Calcium is necessary for strong bones but it’s good for so many other aspects of your health as well. Calcium helps circulation, and it also may reduce PMS symptoms in women. It also may help reduce LDL cholesterol levels. It is found naturally in dairy products. It can also be found in capsule, liquid, and tablet form.
Calcium is an essential mineral. Average adult weight is made up of about 2% calcium, most of which is stored in the skeleton and teeth. A small amount of calcium circulates in the blood, muscles, and fluid between cells to help transmit nerve impulses. Along with keeping teeth and bones strong, calcium also promotes blood coagulation and plays an essential role in enabling muscles, including the heart, to relax and contract. Food sources of calcium include dairy products (milk, yogurt, cheese), sea vegetables, sardines, almonds, hazelnuts, legumes, collards, kale, parsley, and tofu (Pitchford 1993).
|Type of oral calcium salt||Elemental calcium per 1,000 mg (percentage and weight)|
|Carbonate||40% (400 mg)|
|Citrate||21% (210 mg)|
|Lactate||13% (130 mg)|
|Gluconate||9% (90 mg)|
Ca, calcium carbonate, calcium chloride, calcium citrate, calcium gluceptate, calcium gluconate, calcium malate
Actions & Pharmacology
Calcium has anti-osteoporotic, antihypertensive, antihyperlipidemic, and possible anticarcinogenic properties. It is an electrolyte, a nutrient, and a mineral. Calcium functions as a regulator in the release and storage of neurotransmitters and hormones, in the uptake and binding of amino acids, and in vitamin B12 absorption and gastrin secretion. Calcium is required to maintain the function of the nervous, muscular, and skeletal systems and cell membrane and capillary permeability. It is an activator in many enzyme reactions and is essential in the transmission of nerve impulses; contraction of cardiac, smooth, and skeletal muscles; respiration; blood coagulation; and renal function (Product Info: Calcium gluconate 1992; AHFS 1979).
Calcium precipitates soluble colonic luminal surfactants (bile acids and free fatty acids) resulting in reduced cytolytic activity of these substances and, consequently, reduced epithelial damage and colonic proliferation. This antiproliferative effect was found for calcium provided as milk, calcium carbonate, and calcium phosphate and may explain the inverse association between calcium intake and colorectal neoplasia reported in some studies (Govers et al 1994).
Large clinical trials found that calcium supplementation decreased the risk of recurrent colorectal adenomas. In the Calcium Polyp Prevention Study, 930 patients with a recent history of colorectal adenomas were randomized to treatment with calcium carbonate (1200 mg/day) or placebo. Following 4 years of treatment, those who received calcium had a 17% lower risk of one or more colorectal adenomas compared with those in the placebo group (Baron et al 1999). A subsequent study enrolled the same patients to examine the effects of calcium supplementation on colorectal lesions. Using data obtained from the Calcium Polyp Prevention Study, the analysis revealed an even larger reduction in the risk of advanced adenomas. This effect was most pronounced in those with high intakes of dietary calcium and fiber and low intakes of fat, although these interactions were not statistically significant (Wallace et al 2004).
However, in the Women's Health Initiative study involving 36,282 postmenopausal women, a combined regimen of calcium and vitamin D supplementation for 7 years had no effect on the incidence of colorectal cancer. This large-scale placebo-controlled trial, primarily designed to study this regimen for the prevention of osteoporosis, investigated its impact on rates of colorectal cancer as well. Participants were randomized to active treatment received 1000 mg calcium and 400 IU vitamin D daily (n=18,176) or placebo (n=18,106). Although no positive association was found with supplementation, the authors point out that the long latency of colorectal cancer development, coupled with the lengthy duration of the trial, may have contributed to these null findings (Wactawski-Wende et al 2005).
