Calcium

Calcium is the most common mineral in the human body. About 99% of the calcium in the body
is found in bones and teeth, while the other 1% is found in the blood and soft tissue. Calcium
levels in the blood and fluid surrounding the cells (extracellular fluid) must be maintained within
a very narrow concentration range for normal physiological functioning. The physiological
functions of calcium are so vital to survival that the body will demineralize bone to maintain
normal blood calcium levels when calcium intake is inadequate. Thus, adequate dietary calcium
is a critical factor in maintaining a healthy skeleton (1).

Function

Structure: Calcium is a major structural element in bones and teeth. The mineral component of
bone consists mainly of hydroxyapatite [Ca10(PO4)6(OH)2] crystals, which contain large amounts
of calcium and phosphate (2). Bone is a dynamic tissue that is remodeled throughout life. Bone
cells called osteoclasts begin the process of remodeling by dissolving or resorbing bone. Bone-
forming cells called osteoblasts then synthesize new bone to replace the bone that was resorbed.
During normal growth, bone formation exceeds bone resorption. Osteoporosis may result when
bone resorption chronically exceeds formation (1).

Cell signaling: Calcium plays a role in mediating the constriction and relaxation of blood vessels
(vasoconstriction and vasodilation), nerve impulse transmission, muscle contraction, and the
secretion of hormones like insulin (3). Excitable cells, such as skeletal muscle and nerve cells,
contain voltage-dependent calcium channels in their cell membranes that allow for rapid changes
in calcium concentrations. For example, when a muscle fiber receives a nerve impulse that
stimulates it to contract, calcium channels in the cell membrane open to allow a few calcium ions
into the muscle cell. These calcium ions bind to activator proteins within the cell, which release a
flood of calcium ions from storage vesicles inside the cell. The binding of calcium to the protein,
troponin-c, initiates a series of steps that lead to muscle contraction. The binding of calcium to
the protein, calmodulin, activates enzymes that breakdown muscle glycogen to provide energy
for muscle contraction (1).

Cofactor for enzymes and proteins: Calcium is necessary to stabilize a number of proteins and
enzymes, optimizing their activities. The binding of calcium ions is required for the activation of
the seven "vitamin K-dependent" clotting factors in the coagulation cascade (see vitamin K). The
term, "coagulation cascade," refers to a series of events, each dependent on the other that stops
bleeding through clot formation (4).
Regulation of calcium levels: Calcium concentrations in the blood and fluid that surrounds cells
are tightly controlled in order to preserve normal physiological function (diagram). When blood
calcium decreases (e.g., in the case of inadequate calcium intake), calcium-sensing proteins in
the parathyroid glands send signals that result in the secretion of parathyroid hormone (PTH) (5).
PTH stimulates the conversion of vitamin D to its active form, calcitriol, in the kidneys.
Calcitriol increases the absorption of calcium from the small intestine. Together with PTH,
calcitriol stimulates the release of calcium from bone by activating osteoclasts (bone resorbing
cells) and decreases the urinary excretion of calcium by increasing its reabsorption in the
kidneys. When blood calcium rises to normal levels, the parathyroid glands stop secreting PTH
and the kidneys begin to excrete any excess calcium in the urine. Although this complex system
allows for rapid and tight control of blood calcium levels, it does so at the expense of the
skeleton (1).

Deficiency

A low blood calcium level usually implies abnormal parathyroid function and is rarely due to
low dietary calcium intake since the skeleton provides a large reserve of calcium for maintaining
normal blood levels. Other causes of abnormally low blood calcium levels include chronic
kidney failure, vitamin D deficiency, and low blood magnesium levels that occur mainly in cases
of severe alcoholism. Magnesium deficiency results in a decrease in the responsiveness of
osteoclasts to PTH. A chronically low calcium intake in growing individuals may prevent the
attainment of optimal peak bone mass. Once peak bone mass is achieved, inadequate calcium
intake may contribute to accelerated bone loss and ultimately to the development of
osteoporosisDisease.

