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Nutrient Name: Calcium.
Synonyms: Calcium ascorbate, calcium aspartate, calcium carbonate, calcium citrate, calcium gluconate, calcium lactate.
Elemental Symbol: Ca.
Related Substance: Microcrystalline hydroxyapatite (MCHC)

Summary Table
Drug/Class Interaction TypeMechanism and SignificanceManagement
Aminoglycoside antibiotics
Nephrotoxic effects of aminoglycosides can increase calcium excretion. Calcium coadministration may be protective but may potentiate adverse effects, especially of gentamicin, although such nephrotoxic synergy has only been demonstrated with parenteral, not oral, calcium coadministration.Coadminister with extended use; closely monitor renal function and serum calcium, magnesium, and potassium.
Amphotericin B
Toxicity of amphotericin B associated with increased intracellular calcium concentration. This drug can deplete and disrupt calcium and other minerals. Well documented but not well understood.Monitor electrolytes and coadminister minerals as indicated. Consider using less toxic liposomal formulation instead.
Antacids, aluminum- and magnesium-containing
Aluminum-based antacids may reduce calcium absorption and complex with phosphates to deplete calcium. Calcium citrate may increase aluminum absorption.Avoid calcium citrate during therapy. Minimize use of aluminum-based antacids.
Anticonvulsant medications
/ /
Antiepileptic drugs, particularly phenytoin and phenobarbital, can decrease calcium absorption, accelerate vitamin D metabolism in liver (CYP450 induction), and may reduce serum levels of 25(OH) vitamin D. Thus, anticonvulsants impair mineralization, leading to increased risk of bone loss, osteoporosis, and fractures. Mechanisms well established; clinical implications variable.Coadminister calcium and vitamin D. Monitor serum 25(OH)D and bone status. Promote sunlight exposure and weight-bearing exercise.
Beta-1-adrenoceptor antagonists
Simultaneous intake may inhibit absorption and bioavailability of both agents, which over time may increase drug half-life and may cause accumulation.Separate intake by 2 hours. Monitor blood pressure and heart rate as indices of beta-blocker levels.
/ /
Synergistic interaction. Vitamin D assists calcium absorption, and both enable bisphosphonates in maintaining bone mineralization, including with HRT.Coadminister calcium and vitamin D. Promote appropriate sunlight exposure and weight-bearing exercise.

Calcium intake may enhance bone-sparing effect of calcitonin in prevention or treatment of osteoporosis. Pharmacologically reasonable; emerging evidence.Coadminister calcium (and vitamin D if needed).
Calcium acetate

Possible adverse effect from concomitant administration due to additive effect. Generally accepted; direct evidence lacking.Avoid concomitant calcium. Monitor for hypercalcemia with calcium acetate.
Cholestyramine, colestipol
Bile acid sequestrants
Bile acid sequestrants can impair calcium absorption by binding calcium and by reducing absorption of vitamin D and fat-soluble nutrients as a result of decreasing lipid digestion and absorption. Risk of deficiency and sequelae with extended use.Supplement calcium and vitamin D. Promote sunlight exposure and exercise.
Corticosteroids, oral
/ /
Oral corticosteroids reduce calcium absorption and may increase excretion while decreasing vitamin D availability and lowering serum levels. Increased risk of bone loss, osteoporosis, and fractures with long-term oral steroid use.Supplement additional calcium and monitor bone and 25(OH)D status with steroid use > 1 month. Promote sunlight exposure and exercise.
EDTA binds to calcium; thereby increasing calcium excretion and increasing risk of hypocalcemia or negative calcium balance.Assess levels of calcium and other affected nutrients before treatment. Coadminister minerals.
Oral contraceptives (OCs)
Hormone replacement therapy (HRT)
Synergistic interaction, especially with osteoporosis. Calcium can protect bone mineral density (BMD) during attainment of maximal peak bone mass in adolescence and early adulthood (with which OCs can interfere) and minimize later bone loss. Vitamin D assists calcium absorption, and both enable estrogen to inhibit osteoclastic activity and bone resorption and maintain bone mineralization. Progestins may counter benefit.Coadminister with calcium and vitamin D (separate intake), possibly bisphosphonates. Monitor bone, 25(OH)D and HDL. Promote sunlight, nutrient-rich diet, and weight-bearing exercise.
quinolone antibiotics
Chelation between this class of antibiotics and calcium likely to impair absorption of both, as well as other minerals. Calcium depletion and effects of bone loss plausible with extended use but not established or probable.Discontinue calcium or separate intake during short-term therapy. Mineral supplementation may be appropriate with extended therapy; intake separated by several hours.
Gastric acid–suppressive medications
Cimetidine, Histamine (H2) antagonists
Omeprazole, Proton pump inhibitors

