.3 in the calcium citrate group vs 2.7 in the placebo group), height, weight, calcium intake, and L2-L4 bone density. L2-L4 bone density did not change during calcium citrate treatment (+ 1.03% after two years), whereas it declined significantly by -2.38% after two years on placebo (P < .001). Femoral neck bone density did not change in either group. Radial shaft bone density did not change in the calcium citrate group (-0.02% after two years), but it declined significantly in the placebo group (-1.79% after one year and -3.03% after two years, P < .01). The difference in bone density of the L2-L4 vertebrae and radial shaft after two years of treatment was significant between the two groups. An analysis of covariance disclosed no significant effect of calcium citrate on L2-L4 bone density during the first three years after menopause, but a protective effect after three years. Although serum PTH did not change, serum and urinary calcium increased and serum calcitriol and urinary phosphorus decreased in the calcium citrate group, indicative of parathyroid suppression. Serum bone-specific alkaline phosphatase and osteocalcin, and urinary hydroxyproline and N-telopeptide decreased during some calcium citrate treatment periods, indicative of a reduction in bone turnover. Thus, calcium citrate supplementation (400 mg of calcium twice daily) averted bone loss and stabilized bone density in the spine, femoral neck, and radial shaft in women relatively soon after menopause. This bone-sparing action was probably due to the inhibition of bone resorption from parathyroid suppression.

Bone Density↗
PubMed1996

Calcium absorption from apple and orange juice fortified with calcium citrate malate (CCM).

OBJECTIVE: Determine calcium (Ca) absorption from Ca fortified orange and apple juice. METHODS: Absorbability was assessed by measuring 45Ca absorption in healthy women (mean age 57 years, n = 57/group) and whole body 47Ca retention in adult female beagle dogs (n = 6/group) and young adult male rats (n = 6/group). Women received 6.24 mmol (250 mg) Ca as calcium citrate malate fortified orange juice (CCM-OJ) or apple juice (CCM-AJ). Dogs received 3.12 mmol (125 mg) Ca as CCM-OJ or CCM-AJ. Rats were administered 0.15 mmol (6 mg) Ca as either milk, CCM-OJ, or CCM-AJ. Additional 47Ca whole body retention experiments in rats measured the effects of differences in the carbohydrate and organic acid contents of the juices on Ca absorption. RESULTS: Mean +/- SEM percent Ca fractional absorption was greater (p < 0.003) in women who consumed CCM-AJ (42 +/- 2%) than those who consumed CCM-OJ (36 +/- 1%). Ca retention in dogs was 15 +/- 1% for CCM-OJ and 29 +/- 2% for CCM-AJ (p < 0.001). Ca retention was significantly different (p < 0.05) in rats administered milk (42 +/- 2%), CCM-OJ (52 +/- 2%), or CCM-AJ (61 +/- 2%). By manipulating the carbohydrate and organic acid concentrations of test solutions to mimic the composition of Ca fortified juices, we found that the greater fructose and lower organic acid content of apple juice accounted for its greater Ca absorbability. CONCLUSIONS: CCM fortified versions of orange and apple juice have high Ca absorbability and are potentially important vehicles for increasing dietary Ca intake. The greater Ca absorption from CCM-AJ compared with CCM-OJ is accounted for by differences in the carbohydrate and organic acid content of the juices. These data suggest that by modifying common beverage ingredients, products with even greater Ca absorbability could be formulated.

Absorption↗
PubMed2006

Ferrus calcium citrate is absorbed better than iron bisglycinate in patients with Crohn's disease, but not in healthy controls.

Our purpose was to compare the absorption of iron bisglycinate and ferrous calcium citrate in volunteers using an oral iron tolerance test. Twenty volunteers, 10 healthy controls and 10 with stable Crohn's disease, agreed to participate in the study. All were given 50 mg of elemental iron as iron bisglycinate or ferrous calcium citrate. Serum iron levels were monitored for 4 hr. After a week, each received the other regimen. Using the area under the curve as indicator, the oral iron absorption test revealed that absorption of iron post-ingestion of ferrous calcium citrate was better than after ingestion of iron bisglycinate for the group as a whole (P < 0.03). Volunteers with Crohn's disease absorbed ferrous calcium citrate better than iron bisglycinate (P=0.005). No difference was noted in the absorption of either preparation by healthy volunteers. Ferrus calcium citrate is apparently more effective than iron bisglycinate in patients with Crohn's disease.

Adult↗
PubMed1994

The effect of calcium carbonate and calcium citrate on the absorption of zinc in healthy female subjects.