Food sources

Average dietary intakes of calcium in the U.S. are well below the RDA for every age and gender
group, especially in females. Only about 25% of boys and 10% of girls ages 9 to 17 are estimated
to meet the recommendations. Dairy foods provide 75% of the calcium in the American diet.
However, it is typically during the most critical period for peak bone mass development that
adolescents tend to replace milk with soft drinks (1, 3). Dairy products represent rich and
absorbable sources of calcium, but certain vegetables and grains also provide calcium. However,
the bioavailability of the calcium must be taken into consideration. While the calcium rich plants
in the kale family (broccoli, bok choy, cabbage, mustard, and turnip greens) contain calcium that
is as bioavailable as that in milk, some food components have been found to inhibit the
absorption of calcium.
Oxalic acid, also known as oxalate, is the most potent inhibitor of calcium absorption and is
found at high concentrations in spinach and rhubarb and somewhat lower concentrations in sweet
potatoes and dried beans. Phytic acid is a less potent inhibitor of calcium absorption than oxalate.
Yeast possess an enzyme (phytase) which breaks down phytic acid in grains during fermentation,
lowering the phytic acid content of breads and other fermented foods. Only concentrated sources
of phytate, such as wheat bran or dried beans, substantially reduce calcium absorption (1). The
table below lists a number of calcium rich foods, along with their calcium content and the
number of servings of that food required to equal the absorbable calcium from one glass of milk
(49). For more information on the nutrient content of foods, search the USDA food composition
database.

Nutrient interactions

Sodium

High sodium intake results in increased loss of calcium in the urine, possibly due to competition
between sodium and calcium for reabsorption in the kidney or by an effect of sodium on
parathyroid hormone (PTH) secretion. Each 2.3-gram increment of sodium (6 grams of salt;
NaCl salt) excreted by the kidney has been found to draw about 24-40 milligrams (mg) of
calcium into the urine. Because urinary losses account for about half of the difference in calcium
retention among individuals, dietary sodium has a large potential to influence bone loss. In adult
women, each extra gram of sodium consumed per day is projected to produce an additional rate
of bone loss of 1% per year if all of the calcium loss comes from the skeleton. Although animal
studies have shown bone loss to be greater with high salt intakes, no controlled clinical trials
have been conducted to confirm the relationship between salt intake and bone loss in humans (1,
6). However, a 2-year study of postmenopausal women found increased urinary sodium
excretion (an indicator of increased sodium intake) to be associated with decreased bone mineral
density (BMD) at the hip (7). Additionally, a longitudinal study in 40 postmenopausal women
found that adherence to a low sodium diet (2 grams/day) for six months was associated with
significant reductions in sodium excretion, calcium excretion, and aminoterminal propeptide of
type I collagen, a biomarker of bone resorption. However, these associations were only observed
in women with baseline urinary sodium excretions equal to or greater than 3.4 grams/day (i.e.,
the mean sodium intake for the U.S. adult population) (8). Racial differences on the effect of
dietary sodium on urinary sodium and calcium excretion and retention have been reported in
adolescent girls. White girls excreted the extra sodium on a high salt diet, but black girls went
into positive sodium balance, which resulted in reduced urinary calcium loss compared to white
girls (9).
Vitamin D

Vitamin D is required for optimal calcium absorption (See Function or Vitamin D). Several other
nutrients (and non-nutrients) influence the retention of calcium by the body and may affect
calcium nutritional status.

Protein

As dietary protein intake increases, the urinary excretion of calcium also increases.
Recommended calcium intakes for the U.S. population are higher than those for populations of
less industrialized nations because protein intake in the U.S. is generally higher. The RDA for
protein is 46 grams/day for adult women and 56 grams/day for adult men; however, the average
intake of protein in the U.S. tends to be higher (65-70 grams/day in adult women and 90-110
grams per day in adult men) (3). Recently, the overall calcium economy has not been
demonstrated to be affected by dietary protein in part due to offsetting changes in calcium
absorption (10). Inadequate protein intakes have been associated with poor recovery from
osteoporotic fractures and serum albumin values (an indicator of protein nutritional status) have
been found to be inversely related to hip fracture risk (3).

Phosphorus

Phosphorus, which is typically found in protein-rich foods, tends to decrease the excretion of
calcium in the urine. However, phosphorus-rich foods also tend to increase the calcium content
of digestive secretions, resulting in increased calcium loss in the feces. Thus, phosphorus does
not offset the net loss of calcium associated with increased protein intake (1). Increasing intakes
of phosphates from soft drinks and food additives have caused concern among some researchers
regarding the implications for bone health. Diets high in phosphorus and low in calcium have
been found to increase parathyroid hormone (PTH) secretion, as have diets low in calcium (3, 6).
While the effect of high phosphorus intakes on calcium balance and bone health is presently
unclear, the substitution of large quantities of soft drinks for milk or other sources of dietary
calcium is cause for concern with respect to bone health in adolescents and adults.