Finally, the Calcium Follow-up Study recently reported its findings regarding the effects of long-term calcium supplementation on the recurrence of colorectal adenomas. Designed as an observational phase of the Calcium Polyp Prevention Study, the goal was to explore the effect of supplementation post-treatment for an average of 7 years. It found that the protective effect of calcium supplementation observed in the initial trial extended up to 5 years after treatment stopped (Grau et al 2007).
Complications and Outcomes of Pregnancy
The World Health Organization (WHO) conducted a randomized, placebo-controlled, double-blind trial in an attempt to clarify whether calcium supplementation in expectant mothers with a deficiency of the mineral reduced rates of pre-eclampsia and preterm delivery. Women who enrolled prior to gestational week 20 were randomized to treatment with 1.5 mg/day calcium (n=4151) or placebo (n=4161) throughout the remainder of pregnancy. Although supplementation did not prevent pre-eclampsia, it did reduce its severity and reduced its incidence by about 10%; however, this did not approach statistical significance. Maternal morbidity and neonatal mortality were improved in the group receiving calcium supplementation, with reductions observed in the severe maternal morbidity and mortality index (risk ratio [RR], 0.80; 95% CI, 0.70-0.91) and the neonatal mortality rate (RR, 0.70; 95% CI, 0.56-0.88). A Cochrane review cited in this article, involving more than 15,000 pregnant women, found an overall protective effect of calcium supplementation on pre-eclampsia (RR, 0.78; 95% CI, 0.68-0.89) (Villar et al 2006).
An earlier meta-analysis of studies evaluating the effect of calcium supplementation on pregnancy-related hypertension and pre-eclampsia raised controversy. The meta-analysis (n=2,260 subjects) reported a significant and substantial 62% reduction in risk of pre-eclampsia as well as decreases in both systolic (-5.4 mm Hg) and diastolic (-3.4 mm Hg) blood pressure with calcium supplementation (typically, 1 to 2 g per day). Many of the studies reviewed were conducted in countries where there is low dietary calcium intake. The authors acknowledged insufficient data hindered their ability to determine whether calcium supplementation affects the meaningful outcomes of maternal and fetal morbidity and mortality. Nevertheless, they suggested a policy of offering calcium supplementation to all pregnant women in whom there is a concern about the development of pre-eclampsia (Bucher et al 1996). Numerous criticisms of the authors' methods of analysis, of their conclusions, and of their advice have been offered (Cher 1997; Cappuccio 1996; Roberts et al 1996; Levine et al 1996).
A review article explored the effect of maternal calcium supplementation on the blood pressure of offspring. Data were examined from 2 randomized trials and 3 observational studies; follow-up among children ranged from birth to 9 years across studies. Although higher intakes of calcium during pregnancy were associated with lowered systolic blood pressure among offspring in all studies, these effects were statistically significant in just 3 studies. The largest randomized trial observed a clinically and statistically significant reduction in the incidence of hypertension in offspring 7 years of age (RR, 0.59; 95% CI, 0.39-0.90). The reviewers concluded that evidence exists to support an association between maternal calcium intake during pregnancy and offspring blood pressure, although additional research is warranted (Bergel and Barros 2007).
A combination of calcium, ascorbic acid, and vitamin D3 reversed dental, clinical, and early skeletal fluorosis in children in a double-blind, placebo-controlled study. Twenty-five children (aged 6 to 12 years), living in an area where the drinking water contained fluorides at a concentration of 4.5 mg/liter (mg/L), were administered either placebo (n=10) or ascorbic acid 250 mg and calcium compound (125 mg elemental calcium) twice a day and vitamin D3 60,000 IU once a week (n=15) for 180 days. Intake of fluoride-rich water continued as usual. At the end of the treatment period, there was significant improvement in dental, clinical, and skeletal grades of fluorosis in the treated children (p=0.05) but not in the placebo group. There were significantly reduced fluoride levels in the blood and serum and increased urinary fluoride levels in the treated group (p=0.05 for all three parameters) but not in the placebo group, indicating increased removal of fluoride from the body. The results of this small study indicate that calcium, ascorbic acid, and vitamin D3 supplementation can reverse fluorosis in children (Gupta et al 1996).