OBJECTIVES: The aim of this study was to determine the effect of calcium carbonate and calcium citrate on zinc absorption. DESIGN: The zinc tolerance test (ZTT), which is the plasma zinc response to an oral zinc challenge, was used to quantitate zinc absorption. A physiological test dose of zinc (4.5 mg elemental zinc as 20 mg zinc sulphate) was used. Subjects underwent ZTTs on three separate occasions, each time consuming in random order, either 4.5 mg elemental zinc, zinc with 600 mg elemental calcium as calcium carbonate or zinc with 600 mg elemental calcium as calcium citrate. SETTING: Metabolic ward conditions. SUBJECTS: Nine, free-living, healthy female subjects recruited from the University population. INTERVENTIONS: Blood samples were obtained at 30 min intervals for 4 h postdose. RESULTS: The area under the plasma zinc curve (AUC) (mean +/- SEM) following the coingestion of zinc with calcium carbonate (438.4 +/- 129.0 mumol Zn.min/100 g albumin) and calcium citrate (308.0 +/- 110.5) was significantly lower (P < 0.017) than when zinc was ingested alone (1561.7 +/- 240). Urinary excretion of calcium was significantly higher (P < 0.017) at 4 h after supplementation with calcium citrate (0.83 +/- 0.12 mumol Ca/mumol creatinine) compared with calcium carbonate (0.40 +/- 0.11). CONCLUSIONS: The decrease in zinc absorption following the ingestion of zinc with different forms of calcium suggests that an antagonistic competition occurred between the minerals and that elemental calcium is the inhibiting factor.

Administration, Oral↗
PubMed1997

The effect of intermittent slow-release sodium fluoride and continuous calcium citrate therapy on calcitropic hormones, biochemical markers of bone metabolism, and blood chemistry in postmenopausal osteoporosis.

A detailed examination of calcitropic hormones and biochemical markers of bone turnover, serum chemistry, and blood hematology was performed in 75 postmenopausal women allocated to two groups: placebo plus calcium citrate (400 mg Ca B.I.D.) (n = 36) or intermittent slow-release sodium fluoride (SRNaF, 25 mg B.I.D.) plus calcium citrate (n = 39). After 2 years of therapy, a significant reduction in serum immunoreactive parathyroid hormone (PTH) was seen for both groups (43 +/- 18 SD-30 +/- 11 ng/liter, in placebo and 46 +/- 24-36 +/- 10, in SRNaF P < 0.0001 for both groups). Serum 1, 25(OH)2D significantly fell in placebo-treated patients (91 +/- 31-75 +/- 34 pmol/liter, P = 0.001) but did not change for SRNaF-treated patients. This difference in response between placebo and SRNaF-treated groups was significant, P = 0.005. Urinary hydroxyproline significantly declined during treatment in both groups (130 +/- 61-76 +/- 38 micromol/day, for placebo and 138 +/- 84-84 +/- 38 for SRNaF, P = 0.001). Similar decreases in urinary N-telopeptide of type I collagen were also observed for both groups (305 +/- 192-252 +/- 197 nmoles BCE/day for placebo and 356 +/- 230-220 +/- 197, P = 0.0001 for SRNaF). Serum carboxyterminal propeptide of type I collagen (PICP) declined significantly in both the placebo and SRNaF groups (118 +/- 38-101 +/- 36 microg/liter, and 116 +/- 47-105 +/- 39, P = 0.0027). Serum osteocalcin did not change significantly for either group, but bone-specific alkaline phosphatase (BS-ALPase), another marker of bone formation, demonstrated a significant fall in the placebo group at 2 years of therapy (16.2 +/- 6.7 U/liter-12.1 +/- 3.5, P = 0.009) and a small increase in the SRNaF-treated patients (13.0 +/- 4.1-15.0 +/- 4.5). The observed difference in response of BS-ALPase between the placebo and treated groups was significant (P = 0.007). There were no significant changes within or between treatment groups for blood hematology or serum chemistries. Mean values for all parameters remained within established normal ranges. These findings suggest that administration of calcium citrate inhibited PTH secretion and thereby reduced bone resorption in both groups, indicated by a decline in serum PTH, urinary hydroxyproline, and N-telopeptide. A low turnover state of bone may have been produced in the placebo group taking calcium citrate alone, since serum PICP, BS-ALPase, and 1,25(OH)2D also decreased. The addition of SRNaF prevented serum 1, 25(OH)2D from falling by an unknown mechanism. However, its anabolic action on the skeleton was best reflected by changes in BS-ALPase. Moreover, SRNaF appeared to exert no deleterious effects on blood chemistries or hematology during 2 years of administration.

Alkaline Phosphatase↗
PubMed2004

Calcium citrate ameliorates the progression of chronic renal injury.