Caffeine

Caffeine in large amounts increases urinary calcium content for a short time. However, caffeine
intakes of 400 mg/day did not significantly change urinary calcium excretion over 24 hours in
premenopausal women when compared to a placebo (11). Although one observational study
found accelerated bone loss in postmenopausal women who consumed less than 744 mg of
calcium/day and reported that they drank 2-3 cups of coffee/day (12), a more recent study that
measured caffeine intake found no association between caffeine intake and bone loss in
postmenopausal women (13). On average, one 8-ounce cup of coffee decreases calcium retention
by only 2-3 mg (1).

The Recommended Dietary Allowance (RDA)

Updated recommendations for calcium intake based on the optimization of bone health were
released by the Food and Nutrition Board (FNB) of the Institute of Medicine in 2010. The
Recommended Dietary Allowance (RDA) for calcium is listed in the table below by life stage
and gender.

Recommended Dietary Allowance (RDA) for Calcium

Males Females
Life Stage Age
(mg/day) (mg/day)
Infants 0-6 months 200 (AI) 200 (AI)
Infants 6-12 months 260 (AI) 260 (AI)
Children 1-3 years 700 700
Children 4-8 years 1,000 1,000
Children 9-13 years 1,300 1,300
Adolescents 14-18 years 1,300 1,300
Adults 19-50 years 1,000 1,000
Adults 51-70 years 1,000 1,200
Adults 71 years and older 1,200 1,200
Pregnancy 14-18 years - 1,300
Pregnancy 19-50 years - 1,000
Breast-feeding 14-18 years - 1,300
Breast-feeding 19-50 years - 1,000

Disease Prevention

Colorectal Cancer

Colorectal cancer is the most common gastrointestinal cancer and the second leading cause of
cancer deaths in the U.S. Colorectal cancer is caused by a combination of genetic and
environmental factors, but the degree to which these two types of factors influence the risk of
colon cancer in individuals varies widely. In individuals with familial adenomatous polyposis,
the cause of colon cancer is thought to be almost entirely genetic, while dietary factors appear to
influence the risk for other types of colon cancer. Animal studies are strongly supportive of a
protective role for calcium in preventing intestinal cancers (14). In humans, controlled clinical
trials have found modest decreases in the recurrence of colorectal adenomas (precancerous
polyps) with calcium supplementation of 1,200-2,000 mg/day (15, 16), and a recent study found
that the protective effect extended up to five years after the intervention ended (17). A pooled
analysis of ten prospective cohort studies, including 534,536 men and women, found that those
in the highest quintile of calcium intake (from food) had a 14% lower risk of colorectal cancer
compared to those in the lowest quintile; dietary intakes of calcium ranged from 674 to 1,051
mg/day in the ten cohorts (18). In this pooled analysis, subjects in the highest quintile of total
calcium intake (from food and supplements) had a 22% lower risk of colorectal cancer. Total
daily intake of calcium ranged from 732 to 1,087 mg in the examined studies. However, most
large prospective studies, individually, have reported increased calcium intakes are only weakly
associated with a decreased risk of colorectal cancer. These weak associations might be
explained by the presence of groups within the population that differ in their response to calcium.
For instance, there is some evidence that individuals with increased circulating levels of insulin-
like growth factor-1 (IGF-1) are at increased risk of colorectal cancer, and increased calcium
intake may benefit this subgroup more than others. A case-control study of 511 men found that
increased calcium intake was more strongly associated with decreased colorectal cancer risk in
men with higher circulating levels of IGF-1 (19). Before conclusions can be drawn, more
research is needed to clarify whether specific subgroups in the larger population have different
calcium requirements with respect to decreasing the risk of colorectal cancer.

Osteoporosis

Osteoporosis is a skeletal disorder in which bone strength is compromised, resulting in an

increased risk of fracture. Sustaining a hip fracture is one of the most serious consequences of
osteoporosis. Nearly one third of those who sustain osteoporotic hip fractures enter nursing
homes within the year following the fracture, and one person in five dies within one year of
experiencing an osteoporotic hip fracture. Although osteoporosis is most commonly diagnosed in
white postmenopausal women, women of other racial groups and ages, men, and children may
also develop osteoporosis (20).