A meta-analysis examined the effects of calcium supplementation on risk of fracture in children of both genders. Studies meeting inclusion criteria were randomized, placebo-controlled trials of at least 3 months duration with bone measurements taken at baseline and again after at least 6 months follow-up. Of the 19 studies identified involving 2,859 children, no effect of calcium supplementation on bone mineral density (BMD) was found at the hip or lumbar spine—common sites of fractures. A slight effect was observed on total bone mineral content and upper limb BMD. Although the effect to the upper limb persisted after supplementation ceased, it is of little clinical importance, since it is unlikely to result in an overall decrease in fracture risk among children (Wizenberg et al 2007).
One study found that 1200 mg/day calcium reduced the risk of osteoporotic fractures in elderly women compliant with the 5-year regimen. The double-blind, placebo controlled trial corresponded in length to the 5-year risk of fracture, projected to be 15% among this group of women (older than 70 years). Those taking calcium (n=730) noted improvements in quantitative ultrasonography findings of the heel, femoral neck, and whole-body dual x-ray absorptiometry data compared with those randomized to placebo (n=730). Calcium supplementation was also associated with greater bone strength (Prince et al 2006). Another 5-year study in a similar number of postmenopausal women found that 1 g/day of calcium citrate taken for 5 years led to significant positive effects on bone density, including a sustained reduction in bone loss and turnover and cumulative benefits to the proximal femur. The effect on fracture risk was less certain, since fractures still occurred in both groups. This may have been the result of decreasing compliance over the 5-year regimen, possibly due in part to a higher incidence of diarrhea reported among supplement users vs those receiving placebo (18% vs 11%, p=.0002). Given the positive cumulative and sustained effects observed among supplement users in this study, the authors suggest that continuous, long-term calcium supplementation can lead to even greater effects on bone density (Reid et al 2006).
An earlier review of studies in which postmenopausal women were treated with antiresorptive drugs (estrogen or calcitonin) or with antiresorptive drugs plus calcium showed greater increases in bone mass when treatment included supplemental calcium. Calcitonin alone stopped bone loss in the spine, but calcitonin plus calcium increased bone mass of the spine (Nieves et al 1998).
Intermittent fluoride treatment plus calcium increased BMD and was associated with a lower fracture rate than calcium supplementation alone in men with idiopathic osteoporosis. Fifty men with osteoporosis but no history of vertebral fractures were given either calcium 1,000 mg/day, or intermittent monofluorophosphate (MFP, 114 mg=15 mg fluoride ions daily, 3 months on, 1 month off) plus calcium 950 to 1,000 mg/day for 36 months. There was a progressive decrease in back pain in the MFP group over the three years, whereas there was no significant change in the calcium-only group. The fracture rate (new fractures per 100 patient-years) at the end of 3 years was 4.9 for the MFP group and 20.5 for the calcium-only group (Ringe et al 1998).
Although some earlier studies have shown a reduction in fractures associated with concurrent use of vitamin D and calcium, a more recent study examining older community-dwelling women (n=3,314) differed in its findings. Subjects included women aged 70 and above with one or more risk factors for fracture of the hip; all received an informational leaflet on calcium intake and how to reduce falls. Those in the treatment group (n=1,321) were instructed to take the combined daily regimen of 1000 mg calcium and 800 IU vitamin D3 (cholecaliferol), while the control group (n=1,993) received the leaflet only. After 2 years, although clinical fracture rates were lower than anticipated in both groups, the researchers found no evidence of reduced risk with supplementation. However, the lack of a placebo arm and the fact that the study was underpowered may have limited the study's findings (Porthouse et al 2005).