Cimetidine can decrease calcium absorption and transport through effects on vitamin D hydroxylase and vitamin D and impairment of gastric acid environment. Omeprazole can decrease absorption by reducing gastric acid production and increasing gastric pH. Possible deficiency with extended use.Supplement with calcium other than carbonate; take separate from meals. Monitor bone density and 25(OH)D with chronic use, especially postmenopausal women.
Heparin, unfractionated
/ /
Heparin therapy is associated with bone loss. Heparin may also inhibit formation of 1,25-dihydroxyvitamin D by kidneys and thereby reduce calcium absorption. Significant risk of bone loss with extended heparin use and nutrient depletion. Limited evidence supporting protective effect of supplemental calcium (or vitamin D).Coadminister calcium and vitamin D, possibly as hydroxyapatite, where indicated. Monitor bone and 1,25(OH)2status with heparin use > 1 month.
Isoniazid (INH)
Isoniazid can lower levels of both calcium and activated vitamin D levels; inhibit hepatic mixed-function oxidase activity, hepatic 25-hydroxylase and renal 1α-hydroxylase and reduce corresponding vitamin D metabolites. Drug-induced vitamin D deficiency can produce hypocalcemia and elevate parathyroid hormone (PTH). Nutrient support unlikely to interfere with therapeutic activity of medication.Coadminister calcium and vitamin D when INH used for > 1 month. Promote sunlight exposure. Monitor 25(OH)D and bone status.
Thyroid hormones
/ /
Chelation between thyroid medications and calcium impairs absorption of both, particularly with calcium carbonate. Thyroid hormones increase urinary calcium excretion. Calcium depletion and effects of bone loss plausible with extended use, but not established or probable; risk greater in women with history of hyperthyroidism or thyrotoxicosis. Strong evidence for binding but evidence lacking for benefit from calcium coadministration.Comorbid conditions may require both agents. Separate thyroid (morning) and calcium (bedtime). Monitor BMD with long-term use.
/ /
Biguanides, especially metformin, reduce B12absorption and lower serum B12and holotranscobalamin by depressing intrinsic factor secretion and interfering with B12/intrinsic factor uptake through calcium-dependent ileal membrane antagonism. Possible decrease of folate and increase of homocysteine.Supplement B12, folic acid, and calcium. Monitor folate and cobalamin status.
Sulfonamide antibiotics

Sulfonamide can impair calcium absorption, as well as that of magnesium and vitamin B12. Low probability of clinically significant effects on calcium balance with short-term therapy. Calcium depletion and effects of bone loss plausible with extended use, but not established or probable.Intake separated by several hours. Additional calcium supplementation may be appropriate with extended therapy.
Tetracycline antibiotics
/ /
Chelation between calcium and tetracycline antibiotics likely to impair absorption of both to clinically significant degree. Calcium intake, even small amounts, can significantly impair antimicrobial activity. Tetracycline also increases urinary calcium excretion. Calcium depletion and effects on calcium-dependent tissues (e.g., bones, teeth) probable, and adverse effect on bone formation or density possible with extended use; increased concern with adolescents and elderly.Discontinue calcium (including dairy foods), or separate intake during short-term therapy. Calcium supplementation usually appropriate with extended therapy, with intake separated by several hours.
Thiazide diuretics
/ / /
Thiazide diuretics increase calcium retention by decreasing urinary calcium excretion; decreased calcium absorption, suppressed PTH secretion, and inhibited vitamin D synthesis also appear to be effects of thiazides. Concomitant use with supplemental calcium theoretically increases risk of hypercalcemia; low probability of occurrence. Not a substitute for increased calcium intake; benefits of increased calcium retention cease when thiazide discontinued. Evidence incomplete.Monitor calcium levels before initiating and periodically during concomitant use of calcium or vitamin D.
Calcium channel blockers
/ / /
Verapamil may decrease endogenous vitamin D synthesis and induce target-organ PTH resistance. Calcium administration can be used to reduce adverse effects of calcium channel blockers; concurrent use of verapamil and intravenous calcium salts, in particular, can be therapeutically efficacious (e.g., control cardiac tachyarrhythmias) yet avoid hypotensive effect of calcium channel blocker. Conversely, increased calcium availability may oppose verapamil's activity as calcium antagonist, particularly when antihypertensive effect desired. Theoretically, excess calcium (or vitamin D) might contribute to hypercalcemia, which in turn might precipitate cardiac arrhythmia in patients on verapamil. Minimal evidence; rare occurrence but potentially severe.Concurrent supplementation with calcium (and vitamin D) may be appropriate, but only under close supervision. Consider bone support needs.
EDTA, Ethylenediaminetetraacetic acid; HDL , high-density lipoprotein; INH , international normalized ratio.
nutrient description

Chemistry and Forms

Calcium ascorbate, calcium aspartate, calcium carbonate, calcium citrate, calcium citrate-malate (citramate), calcium gluconate, calcium lactate, calcium malate; microcrystalline hydroxyapatite (MCHC); calcium acetate; bonemeal, dolomite; calcium glycerophosphate, dicalcium phosphate, tricalcium phosphate; calcium phosphate (dairy calcium).

Physiology and Function

Calcium is the most abundant mineral in the human body, with 99% of it stored in bone and teeth. The remaining 1% of body calcium is found in the blood, extracellular fluid (ECF), and soft tissue. Normal physiological functioning requires that homeostatic systems in the intestines, bones, and kidneys, in concert with parathyroid hormone (PTH), calcitonin, vitamin D, and other hormones, maintain calcium levels in the blood and ECF within very narrow concentration parameters. Calcium absorption in the intestines will increase if blood levels decrease. Likewise, renal excretion can be reduced to maintain calcium levels. Ultimately, however, bone will be demineralized to maintain normal calcium parameters when intake is inadequate to sustain the physiological functions of calcium in bone and teeth, cellular structure, endocrine function, cell signaling, nerve transmission, blood clotting, blood pressure regulation, enzyme activation, and muscle contraction.