Osteoporosis is a multifactorial disorder, and nutrition is only one factor contributing to its
development and progression (2). Other factors that increase the risk of developing osteoporosis
include, but are not limited to, increased age, female gender, estrogen deficiency, smoking,
metabolic disease (e.g., hyperthyroidism), and the use of certain medications (e.g.,
corticosteroids and anticonvulsants). A predisposition to osteoporotic fracture is related to one's
peak bone mass and to the rate of bone loss after peak bone mass has been attained. After adult
height has been reached, the skeleton continues to accumulate bone until the third decade of life.
Genetic factors exert a strong influence on peak bone mass, but lifestyle factors can also play a
significant role. Strategies for reducing the risk of osteoporotic fracture include the attainment of
maximal peak bone mass and the reduction of bone loss later in life. Although calcium is the
nutrient consistently found to be most important for attaining peak bone mass and preventing
osteoporosis, adequate vitamin D intake is also required for optimal calcium absorption (20).

Physical exercise is another lifestyle factor of benefit in the prevention of osteoporosis and
osteoporotic fracture. There is evidence to suggest that physical activity early in life contributes
to the attainment of higher peak bone mass. Exercise in the presence of adequate calcium and
vitamin D intake probably has a modest effect on slowing the rate of bone loss later in life. One
compilation of published calcium trials indicated that the beneficial skeletal effect of increased
physical activity was achievable only at calcium intakes above 1,000 mg/day (21). High impact
exercise and resistance exercise (weights) are likely the most beneficial for preventing bone loss.
Lower impact exercise like walking, swimming, and cycling have beneficial effects on other
aspects of health and function, but their effects on bone loss are minimal. However, exercise later
in life, even beyond 90 years of age, can still increase strength and reduce the likelihood of a fall,
another important risk factor for hip fracture (20). Supplemental calcium alone cannot usually
restore lost bone in individuals with osteoporosis. However, optimal treatment of osteoporosis
with any drug therapy also requires adequate intake of calcium (1,200 mg/day) and vitamin D
(600 IU/day) (2, 20). For more information about osteoporosis, visit the National Osteoporosis
Foundation Web site.

Kidney stones

Approximately 12% of the U.S. population will have a kidney stone at some time. Most kidney
stones are composed of calcium oxalate or calcium phosphate. Although their cause is usually
unknown, abnormally elevated urinary calcium (hypercalciuria) increases the risk of developing
calcium stones. Increasing dietary calcium increases urinary calcium slightly, and the rise is
more pronounced in those with hypercalciuria. However, other dietary factors such as sodium
and protein are also known to increase urinary calcium (22, 23). A large prospective study that
followed men over a period of 12 years found the incidence of symptomatic kidney stones to be
44% lower in men in the highest quintile (1/5) of calcium intake, averaging 1,326 mg/day,
compared with men in the lowest quintile of calcium intake, averaging 516 mg/day (24). Similar
results were observed in a large prospective study of women followed over 12 years (25). A 14-
year follow-up analysis of the study in men reported that calcium intake was related to a lower
risk of kidney stones in those less than 60 years of age but not in men older than 60 years (26).
Additionally, a prospective study in a cohort of 96,245 younger women, aged 27 to 44 years,
found that higher dietary calcium intakes were associated with a lower risk of kidney stones (27).
The authors of these two studies suggest that increased dietary calcium might inhibit the
absorption of dietary oxalate and reduce urinary oxalate, a risk factor for calcium oxalate stones.
Support for this idea comes from a study in which people ingested oxalate with or without
supplemental calcium (28). Providing 200 mg of elemental calcium along with oxalate
significantly reduced both oxalate absorption and excretion.