In a smaller 3-year study involving 318 women and men over the age of 65 who lived at home, calcium 500 mg/day (as calcium citrate malate) plus 700 IU of cholecalciferol/day, in comparison to placebo, reduced the rate of bone loss in both men and women and significantly reduced the incidence of nonvertebral fractures. Rates of loss of bone mass were lower for femoral neck, spine, and total body in treatment groups after 1 year. However, significant differences between treatment groups in years 2 and 3 were maintained only for total-body BMD (Dawson-Hughes et al 1997).
In a larger study, concurrent administration of oral vitamin D3 and calcium reduced the incidence of nonvertebral fractures and hip fractures and increased bone density of the total proximal femoral region in elderly women (mean age 84 years). Compared with the placebo group (n=888), the treated women (n=877) had 32% fewer nonvertebral fractures and 43% fewer hip fractures. Eighteen months of treatment resulted in an increase of 2.7% in bone density of the total proximal femoral region compared with a decrease of 4.6% in the placebo group (p<0.001). The dosage of vitamin D3 was 20 mcg (800 IU)/day and elemental calcium was 1.2 g/day (Chapuy et al 1992).
Calcium supplementation was effective in reducing premenstrual pain, but not menstrual pain, in a prospective, randomized, double-blind, placebo-controlled, parallel-group, multicenter clinical trial of premenstrual syndrome. Subjects (n=497) were given calcium 1,200 mg daily or placebo for three menstrual cycles. Outcome measures included a daily subjective rating scale with 17 core symptoms, of which three were pain-related, and four symptom factors, of which one was pain-related. Significantly lower scores occurred for all pain measures in the treatment group during the luteal phase of the third menstrual cycle (p=0.001) while scores did not change significantly in controls. Pain scores did not decrease significantly during the menstrual phase of the third menstrual cycle for both calcium and placebo groups (Thys-Jacobs et al 1998).
Indications & Usage
Approved by the FDA:
- Prophylaxis of calcium deficiency and treatment of osteoporosis
- Calcium acetate: Treatment of hyperphosphatemia related to renal failure and hemodialysis
- Calcium carbonate: Used alone or in combination products as an antacid to relieve symptoms of heartburn, acid indigestion, and stomach upset
Calcium supplementation may reduce premenstrual pain, total and LDL cholesterol, hypertension, and the occurrence of colorectal polyps. Studies show it may also reverse fluorosis in children (when combined with vitamins C and D), control age-related increases in parathyroid hormone, and reduce plasma bilirubin in patients with Crigler-Najjar syndrome (calcium phosphate only).
Weaker evidence shows calcium supplementation may be helpful for leg cramps, pre-eclampsia, and prophylaxis of urinary crystallization of calcium oxalate in patients with nephrolithiasis (calcium citrate only).
Calcium supplements are contraindicated in patients with hypercalcemia (Gilman et al 2001).
Precautions & Adverse Reactions
Calcium enhances the effect of cardiac glycosides on the heart and may precipitate arrhythmias (Dukes 1980).
Oral calcium supplementation can cause constipation. Additionally, oral calcium—including antacids containing calcium carbonate or other absorbable calcium salts—can cause hypercalcemia (especially in patients with hypothyroidism) and milk-alkali syndrome with doses higher than 4 g daily. Hypercalcemia may result in nephrolithiasis, anorexia, nausea, vomiting, and ocular toxicity. Symptoms of milk-alkali syndrome include hypercalcemia, uremia, calcinosis, nausea, vomiting, headache, weakness, azotemia, and alterations in taste.
High intake of calcium, whether from food alone or including supplements, was associated in an epidemiological study with an increased incidence of prostate cancer, possibly due to calcium's inhibitory effect on vitamin D conversion (Giovannucci et al 1998).
FDA-rated as Pregnancy Category C. Calcium is safe in normal dietary amounts.
Calcium is safe in normal dietary amounts.
Phosphorus, found in dairy products, may inhibit calcium absorption by forming insoluble compounds with calcium ions. This binds the mineral into a form that is poorly absorbed through the intestinal wall. Clinical Management: Calcium products should not be taken within 2 hours of a dairy product or other foods high in phosphorous.