A dynamic and complex system involving calcium absorption, bone formation and resorption, renal reabsorption and excretion, and hormonal regulatory networks enables rapid and tight control of blood calcium levels. Calcium is absorbed in the duodenum, jejunum, and ileum by an active saturable process that involves vitamin D and PTH. Calcium exhibits threshold absorption that depends on the interplay among dietary intake, blood and tissue levels, gender, life stage and activity level, gastric pH, hormonal milieu, vitamin D receptor genotype, and numerous other factors. Except for dietary intake, the major factors influencing the efficiency of absorption are physiological requirements and age. Thus, in childhood, adolescence, pregnancy, and lactation, the intestinal calcium absorption process becomes more efficient; conversely, it is impaired in the elderly, especially with decreased physical activity levels. Calcium bioavailability depends to some extent on vitamin D status. PTH stimulates the conversion of vitamin D to calcitriol, its active form, primarily in the kidneys and to some degree in other tissues. Calcitriol increases the absorption of calcium from the small intestine. At high intakes, some calcium is absorbed by passive diffusion (independent of vitamin D). Some absorption can also occur from the colon. Together with PTH, calcitriol activates osteoclasts to stimulate the release of calcium from bone and increases renal tubular reabsorption to reduce excretion of calcium through the urine. On reaching normal blood calcium levels, the parathyroid glands suspend PTH secretion, and the kidneys resume excretion of any excess calcium through the urine. Unabsorbed and endogenously secreted calcium is eliminated through the feces. Perspiration and breast milk also act as pathways of calcium excretion.

Calcium ions play a major role in the structural aspect of physiology. Hydroxyapatite [Ca10(PO4)6(OH)2], a crystalline calcium carbonate/calcium phosphate compound, is the form of calcium primarily responsible for providing rigidity and strength to bones and teeth. Positive calcium balance is maintained during development and growth until peak bone density is attained, becomes neutral as adults mature, and is often negative in the elderly. Thus, bone density increases during the first three decades of life until it reaches its peak at about age 30. Thereafter, bone density stabilizes before moving into a pattern of gradual decline. Both men and women experience diminishing bone density as they age, but women experience more significant and rapid decline after menopause. Calcium and vitamin D insufficiency during adolescence and young adulthood can significantly curtail peak bone density, dramatically increasing the risk of osteoporosis in later life.

Calcium facilitates muscle activity by aiding transport across cell membranes. Muscles require calcium for proper contractile function. Without calcium, the muscles tend to stay in the contracted state. The cell membranes of skeletal muscle cells, nerve cells, and other electrically excitable cells are characterized by voltage-dependent calcium channels that enable rapid changes in calcium concentrations. For example, the nerve impulse entering a muscle fiber to stimulate contraction triggers calcium channels in the cell membrane to allow influx of calcium ions into the muscle cell. Calcium ions are released from intracellular storage vesicles as these calcium ions bind to troponin- c and set in motion the process of muscle contraction. Meanwhile, the binding of calcium to calmodulin activates glycogenolysis in the muscle to provide energy necessary for contraction.

As with striated muscle throughout the body, the heart requires calcium for proper contractility. A sudden decrease of ionized serum calcium can cause tetany, leading to cardiac or respiratory failure. Likewise, calcium plays a role in mediating the constriction and relaxation of blood vessels (vasoconstriction and vasodilation).

An array of proteins and enzymes require calcium as a cofactor for optimal activity and stabilization. For example, activation of seven of the clotting factors in the coagulation cascade requires the binding of calcium ions. Ionized calcium initiates the formation of blood clotting by stimulating the release of thromboplastin from blood platelets. It is also a cofactor in the conversion of prothrombin to thrombin, which converts fibrinogen to fibrin, and then aids in its polymerization to form a stable clot.

Calcium also regulates membrane stabilization. Certain cells (e.g., mast cells) tend to rupture when calcium ions are depleted. In addition, neurotransmitters at synaptic junctions are regulated by calcium. This may have effects on such conditions such as anxiety, insomnia, and other stress-related conditions.

nutrient in clinical practice

Known or Potential Therapeutic Uses

Calcium plays many essential roles in human physiology, but it primarily receives attention in conventional medicine and patient inquiries in regard to bone health, aging, and osteoporosis. Nevertheless, calcium has a proven influence on risk for numerous pathological patterns and needs to be emphasized as a critical nutrient beginning at an early age. Calcium intake during childhood and especially during adolescence is perhaps the most significant factor in establishing healthy bone mass and preventing osteoporosis, although exercise is an equally and possibly more important factor. 1 Calcium too often becomes a concern as aging progresses and the threat of bone loss is looming or initial signs of osteoporosis are already present. Unfortunately, when awareness of need develops during middle age and menopause, it is usually too late for optimal calcium nutriture to function in a preventive mode. 2-5

Evidence for beneficial effects of calcium supplementation on bone mineral density (BMD), most often studied in women before and after menopause, is mixed, with slowing the pace of further bone loss becoming the realistic clinical objective in most cases. Inherently, the significance of variables such as calcium intake, beverage habits, hormone history and status, and lifestyle factors (e.g., exercise, smoking) all complicate the issues and confound analysis of the available data. 6,7Thus, although the current dietary and calcium supplementation recommendations are almost always advisable, they are unlikely to reverse the process of age-related bone loss without a comprehensive and strategic approach utilizing multidisciplinary interventions.

The collective evidence indicates that a diet rich in calcium from plant sources deserves much more attention, and that the common advice to consume dairy products may be less well founded than generally presumed. Furthermore, the tendency of adolescents to displace milk consumption with carbonated beverages during the most critical life stage for peak bone mass development tips the calcium balance in a deleterious direction, given the calcium-depleting action of phosphates found in many soft drinks, as well as drawing on the skeletal mineral reserve to buffer the acid load imposed by habitual consumption of large quantities of these acidified carbonated drinks. Experts in clinical nutrition generally recommend that individuals obtain as much calcium as possible from a diverse, notrient-rich, and balanced diet. Foods that provide calcium usually contain other important nutrients, such as magnesium, manganese, copper, zinc, vitamin D, and vitamin K, that work synergistically with calcium. Moreover, intake of calcium levels above 800 mg (elemental calcium) per day is probably unnecessary for maintaining calcium metabolism in most individuals, provided that vitamin D status is adequate, except for pregnancy and lactation. 8

Calcium absorption is variable, both between different individuals and also with differing forms of calcium. Individuals of Asian and African heritage absorb calcium more efficiently than do Caucasians. 9 Different forms of calcium are absorbed at different rates. The pH of the stomach often influences how well certain calcium salts will be absorbed. The more water-soluble forms of calcium, such as citrate and citrate-malate, tend to have a greater absorption rate, especially in people who are deficient in hydrochloric acid, such as the elderly, or those taking gastric acid–suppressive medications. Furthermore, vitamin D intake and blood levels, as well as vitamin D receptor genotype, can significantly influence calcium bioavailability and absorption. 10 Bran and high-fiber cereals are high in phytates, which can reduce calcium absorption, although this is probably not clinically significant for most individuals over time at typical levels of consumption.