Although calcium stone formers have been advised to restrict calcium intake in the past, a cross-
sectional study of 282 patients with calcium oxalate stones found that dietary salt, as measured
by urinary sodium excretion, was the dietary factor most strongly associated with urinary
calcium excretion (29). A study of 85 calcium stone- forming patients found that those with low
bone mineral density were significantly more likely to have a high salt intake and high urinary
sodium excretion, leading the authors to suggest that reduced salt intake should be recommended
for calcium stone-forming patients (30). Findings that calcium stone-forming patients with lower
calcium intakes are more likely to have decreased bone mineral density also call into question
the therapeutic use of dietary calcium restriction. At present, the only dietary change proven
effective in reducing kidney stone recurrence is increasing fluid intake. However, a recent
randomized, double-blind, placebo-controlled trial in 36,282 postmenopausal women reported
that a combination of supplemental calcium (1,000 mg/day) and vitamin D (400 IU/day) was
associated with a significantly increased risk for kidney stones. More controlled trials are
necessary to determine whether supplemental calcium affects the development of kidney stones
(31).
Pregnancy-induced hypertension (preeclampsia)

Pregnancy-induced hypertension (PIH) occurs in 10% of pregnancies and is a major health risk
for pregnant women and their offspring. PIH is a term that includes gestational hypertension,
preeclampsia, and eclampsia. Gestational hypertension is defined as an abnormally high blood
pressure that usually develops after the 20th week of pregnancy. In addition to gestational
hypertension, preeclampsia includes the development of edema (severe swelling) and proteinuria
(protein in the urine). Preeclampsia may progress to eclampsia (also called toxemia) in which
life-threatening convulsions and coma may occur (32). Although the cause of PIH is not entirely
understood, calcium metabolism appears to play a role. Risk factors for PIH include first
pregnancies, multiple gestations (e.g., twins or triplets), chronic high blood pressure, diabetes,
and some autoimmune diseases. Data from epidemiological studies suggest an inverse
relationship between calcium intake and the incidence of PIH, but the results of experimental
research on calcium supplementation and PIH have been less clear. A systematic review of
randomized placebo-controlled studies found that calcium supplementation reduced the
incidence of high blood pressure in pregnant women at high risk of PIH, as well as in pregnant
women with low dietary calcium intake. However, in women at low risk of PIH and with
adequate calcium intake the benefit of calcium supplementation was judged small and unlikely to
be clinically significant (33). A large multi-center clinical trial of Calcium for Preeclampsia
Prevention (CPEP) in over 4,500 pregnant women found no effect of 2,000 mg of supplemental
calcium on PIH. However, women in the placebo group had a mean intake of 980 mg/day, while
those in the supplemental group had a mean intake of 2,300 mg/day (34). For the general
population, meeting current recommendations for calcium intake during pregnancy may help
prevent PIH. Further research is required to determine whether women at high risk for PIH
would benefit from calcium supplementation above the current recommendations.

Lead toxicity

Children who are chronically exposed to lead, even in small amounts, are more likely to develop
learning disabilities, behavioral problems, and to have low IQ's. Abnormal growth and
neurological development may occur in the infants of women exposed to lead during pregnancy.
In adults, lead toxicity may result in kidney damage and high blood pressure. Although the use of
lead paint and leaded gasoline has been discontinued in the U.S., lead toxicity continues to be a
significant health problem, especially in children living in urban areas. A study of over 300
children in an urban neighborhood found that 49% of children aged 1 to 8 years had blood lead
levels above current guidelines, indicating excessive lead exposure. In this study, only 59% of
children ages 1-3 years and 41% of children ages 4-8 years had calcium intakes meeting the
recommended levels (35). Adequate calcium intake could be protective against lead toxicity in at
least two ways. Increased dietary intake of calcium is known to decrease the gastrointestinal
absorption of lead. Once lead enters the body it tends to accumulate in the skeleton, where it may
remain for more than 20 years. Adequate calcium intake also prevents exposure to lead
mobilized from the skeleton during bone demineralization. A recent study of blood lead levels
during pregnancy found that women with inadequate calcium intake during the second half of
pregnancy were more likely to have elevated blood lead levels, probably related to increased
bone demineralization with the release of accumulated lead into the blood (36). Lead in the blood
of a pregnant woman is readily transported across the placenta resulting in fetal lead exposure at
a time when the developing nervous system is highly vulnerable. Additionally, in
postmenopausal women, increased calcium intake has been associated with decreased blood lead
levels. Other factors known to decrease bone demineralization, including estrogen replacement
therapy and physical activity, have also been inversely associated with blood lead levels (37).