BACKGROUND: Metabolic acidosis is a consequence of chronic renal failure and it may produce bone demineralization, muscle proteolysis, and progression of chronic renal failure. The aim of this study was to evaluate the effects of correction of metabolic acidosis with calcium citrate in an experimental model of renal mass ablation. METHODS: Wistar rats were subjected to 5/6 nephrectomy and were randomly assigned to one of 4 groups: nontreated (NFX); treated with calcium citrate (1.45 g/100 g feed) (NFX-CIT); treated with captopril (500 mg/L water) (NFX-CAP); or treated with both (NFX-CAP-CIT) during 1, 10, or 20 weeks. Body weight, systolic blood pressure, proteinuria, arterial bicarbonate concentration, urine citrate excretion, plasma calcium, and inulin clearance were measured. Histologic glomerular and tubulointerstitial damage scores were measured at 1, 10, and 20 weeks, and glomerular and tubular proliferating cell nuclear antigen (PCNA)-positive cells, alpha-smooth muscle actin, and desmin staining were studied by immunohistochemistry at 1 and 10 weeks. RESULTS: The treated groups showed significantly less glomerular and tubulointerstitial cellular proliferation in the first week (P < 0.05), less glomerular cell transdifferentiation and higher plasma bicarbonate at 10 weeks (P < 0.05), as well as diminished histologic glomerular and tubulointerstitial damage scores at 20 weeks (P < 0.05). Inulin clearances were higher (P < 0.05), and urine protein excretion rates were lower (P < 0.05) than in the NFX non-treated group, but arterial blood pressure was not significantly different in the NFX-CIT group. CONCLUSION: Calcium citrate slows the progression of chronic renal injury in the 5/6 NFX model. It improves metabolic acidosis and diminishes cell proliferation and transdifferentiation without changes in systolic blood pressure.

Alkalies↗
PubMed2006

Severe hypercalcemia after transition from calcium carbonate to calcium citrate in an elderly woman treated with ergocalciferol 50,000 IU per day.

BACKGROUND: Absorption of calcium carbonate in the fasting state has been reported to be significantly compromised in subjects with achlorhydria. Although calcium carbonate malabsorption in the fasting state cannot be predicted, it might be corrected if the compound is administered with meals. However, administering calcium carbonate with meals is logistically challenging in long-term care facilities. OBJECTIVE: The aim of this study was to report the case of a woman who was transitioned to calcium citrate and subsequently experienced symptomatic severe hypercalcemia. METHODS: An 89-year-old female resident of the Wisconsin Veterans Home, a skilled nursing facility in King, Wisconsin, was receiving long-term treatment with ergocalciferol (vitamin D2) 50,000 IU/d. The patient also was receiving calcium carbonate supplements in the morning, and she rarely ate breakfast (fasting state). The patient was transitioned from 2000 mg/d of elemental calcium as carbonate to 1230 mg/d as citrate. RESULTS: After being switched from calcium carbonate to calcium citrate, the patient developed severe symptomatic hypercalcemia (16.8 mg/dL), the primary cause of which was the administration of an inappropriately high dose of vitamin D. CONCLUSIONS: We report a case of symptomatic severe hypercalcemia in a skilled nursing facility resident treated with an inappropriately high daily dose of vitamin D. Hypercalcemia manifested when calcium carbonate was replaced with calcium citrate.

Aged, 80 and over↗
PubMed1999

Comparative absorption of calcium sources and calcium citrate malate for the prevention of osteoporosis.

Anthropologically speaking, humans were high consumers of calcium until the onset of the Agricultural Age, 10,000 years ago. Current calcium intake is one-quarter to one-third that of our evolutionary diet and, if we are genetically identical to the Late Paleolithic Homo sapiens, we may be consuming a calcium-deficient diet our bodies cannot adjust to by physiologic mechanisms. Meta-analyses of calcium and bone mass studies demonstrate supplementation of 500 to 1500 mg calcium daily improves bone mass in adolescents, young adults, older men, and postmenopausal women. Calcium citrate malate has high bioavailability and thus has been the subject of calcium studies in these populations. Positive effects have been seen in prepubertal girls, adolescents, and postmenopausal women. The addition of trace minerals and vitamin D in separate trials has improved the effect of calcium citrate malate on bone density and shown a reduction of fracture risk.

Absorption↗
PubMed2002

Effect of estrogen treatment and vitamin D status on differing bioavailabilities of calcium carbonate and calcium citrate.

The authors hypothesized that estrogen treatment or vitamin D status may affect the bioavailability of two common calcium supplements differently. Using data derived from a recent trial in 25 postmenopausal women, the authors found that deltaAUC of serum calcium after subtraction of placebo was significantly higher after calcium citrate (median, 0.85; 25th to 75th percentile, 0.70 to 3.15) than after calcium carbonate (0.25; -0.58 to 1.00) in non-estrogen-treated patients. There was no difference in the bioavailability of calcium between the two calcium formulations in estrogen-treated patients. Bioavailability was also significantly higher with the citrate salt for the subgroups with lower serum 25-hydroxyvitamin D and higher serum 1,25-dihydroxyvitamin D concentrations. In summary, bioavailability of calcium from the calcium carbonate product was more dependent on estrogen treatment and vitamin D status than that of calcium citrate. This may explain the variable results of reported calcium supplementation studies.

Adult↗