Historical/Ethnomedicine Precedent

Dark-green leafy vegetables, hard cheeses, sesame seeds, seaweed, and other components of traditional indigenous diets have long been emphasized for their contributions to health and longevity. Dairy consumption has been part of some cultural traditions for long periods, although controversy continues as to whether it is always in association with a genetic capacity to digest, assimilate, and metabolize dairy foods.

Possible Uses

Amenorrhea (bone loss prevention), anxiety, arthritis, blood clotting, blood pressure regulation, cardiovascular disease, celiac disease (related deficiency), colon cancer (risk reduction), colorectal cancer, depression, dysmenorrhea, gestational hypertension, gingivitis, hyperactivity, hypercholesterolemia, hypertension, hypertriglyceridemia, hypoparathyroidism, insomnia, insulin resistance syndrome, kidney stones (calcium oxalate stone prevention), migraine, multiple sclerosis, obesity, osteoporosis, periodontal disease, postpartum support, preeclampsia (related deficiency), pregnancy support, premenstrual syndrome, restless legs syndrome, rickets, stroke.

Related Therapeutic Applications

Calcium carbonate is used as an antacid. Calcium carbonate and calcium acetate can be used as phosphate binders in renal failure. Calcium chloride and calcium gluconate are used intravenously in treating severe hypocalcemia.

Deficiency Symptoms

Simple calcium deficiency is not a recognized clinical disorder, and standard laboratory tests, except bone scans during middle age, offer little useful data to evaluate calcium status for individuals with suboptimal or even moderately compromised intake, development, and peak bone mass. Long-term calcium deficiency contributes to growth deficiency in children; poor tooth development is also characteristic. A lack of calcium in adults may cause osteoporosis and osteomalacia and result in bone deformities, bone pain, and fractures. Other symptoms related to a deficiency are tetany or other muscle spasms. These usually occur in the legs. However, they may also occur in the blood vessels and may lead to hypertension. Other, typically more advanced, symptoms of calcium deficiency include nausea and vomiting, headaches, candidiasis, dry skin and nails, alopecia, neuromuscular irritability, muscular spasms and contracture, tetany, arrhythmias, convulsions, anxiety, depression, insomnia, and psychosis.

Calcium insufficiency, depletion, and deficiency can result from a wide range of factors and are usually gradual in onset and difficult to reverse once established. Decreased intake, inadequate weight-bearing exercise, blood loss (both internal and external), menorrhagia, lead toxicity, and malabsorption all can lead to calcium deficiency. Deficiencies in vitamin D and magnesium can contribute to calcium deficiency. A growing body of evidence indicates that vitamin D status is compromised in a large portion of the population, particularly adolescents and the elderly, because of inadequate intake and lack of exposure to sufficient sunlight. Magnesium deficiency results in decreased responsiveness of osteoclasts to PTH. Compromised calcium status during development will prevent the attainment of optimal peak bone mass. Once that opportune phase is passed, inadequate calcium intake may contribute to accelerated bone loss and ultimately the development of osteoporosis.

However, increased absorption of dietary calcium, rather than an increased intake or decreased excretion of calcium, appears to be the most influential factor in rapid acquisition of bone mineral during pubertal growth. Thus, the effects of dietary factors on calcium absorption efficiency are modulated by calcium status, genetic factors (e.g., specific vitamin D receptor gene polymorphisms), and height and body size. 10-14Furthermore, malabsorption conditions (e.g., Crohn's disease, celiac disease, surgical intestinal resection), prolonged bed rest, excessive menstrual blood loss, and a range of pathologies and medical interventions can also contribute to calcium depletion and potential deficiency.

Dietary Sources

  • Hard cheese, almonds, sesame seeds, filberts, and dark-green leafy vegetables are considered high in calcium, with greater than 200 mg/100 g food.
  • Milk, yogurt, sunflower seeds, Brazil nuts, broccoli, parsley, and watercress are considered medium in calcium, with greater than 100 mg/100 g food.

Average dietary intakes of calcium in the United States (U.S.) are well below the adequate intake (AI) recommendation for every age and gender group, especially in females and most significantly in children 9 to 17 years old. Furthermore, surveys consistently find that up to 85% of postmenopausal women do not consume adequate calcium every day, and on average consume about 500 mg less than the U.S. recommended dietary allowance (RDA). “Despite increasing public awareness and patient education about the importance of calcium [intake], this analysis shows the average daily calcium intake has not improved since the landmark Study of Osteoporotic Fractures (SOF),” conducted from 1986 to 1988, which found that postmenopausal women's average daily calcium intake was 714 mg daily. 15

The issue of calcium bioavailability from milk and dairy products remains a contentious issue, more often dominated by cultural habit and marketing than by nutritional science. In a systematic review of 58 clinical, longitudinal, retrospective, and cross-sectional studies on the relationship between milk, dairy products, or calcium intake and bone mineralization or fracture risk in children and young adults (1-25 years old), Lanou et al. 16 concluded: “Scant evidence supports nutrition guidelines focused specifically on increasing milk or other dairy product intake for promoting child and adolescent bone mineralization.” Furthermore, large segments of the populations may not have the genetic background for digestion and assimilation of cow's milk, or any milk, past infancy, with resulting food intolerances, lactase deficiency, and food allergies being increasingly recognized for their clinical import.