Disease Treatment

High blood pressure (hypertension)

The relationship between calcium intake and blood pressure has been investigated extensively
over the past two decades. An analysis of 23 large observational studies found a reduction in
systolic blood pressure of 0.34 millimeters of mercury (mm Hg) per 100 mg of calcium
consumed daily and a reduction in diastolic blood pressure of 0.15 mm Hg per 100 mg calcium
(38). A large systematic review of 42 randomized controlled trials examining the effect of
calcium supplementation on blood pressure compared to placebo found an overall reduction of
1.44 mm Hg in systolic blood pressure and a reduction of 0.84 mm Hg in diastolic blood
pressure (39). Calcium supplementation in these randomized controlled trials ranged from 500-
2,000 mg/day, with 1,000-1,500 mg/day being the most common dose. In the DASH (Dietary
Approaches to Stop Hypertension) study, 549 people were randomized to one of three diets for
eight weeks: (1) a control diet that was low in fruit, vegetables, and dairy products; (2) a diet rich
in fruits (~5 servings/day) and vegetables (~3 servings/day); and (3) a combination diet rich in
fruits and vegetables as well as low-fat dairy products (~3 servings/day) (40). The combination
diet represented an increase of about 800 mg of calcium/day over the control and fruit/vegetable
rich diets for a total of about 1,200 mg of calcium/day. The combination diet reduced systolic
blood pressure 5.5 mm Hg and diastolic blood pressure 3.0 mm Hg more than the control diet,
while the fruit/vegetable diet reduced systolic blood pressure 2.8 mm Hg and diastolic blood
pressure 1.1 mm Hg more than the control diet. Among those participants diagnosed with
hypertension, the combination diet reduced systolic blood pressure by 11.4 mm Hg and diastolic
pressure by 5.5 mm Hg more than the control diet, while the reduction for the fruit/vegetable diet
was 7.2 mm Hg systolic and 2.8 mm Hg diastolic compared to the control diet (41). This
research indicates that a calcium intake at the recommended level (1,000-1,200 mg/day) may be
helpful in preventing and treating moderate hypertension (42). More information about the
DASH diet is available from the National Institutes of Health (NIH).

Premenstrual Syndrome (PMS)

PMS refers to a cluster of symptoms, including but not limited to fatigue, irritability,
moodiness/depression, fluid retention, and breast tenderness, that begins sometime after
ovulation (mid-cycle) and subsides with the onset of menstruation (the monthly period) (43).
Low dietary calcium intakes have been linked to PMS in several studies, and supplemental
calcium has been shown to decrease symptom severity (44). In a randomized, double-blind,
placebo-controlled clinical trial of 466 women, supplemental calcium (1,200 mg/day) for three
menstrual cycles was associated with a 48% reduction in total symptom scores, compared to a
30% reduction observed in the placebo group (45). Similar positive effects were reported in two
double-blind, placebo-controlled, cross-over trials that administered 1,000 mg of calcium daily
(46, 47). A case-control study in women participating in the Nurses' Health Study II found that
those who consumed the most calcium (median of 1,283 mg/day) from foods had a 30% lower
risk of developing PMS compared to those with the lowest calcium intake (median of 529
mg/day from foods) (48). However, calcium intake from supplements had no effect on PMS in
this study. Large-scale clinical trials are needed to determine whether increasing dietary calcium
intake or taking calcium supplements has therapeutic benefits in treating and preventing PMS.

Sources

Servings needed to
Food Serving Calcium (mg) equal the absorbable
calcium in 8 oz of milk
Milk 8 ounces 300 1.0
Yogurt 8 ounces 300 1.0
Cheddar cheese 1.5 ounces 303 1.0
Pinto beans 1/2 cup, cooked 45 8.1
Red beans 1/2 cup, cooked 41 9.7
White beans 1/2 cup, cooked 113 3.9
Tofu, calcium set 1/2 cup 258 1.2
Bok choy 1/2 cup, cooked 79 2.3
Kale 1/2 cup, cooked 61 3.2
Broccoli 1/2 cup, cooked 35 4.5
Spinach 1/2 cup, cooked 115 16.3
Rhubarb 1/2 cup, cooked 174 9.5
Fruit punch with
8 ounces 300 0.62
calcium citrate malate