Foods containing oxalic acid or phytic acid
Oxalic acid (found in foods such as spinach, parsley, rhubarb, and beans) and phytic acid (found in bran and whole cereals) may inhibit calcium absorption by forming insoluble compounds with calcium ions. This binds the mineral into a form that is poorly absorbed through the intestinal wall. Clinical Management: Calcium products should not be taken within 2 hours of eating foods high in oxalic acid or phytic acid.
Concurrent use may result in reduced absorption of iron, although the effect is usually not clinically significant.
Concurrent use may result in reduced absorption of zinc, although the effect is usually not clinically significant.
Coadministration of digitoxin and parenteral calcium is contraindicated (Product Info: Crystodigin 1995). Early case reports describe cardiovascular collapse after administration of intravenous calcium in patients receiving digitalis. Clinical Management: Administration of parenteral calcium to digitoxin-treated patients is contraindicated.
Most textbooks and reviews state that a contraindication exists in giving calcium intravenously in the presence of digitalis glycosides, though this is based on relatively few reports. The similar actions of digitalis glycosides and calcium are documented, and deaths have occurred during simultaneous administration. Clinical Management: If calcium is needed in a digitalized patient, it should be infused over several hours or given orally.
A retrospective study conducted on 267 patients who had undergone elective coronary artery bypass graft (CABG) surgery showed an increased incidence of renal failure in patients who had received gentamicin and bypass prime solutions containing high amounts of calcium (Schneider et al 1996). Clinical Management: Avoid concurrent use of gentamicin and solutions containing a high amount of calcium during CABG surgery.
Concurrent use may result in decreased effectiveness of aspirin due to increased urinary pH and subsequent increased renal elimination of salicylates. Clinical Management: Monitor for reduced aspirin effectiveness upon initiation of calcium-containing products or for possible aspirin toxicity upon withdrawal of calcium-containing products. Adjust the dose accordingly. Using buffered aspirin may limit the degree to which the urine is alkalinized.
Concomitant use may result in decreased effectiveness of cefpodoxime. Clinical Management: Concurrent administration of cefpodoxime and calcium-containing products is not recommended. If concurrent use cannot be avoided, cefpodoxime should be taken at least 2 to 3 hours before the administration of calcium. Because staggered administration may not be completely reliable, aggressively monitor patients for continued antibiotic efficacy. Alternative antibiotic therapy (eg, another third-generation cephalosporin or a second-generation cephalosporin with similar activity) may need to be considered.
Thiazide and thiazide-like diuretics may cause hypercalcemia by decreasing renal calcium excretion. Concomitant ingestion of calcium salts and thiazide diuretics may predispose patients to developing the milk-alkali syndrome. Clinical Management: Instruct patients to avoid excessive ingestion of calcium in any form (eg, antacids, dairy products) during thiazide diuretic therapy. Consider monitoring the patient's serum calcium level and/or parathyroid function if calcium replacement therapy is clinically necessary.
Concomitant use may result in decreased effectiveness of fluoroquinolones such as ciprofloxacin and enoxacin. Clinical Management: Concurrent administration of fluoroquinolones with calcium—including calcium-fortified foods and drinks such as orange juice—should be avoided. Fluoroquinolones may be taken 2 hours before or 6 hours after taking calcium-containing products.
Concomitant use may result in decreased effectiveness of itraconazole. Clinical Management: Calcium-containing products should be taken at least 1 hour before or 2 hours after itraconzaole.
Concomitant use may result in decreased effectiveness of ketoconazole. Clinical Management: Concurrent administration of ketoconazole and calcium-containing products is not recommended. If concurrent use cannot be avoided, ketoconazole should be taken at least 2 hours before calcium-containing products. Because staggered administration may not be completely reliable, aggressively monitor patients for continued antifungal efficacy.
Concurrent use with calcium carbonate may result in decreased absorption of levothyroxine. Clinical Management: Separate the administration of levothyroxine and calcium carbonate by at least 4 hours.