Consumption of cola-containing drinks, but not other carbonated beverages, appears to be associated with lower BMD in older women. 17

Nutrient Preparations Available

The issue of which form of supplemental calcium is “best” belies the broader issues of biochemical individuality in general and gastrointestinal function in particular. Organically bound calcium, such as aspartate, citrate, gluconate, or chelated forms, generally demonstrates higher bioavailability than inorganic calcium, such as carbonate, phosphate, or sulfate; such bioavailability is particularly significant in individuals with insufficient gastric acid or poor bowel constitution and in the elderly. Calcium carbonate is the least expensive and most well-known form of calcium, but it frequently causes constipation and bloating and may not be well absorbed by individuals with reduced levels of stomach acid. 18 When calcium carbonate is taken with orange or other citrus juice, a significant amount of calcium citrate is formed, and absorption appears to be enhanced, even in subjects with low gastric acidity. Calcium citrate and heated oyster shell–seaweed calcium may be better absorbed than calcium carbonate; other evidence indicates no significant difference in bioavailability. Studies have shown a normally functioning bowel can ionize calcium carbonate and the lumen can absorb it well; after it is absorbed, it can be converted to aspartate, then an orotate, so that it can be absorbed into the cells. 19-21

Calcium lactate and calcium gluconate are also more efficiently absorbed than calcium carbonate. Calcium citrate-appears to be better tolerated in the elderly and by those with sensitive digestive systems and may offer superior efficacy in preventing the progression of osteoporosis. Calcium citrate-malate (citramate) is absorbed better and tolerated more consistently than calcium carbonate. 22 Many physicians and other health care professionals experienced in nutritional therapy have increasingly turned to calcium citramate as their preferred form of calcium. Some evidence suggests efficacy of microcrystalline hydroxyapatite (MCHC) in cases where osteoporosis is the greatest concern. This form of calcium is purported to have a special affinity for bone formation, but some have asserted that it may not be absorbed well.

Dosage Forms Available

Capsule, chewable tablet, functional foods (e.g., orange juice fortified with calcium citrate), liposomal spray, liquid, powder, tablet; injection (prescription only).

Source Materials for Nutrient Preparations

Oyster shells (calcium carbonate), dolomite, bonemeal (calcium hydroxyapatite); calcium ascorbate, calcium aspartate, calcium citrate, calcium citrate-malate, calcium gluconate, calcium glycerophosphate, calcium lactate, calcium malate, dicalcium phosphate, and tricalcium phosphate are calcium salts of the corresponding organic acid, produced by titrating the acid with calcium hydroxide or other basic form. Soluble forms of calcium phosphate along with other minerals present in milk have been extracted from milk and are being used to fortify other foodstuffs.

Most calcium supplements (85%) currently sold in the U.S. are made from calcium carbonate, which contains the greatest percentage of elemental calcium on a weight basis, but is also the least water-soluble calcium salt.

  • Note:   Lead contamination has been observed in some forms of supplemental calcium, particularly dolomite, bonemeal, and oyster shell. 23-25The U.S. federal limit for lead content is 7.5 micrograms (µg) per 1000 milligrams (mg) elemental calcium. Good manufacturing practice has established an industry standard of keeping the amount of lead in calcium supplements to less than 0.5 µg/1000 mg elemental calcium. A product survey published in 2000 reported measurable lead in 8 of 21 supplements, in amounts averaging 1 to 2 µg/1000 mg elemental calcium. 26 Calcium inhibits intestinal absorption of lead, and adequate calcium intake is protective against lead toxicity. Consequently, calcium deficiency could potentially present a greater risk of lead intake due to general lead exposure than associated with trace amounts in calcium supplements.

Dosage Range

No multivitamin/multimineral capsule or tablet contains 100% of the recommended daily dose of calcium because it would be too bulky and too large to swallow. For example, 1 g calcium carbonate contains 400 mg elemental calcium and 1 g calcium citrate contains 211 mg elemental calcium. Furthermore, because calcium exhibits an absorption threshold, absorption is maximized by limiting each dose to 500 mg elemental calcium. 27 Thus, supplemental calcium intake is most efficacious when the daily intake is divided into two or more doses, preferably with meals (and away from most medications). Concomitant vitamin D will enhance calcium absorption.


Dietary: In the United Kingdom, the average daily diet provides 961 mg for men and 764 mg for women.

Supplemental/Maintenance: 500 to 2500 mg per day.

  • For individuals age 19 to 50: 1000 mg/day (including diet)
  • For adults age 51 and older:
    • Women: 1500 mg/day (including diet)
    • Men: 1200 mg/day (including diet)
  • Pregnant and breastfeeding females under 19 years: 1300 mg/day (including diet)
  • Pregnant and breastfeeding females age 19 and older: 1000 mg/day (including diet)
  • Note:   These recommendations do not incorporate research demonstrating that doses above 800 mg/day may be unnecessary with adequate vitamin D levels.

Pharmacological/Therapeutic: Calcium intake as high as 3000 mg/day, together with 10 to 50 µg/day vitamin D3(cholecalciferol), may be appropriate if plasma calcium and phosphate levels are stable and within normal range (e.g., in treatment of secondary hyperparathyroidism in uremia). 28

Calcium deficits associated with vitamin D deficiency may warrant daily doses up to 6000 mg of calcium acetate or calcium carbonate.

Toxic: Total calcium intake, from combined dietary and supplemental sources, should not exceed 2500 mg/day for long-term use. Large, acute doses normally exhibit no toxic effects. The tolerable upper intake level (UL) established by the U.S. Food and Nutrition Board (FNB), Institute of Medicine, for vitamin C in adults (≥19 years) is 2500 mg/day.

Pediatric (<18 years)


  • Infants, birth to 6 months: 210 mg/day; breast-feeding optimal
  • Infants, 7 months to 1 year: 270 mg/day
  • Children, 1 to 3 years: 500 mg/day
  • Children, 4 to 8 years: 800 mg/day

Supplemental/Maintenance: A daily intake of 1300 mg total calcium (diet plus supplements) is generally considered necessary to promote the attainment of maximal peak bone mass in children and adolescents.

Pharmacological/Therapeutic: 500 to 2500 mg/day.

Toxic: UL for calcium:

  • Infants, 0 to 12 months: Not established; dietary source only recommended
  • Children, 1 to 13 years: 2500 mg
  • Adolescents, 14 to 18 years: 2500 mg

Laboratoary Values

Serum Calcium

Normal levels: 2.2 to 2.6 mmol/L (8.4-10.2 mg/dL).

Serum calcium levels are maintained within tight parameters under most circumstances and do not provide accurate or sensitive markers for calcium status. Low blood calcium level usually implies abnormal parathyroid function and/or vitamin D deficiency, or low serum albumin. Elevated blood calcium levels are more likely to occur in response to higher absorption during calcium deficiency than with true excess. More often, elevated blood calcium occurs from hyperparathyroid states, vitamin D excess (usually in lymphoma, or sarcoid, or other granulomatous diseases where pathological tissues convert 25-OH vitamin D to calcitriol autonomously), or hypercalcemia of malignancy, which is usually caused by tumor-produced hormones that have PTH-like activity. Milk-alkali syndrome, as discussed later, is of historical interest only as a cause of hypercalcemia.

Ionized (Unbound) Serum Calcium

Normal levels: 1.17 to 1.29 mmol/L.

Low levels may indicate negative calcium balance.

Urinary Calcium

Normal levels:

  • Women: Approximately 150 to 250 mg/day
  • Men: Approximately 200 to 300 mg/day

safety profile


Calcium is generally considered safe at usual doses. Even in large doses, calcium absorption is limited, blood and tissue levels are tightly regulated, it is efficiently excreted, and toxicity rarely results. Some forms of calcium, notably calcium carbonate, may cause abdominal bloating, flatulence, and constipation in some individuals. Interference with absorption of other nutrients, particularly magnesium, iron, and zinc, as well as some medications, is the primary adverse effect associated with large doses of calcium. However, concern has been raised in recent years about excessively high levels of lead in some forms of calcium, particularly those derived from bonemeal, dolomite, and oyster shell.

Nutrient Adverse Effects

General Adverse Effects

Hypercalcemia has been reported in association with calcium supplements and antacids but has never been attributed to dietary (i.e., food) sources of calcium. Ingestion of extremely large amounts of calcium (5000 mg/day, or >2000 mg/day over long period) can produce a toxic response. However, excess calcium levels are more likely to result from pathological processes such as hyperparathyroidism, certain types of cancer, kidney failure, breakdown of bone, or excessive levels of vitamin D.

Mild hypercalcemia is usually asymptomatic, but higher levels (>12 mg/dL) often result in symptoms that include loss of appetite, nausea, vomiting, constipation, abdominal pain, dry mouth, thirst, and frequent urination. More severe hypercalcemia may result in renal toxicity, cardiac arrhythmias, confusion, delirium, coma, and if not treated, death.

Milk-alkali syndrome, resulting from concomitant consumption of large quantities of milk, calcium carbonate (antacid), and sodium bicarbonate (absorbable alkali), represents the most well-known form of hypercalcemia. This obsolete treatment for peptic ulcers often involved calcium supplement levels from 1.5 to 16.5 g/day for 2 days to 30 years.

Increased excretion of calcium by the kidneys (hypercalciuria) constitutes a more significant risk factor for nephrolithiasis than does high calcium intake per se. In fact, most evidence indicates that enriched dietary calcium is associated with a decreased risk of oxalate kidney stones (which represent 80% of renal stones), presumably due to binding of dietary oxalate in the gut, thus decreasing its absorption. However, one large prospective study found that women taking supplemental calcium (of unspecified form) had a 20% higher risk of developing kidney stones than those who did not. These researchers also observed that women consuming low-calcium diets were at greater risk for stones than those with higher calcium intakes, perhaps, as they speculated, because of reciprocal hyperoxaluria. 29 Nevertheless, a diet low in animal protein and sodium, but with normal calcium levels, is more effective in preventing recurrence of calcium oxalate kidney stones than a diet low in calcium. 30 The form of calcium may be the differentiating factor deserving further investigations. Some clinicians have reported that calcium citrate can be beneficial in preventing or reversing kidney stones and bone spurs, and that calcium carbonate is more frequently associated with pathological calcification processes. As noted, higher levels of calcium from food may complex with dietary oxalates in the intestines and reduce their absorption; likewise, taking calcium supplements separate from food will significantly reduce their beneficial effect of decreasing intestinal oxalate absorption.

Adverse Effects Among Specific Populations

Risks from calcium supplementation are significantly greater in individuals with hyperparathyroidism, certain types of cancer, kidney failure, or other conditions that interfere with normal calcium regulation.

Pregnancy and Nursing

Evidence of adverse effects in pregnancy resulting from calcium supplementation is lacking. Calcium supplementation is generally advised during pregnancy and lactation and can reduce risk of preeclampsia.