Concomitant administration of calcium-containing antacids and sodium polystyrene sulfonate resin therapy has resulted in the elevation of serum carbon dioxide content levels, associated with varying degrees of metabolic alkalosis. Clinical Management: Separate the oral administration of sodium polystyrene sulfonate and calcium-containing products by as much time as possible. Another alternative is to administer the sodium polystyrene sulfonate rectally. If concurrent oral administration cannot be avoided, monitor the patient for evidence of alkalosis.
Concurrent use may result in decreased effectiveness of tetracyclines. Clinical Management: Concurrent administration of any of the tetracyclines and calcium-containing products is not recommended. If concurrent use cannot be avoided, tetracyclines should be taken at least 1 to 3 hours before calcium-containing products. Because staggered administration may not be completely reliable, aggressively monitor patients for continued antibiotic efficacy.
Concurrent use may result in decreased effectiveness of ticlopidine. Clinical Management: Concurrent administration of ticlopidine and calcium-containing products is not recommended. If concurrent use cannot be avoided, ticlopidine should be taken at least 1 to 2 hours before the administration of calcium.
Concomitant use may result in decreased effectiveness of verapamil, a calcium channel blocker, and result in reversal of hypotensive effects. Clinical Management: Calcium generally is given to reverse hypotension and improve cardiac conduction defects. Monitor the patient for expected cardiovascular response.
Concurrent use may result in decreased effectiveness of zalcitabine. Clinical Management: Separate the administration of zalcitabine and calcium-containing products as far apart as possible.
Concomitant use may decreased bioavailability of atenelol. Clinical Management: Instruct patients to avoid taking atenolol and calcium-containing products at the same time. Atenolol should be administered 2 hours before or 6 hours after calcium-containing products.
Concomitant use may result in decreased effectiveness of bismuth subcitrate. Clinical Management: Bismuth subcitrate and calcium-containing products should be administered at least 30 minutes apart.
Concurrent use may interfere with the absorption of bisphosphonates such as alendronate, etidronate, and risedronate. Clinical Management: Administer bisphosphonates 2 hours before and 3 to 4 hours after a dose of calcium.
Concomitant use may result in decreased absorption of hyoscyamine. Clinical Management: Hyoscyamine should be taken prior to meals and calcium-containing products should be taken after meals.
Concomitant use may result in decreased absorption of methscopolamine, although the effect is minor. Clinical Management: Monitor the patient for drug effectiveness.
Ranitidine bismuth citrate
Concurrent use may result in decreased plasma concentrations of ranitidine; however, the effect is clinically insignificant.
Concurrent use may result in decreased effectiveness of sucralfate. Clinical Management: Calcium-containing products should not be taken 30 minutes before or after sucralfate administration.
Concomitant sulfasalazine and calcium gluconate therapy has been reported to result in delayed absorption of sulfasalazine.
Active treatment is required when serum calcium levels reach 12 mg/dL, and intensive treatment is necessary for levels greater than 15 mg/dL (AMA 1980).
Mode of Administration
Capsule, liquid, tablet
The National Institute of Medicine recommends the following Adequate Intakes (AIs) for males and females: 0 to 6 months — 210 mg/day; 7 to 12 months — 270 mg/day; 1 to 3 years — 500 mg/day; 4 to 8 years — 800 mg/day; 9 to 18 years — 1,300 mg/day; 19 to 50 years — 1,000 mg/day; 51+ years — 1,200 mg/day. The same AIs apply to pregnant or lactating women.
- Colorectal cancer prevention: 1,200 to 2,000 mg/d (Hofstad et al 1998; Duris et al 1996; Lipkin & Newmark 1993; Zimmerman 1993).
- Crigler-Najjar Syndrome: 4,000 mg/d (Van der Veere et al 1997).
- Dysmenorrhea: 1,000 to 1,300 mg/d (Penland et al 1993; Thys-Jacobs et al 1989).