Infants and Children

Some sources have suggested that calcium supplements should be used under medical supervision in young children because of a risk of bowel perforation. Nondairy foods rich in calcium are preferred, with human breast milk being the superior food source for infants. Liquid forms are available when supplementation is appropriate. Children may also do well with some chewable forms, although some products contain sugar, which is not recommended.


Calcium supplementation is contraindicated in some individuals with hyperparathyroidism, chronic renal impairment or kidney disease, sarcoidosis or other granulomatous diseases, cancer patients with a history of hypercalcemia, or patients with a history of idiopathic calcium stones (except the common calcium oxalate stones, in which calcium supplementation with meals may reduce the risk of stone formation by binding dietary oxalate).

Precautions and Warnings

Caution is generally appropriate in conditions associated with hypercalcuria and hypercalcemia. Soft tissue calcification may occur with hyperparathyroidism, hyperphosphatemia, magnesium deficiency, or vitamin D overdoses. Calcium supplements should be used with caution and with medical supervision in hypertensive individuals because blood pressure control may be altered. As previously suggested, judicious selection of the form of calcium used may reduce or even reverse the risk factors involved with supplementation in individuals with these conditions.

High calcium intake, primarily from milk and dairy products, may increase prostate cancer risk by lowering concentrations of 1,25-dihydroxyvitamin D3[1,25(OH)2D3], a hormone thought to protect against prostate cancer. The epidemiological evidence, however, is mixed. Other evidence indicates that calcium supplementation is not associated with increased risk of prostate cancer. 31-36Nevertheless, calcium supplementation is sometimes considered as contraindicated in men diagnosed with prostate cancer. If calcium were found to have such an adverse effect, concomitant supplementation with vitamin D might provide a safe, simple, and effective counterpoint.

interactions review

Strategic Considerations

The many interactions involving calcium reveal several consistent patterns. Nevertheless, most of the available clinical research has inadequate specificity, depth, complexity, and duration and cannot capture many of the nuances that will enable clinicians to navigate their diverse implications. Calcium and many medications can interfere with each other in ways that are easily avoided or that require tactical choices within a strategic approach. On occasion, the adverse effects on calcium-rich tissue can be swift and permanent (e.g., tetracycline, sometimes corticosteroids). More often, medications interfere with calcium function or cause steady depletion that will increase risks of adverse effects over time. Notably, physicians prescribing such agents over extended periods (e.g., anticonvulsants, opioids and oral glucocorticoids) usually do not advise or prescribe adequate countermeasures, whether calcium and vitamin D, bisphosphonates, or the combination, to address effectively the common occurrence of drug-induced decreases in BMD and increased risk of fracture. 37,38Conversely, the risk of hypercalcemia/hypercalciuria from calcium intake through supplements or dietary sources is improbable outside of metabolic pathologies influencing the calcium and vitamin D regulatory systems. Overall, calcium tends to follow the patterns of other dense aspects of nature and physiology, which come on gradually, move slowly, and can be difficult to reverse once established.

Calcium and many medications complex or otherwise bind to each other, thus reducing absorption of both agents. During short courses of treatment, this interaction may reduce drug absorption and activity to a clinically significant degree. In contrast, any short-term interference with calcium assimilation will not interfere with the intended therapeutic action in a strategically important degree, given that most uses of calcium are long term, preventive, or cumulative. In most situations, simple temporal separation of intake is adequate to avoid such interference; when not sufficient, however, the calcium may need to be temporarily discontinued, usually with minimal or no impact on therapeutic intentions. Importantly, calcium-fortified foods, such as orange juice, are often not thought of as “calcium supplements” and can significantly interfere with absorption of pharmaceutical medications that bind to calcium, when taken with such beverages.

Significant and often severe limitations in the ability to reach conclusions about interactions involving “calcium” occur because of the various calcium salts potentially involved. Too often, an easy but potentially misleading tendency is to generalize from research that often is not clear, especially in secondary sources and derivative literature, and particularly in abstract form. An even greater interpretive error is to extrapolate from findings involving parenteral calcium to the use of oral calcium supplements; the two situations are physiologically vastly different, and almost never comparable. Calcium carbonate and calcium phosphate are best taken with meals to optimize absorption. 21 Other calcium salts can be taken without regard to food intake or meals; this may make them preferable for hypochlorhydric individuals and patients prescribed H2antagonists or other medications that reduce gastric acidity, particularly proton pump inhibitors (PPIs).

The literature is further complicated by the presence of research and case reports involving calcium salts as antacids, particularly when observations regarding such substances are extrapolated to calcium supplements. Except for differences in the substances themselves, gastric acidity, achlorhydria, and acid suppression are all complicating issues of significant import. Likewise, some studies and many commentators fail to distinguish between calcium intake from calcium supplements and that from dietary intake of milk and dairy products.

Multiple variables (e.g., individual biochemical variability, gender, life stage, diet, vitamin D status) that influence how “calcium” will be absorbed and function in any given individual need to be further evaluated before considering the medications and conditions being treated.

The inadequacies of standard knowledge and clinical practice regarding the prevalence and assessment of vitamin D deficiency emerging in recent years will increasingly reveal deep implications for calcium balance, bone health, and much more. Many agents that deplete calcium or otherwise interfere with its metabolism do so indirectly through their adverse effects on vitamin D status. Although direct effects on calcium may also be present, the effects on vitamin D can significantly impair calcium absorption and activity. Conversely, elevated levels of vitamin D can cause an increased absorption of calcium.

Pervasive vitamin D deficiency status and underutilization of laboratory assessment for 25-hydroxyvitamin D [25(OH)D] levels influence and limit research design, interpretation, and clinical practice within conventional medicine. For example, in 2005, two randomized controlled trials of calcium carbonate and cholecalciferol (vitamin D3) reported that administration for prevention of fractures in primary care produced widely publicized conclusions declaring that such nutrient supplementation provided no value in preventing fractures. 39,40Such assertions were made despite disclosures that (1) vitamin D levels had been tested in only a small sample of the subjects in one of the studies; (2) vitamin D deficiency appeared to be common within the subject populations, as indicated by responses to vitamin D supplementation; (3) quality control of the supplements was very poor; (4) compliance was marginal and declined over time (e.g., 63%, or as low as 45%); and (5) the use of calcium carbonate in a population of older and often hypochlorhydric subjects would be considered suboptimal by many, if not most, experienced practitioners of nutritional therapeutics. Digestion of calcium carbonate relies on the integrity of gastric function and the bowel culture to produce the ionizing acids. Thus, gastrointestinal adverse effects, typical of calcium carbonate, were cited as a major factor in greater noncompliance with calcium intake.

In the study in which 1% of the subjects had their vitamin D levels actually measured, there was only a marginal increase after 1 year of supplementation with 800 IU of vitamin D per day (although when analyzed, some of the supplements contained as little as 372 IU, mean value, per tablet). Average 25(OH)D levels at beginning of the study (15 ng/mL) were in the range of severe deficiency, and after 1 year improved only to 24 ng/mL, still well below what many vitamin D researchers consider to be adequate levels (30-40 ng/mL). 41 Subsequently, in a trial involving 944 healthy Icelandic adults, Steingrimsdottir et al. 8 found that with 25(OH)D levels below 10 ng/mL, maintaining calcium intake above 800 mg/day appeared to normalize calcium metabolism, as determined by the PTH level, but in individuals with higher 25(OH)D levels, no benefit was observed from calcium intake above 800 mg/day. Clearly, further research on calcium and other minerals involved in bone metabolism need to take into account, and preferably optimize, vitamin D status.

Notably, in conventional practice, the main pharmacological intervention for the prevention of bone loss is antiresorptive drugs, such as bisphosphonates, for which almost every clinical trial has included coadministration of calcium or vitamin D. Moreover, the decontextualization and narrow focus of these studies highlight the shortcomings of standard research methodology and clinical practice to consider the broad factors of aging, lifestyle, activity level, drug depletions, and poor nutritional status characteristic of the populations in question, as well as the complex nature of bone health and its reliance on interdependencies of multiple nutrients and tissues, rather than using such a narrow focus on supplemental calcium and vitamin D. As public and practitioner attention on vitamin D grows, it may prove a pivotal issue in expanding perceptions and awareness, analysis, and intervention through a broad integrative model more accurately reflecting patient needs, with a scientific understanding of the breadth and complexity of the processes involved.

Ultimately, perhaps the most limiting aspects of the research findings generally available involve the questions asked, the assessment methods used, and the time frames considered. As noted in many sections, the markers of blood calcium levels and other short-term indices do not adequately address the issue of calcium depletion over time; the feedback systems of calcium homeostasis involve vitamin D synthesis and activation, calcium absorption, tubular reabsorption and urinary excretion, PTH production and secretion, and bone formation, catabolism, and resorption. Thus, as a drug interferes with calcium absorption and metabolism and induces a depletion pattern anywhere along the way, superficial parameters may remain within normal parameters, but the long-term state of bone density may be in steady decline. For this reason, it is often clinically useful to assess markers of bone breakdown, such as urinary pyridinium cross-links (pyridinium and deoxypyridinium), as a baseline, when starting a pharmaceutical intervention with the potential to impact calcium balance negatively. An increase in urinary markers of bone breakdown signifies the development of negative calcium balance, despite all other markers related to calcium appearing normal, because of intrinsic calcium homeostatic mechanisms. This can serve as an early warning sign and allow for nutritional interventions to correct negative calcium balance without waiting to find a decrease in bone density on a subsequent bone density scan.

See also Vitamin D in Nutrient-Nutrient Interactions.

nutrient-drug interactions
Aminoglycoside Antibiotics, Including Gentamicin and Neomycin
Amphotericin B
Antacids Containing Aluminum and Magnesium
Anticonvulsant Medications
Atenolol and Related Beta-1-Adrenoceptor Antagonists (Beta-1-Adrenergic Blocking Agents)
Bile Acid Sequestrants
Calcium Acetate
Cholestyramine, Colestipol, and Related Bile Acid Sequestrants
Corticosteroids, Oral, Including Prednisone
Oral Contraceptives: Monophasic, Biphasic, and Triphasic Estrogen Preparations (Synthetic Estrogen and Progesterone Analogs)
Hormone Replacement Therapy (HRT): Estrogen-Containing and Synthetic Estrogen and Progesterone Analog Medications
Fluoroquinolone (4-Quinolone) Antibiotics
Cimetidine and Related Histamine (H 2 ) Receptor Antagonists
Omeprazole and Related Proton Pump Inhibitors
Heparin, Unfractionated
Levothyroxine and Related Thyroid Hormones
Metformin and Related Biguanides
Sulfamethoxazole and Related Sulfonamide Antibiotics
Tetracycline Antibiotics
Thiazide Diuretics
Verapamil and Related Calcium Channel Blockers
unproven, speculative, and overstated interactions claims
Albuterol/Salbutamol and Related Beta-2-Adrenoceptor Agonists
Caffeine (and Coffee)
Diclofenac and Related Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)
Digoxin and Related Cardiac Glycosides
Erythromycin and Related Macrolide Antibiotics
Hydroxychloroquine and Chloroquine
Laxatives, Stimulant
Loop Diuretics
Mineral Oil
Potassium-Sparing Diuretics
Retinoic Acid and Related Retinoids
Sodium Fluoride
nutrient-nutrient interactions
Caffeine and Coffee
Essential Fatty Acids
Milk and Dairy Products
Vitamin D
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