- Hypercholesterolemia: 250 to 400 mg/d with meals (Denke et al 1993; Bell et al 1992; Karanja et al 1994).
- Hyperphosphatemia: 1,334 mg of calcium acetate with each meal initially. Most patients will require 2,001 to 2,668 mg with each meal. The dosage may be increased as necessary to obtain serum phosphate levels below 6 mg/dL as long as hypercalcemia does not occur (Product Info: PhosLo 1996); or alternatively, 1 to 17 grams of calcium carbonate daily in divided doses (Malberti et al 1988; Slatopolsky et al 1986).
- Hyperphosphatemia of renal failure and hemodialysis: 4,000 to 8,000 mg/d of calcium acetate (Product Info: PhosLo 1996) or 2,500 to 8,500 mg/d of calcium carbonate (Malberti et al 1988; Slatopolsky et al 1986).
- Hypertension, idiopathic: 1,000 to 2,000 mg/d (Bucher et al 1996; Takagi et al 1991; Lyle et al 1987; Tabuchi et al 1986).
- Hypertension, pregnancy-related: 1,000 to 2,000 mg/d (Bucher et al 1996).
- Hypocalcemia: calcium carbonate, 1 to 2 grams 3 times a day with meals (AMA 1986); calcium citrate, 950 mg to 1.9 g given 3 or 4 times a day after meals (AMA 1986); calcium gluconate, 15 g daily in divided doses (AMA 1986); calcium lactate, 7.7 grams daily in divided doses with meals (USPDI 2004; AMA 1980); calcium glubionate, 15 grams/d in divided doses (AMA 1986); dibasic calcium phosphate, 4.4 g daily in divided doses with or after meals (USPDI 2004; AMA 1980); tribasic calcium phosphate, 1.6 grams twice daily with or after meals (USPDI 2004).
- Nephrolithiasis, prevention: 200 to 300 mg with meals or as the citrate salt between meals (Liebman et al 1997; Levine et al 1994; Barilla et al 1978).
- Osteoporosis, glucocorticoid-induced, prevention of bone loss:1,000 mg/d (Buckley et al 1996).
- Osteoporosis, idiopathic, prevention of bone loss and fractures: 500 to 2,400 mg/d including a bedtime dose (Nieves et al 1998; Dawson-Hughes et al 1997; Fujita et al 1997; McKane et al 1996; Blumsohn et al 1994; Reid et al 1993; Chapuy et al 1992).
- Pre-eclampsia, prevention: 1,000 to 2,000 mg/d (Bucher et al 1996).
- Premenstrual syndrome: 1,000 to 1,200 mg/d (Thys-Jacobs et al 1998; Penland et al 1993; Thys-Jacobs et al 1989).
- Bone mass accretion (adolescents): 500 mg/d (Lloyd et al 1993).
- Fluorosis: 250 mg/d (Gupta et al 1996).
- Hypertension, prevention: 600 mg/d (Gillman et al 1995).
- Hypocalcemia: calcium chloride, 200 mg/kg/d in divided doses every 4 to 6 hours (Benitz et al 1988); calcium glubionate: infants up to 1 year old should receive 1.8 grams of calcium glubionate 5 times a day before meals, and children 1 to 4 years old should receive 3.6 grams 3 times a day before meals. Children over age 4 should receive adult and adolescent doses (USPDI 2004); calcium gluconate, 200 to 800 mg/kg/d in divided doses (USPDI 2004; Benitz et al 1988); calcium lactate, 500 mg/kg/24 hours given orally in divided doses (USPDI 2004; Benitz et al 1981; Shirkey 1980; AMA 1980; Pagliaro et al 1979); calcium levulinate: 500 mg/kg/24 hours (12 g/square meter/24 hours) given orally in divided doses (Shirkey 1980); dibasic calcium phosphate: 200 to 280 mg/kg of body weight a day, in divided doses with or after meals (USPDI 2004).