Supplements

Most experts recommend obtaining as much calcium as possible from foods because calcium in
foods is accompanied by other important nutrients that assist the body in utilizing
calcium. However, calcium supplements may be necessary for those who have difficulty
consuming enough calcium from foods. No multivitamin/multimineral tablet contains 100% of
the recommended daily value (DV) for calcium because it is too bulky, and the resulting pill
would be too large to swallow. The "Supplement Facts" label, now required on all supplements
marketed in the U.S., lists the calcium content of the supplement as elemental calcium. Calcium
preparations used as supplements include calcium carbonate, calcium lactate, calcium gluconate,
calcium citrate, and calcium citrate malate. To determine which calcium preparation is in your
supplement, you may have to look at the ingredient list. Calcium carbonate is generally the most
economical calcium supplement. To maximize absorption, take no more than 500 mg of
elemental calcium at one time. Most calcium supplements should be taken with meals, although
calcium citrate and calcium citrate malate can be taken anytime (50).

Lead in calcium supplements

Several years ago concern was raised regarding the lead levels in calcium supplements obtained
from natural sources (oyster shell, bone meal, dolomite). In 1993, investigators found measurable
quantities of lead in most of the 70 different preparations they tested (51). Since then,
manufacturers have made an effort to reduce the amount of lead in calcium supplements to less
than 0.5 micrograms (mcg)/1,000 mg of elemental calcium. The federal limit is 7.5 mcg/1,000
mg elemental calcium. Because lead is so widespread and long lasting, no one can guarantee
entirely lead-free food or supplements. A recent study found measurable lead in eight out of 21
supplements, in amounts averaging between 1 and 2 mcg/1,000 mg of elemental calcium (52).
Calcium inhibits intestinal absorption of lead, and adequate calcium intake is protective against
lead toxicity, so trace amounts of lead in calcium supplementation may pose less of a risk of
excessive lead exposure than inadequate calcium consumption. While most calcium sources
today are relatively safe, look for supplements that are labeled "lead-free" and avoid large doses
of supplemental calcium (more than 1,500 mg/day).

Safety

Toxicity

Abnormally elevated blood calcium (hypercalcemia) resulting from the over consumption of
calcium has never been documented to occur from foods, only from calcium supplements. Mild
hypercalcemia may be without symptoms or may result in loss of appetite, nausea, vomiting,
constipation, abdominal pain, dry mouth, thirst, and frequent urination. More severe
hypercalcemia may result in confusion, delirium, coma, and if not treated, death. Hypercalcemia
has been reported only with the consumption of large quantities of calcium supplements usually
in combination with antacids, particularly in the days when peptic ulcers were treated with large
quantities of milk, calcium carbonate (antacid), and sodium bicarbonate (absorbable alkalai) (1).
This condition was termed milk alkalai syndrome and has been reported at calcium supplement
levels from 1.5 to 16.5 grams/day for two days to 30 years. Since the treatment for peptic ulcers
has changed, the incidence of this syndrome has decreased considerably (3).

Although the risk of forming kidney stones is increased in individuals with abnormally elevated
urinary calcium (hypercalciuria), this condition is not usually related to calcium intake, but rather
to increased excretion of calcium by the kidneys. Overall, increased dietary calcium has been
associated with a decreased risk of kidney stones. However, in a large prospective study, the risk
of developing kidney stones in women taking supplemental calcium was 20% higher than in
those who did not take supplements (25). This effect may be related to the fact that calcium
supplements can be taken without food, eliminating their beneficial effect of decreasing
intestinal oxalate absorption.
In 2010, the Food and Nutrition Board of the Institute of Medicine updated the tolerable upper
intake level (UL) for calcium. The UL is listed below by age group.

Tolerable Upper Intake Level (UL) for Calcium

Age Group UL (mg/day)
Infants 0-6 months 1,000
Infants 6-12 months 1,500
Children 1-8 years 2,500
Children 9-13 years 3,000
Adolescents 14-18 years 3,000
Adults 19-50 years 2,500
Adults 51 years and older 2,000

Do high calcium intakes increase the risk of prostate cancer?

Recent epidemiological studies have raised concern that high calcium intakes are associated with
increased risk of prostate cancer. A large prospective cohort study in the U.S. followed more
than 50,000 male health professionals for eight years and found that men whose calcium intake
was 2,000 mg/day or more had a risk of developing advanced prostate cancer that was three
times higher than men whose calcium intake was less than 500 mg/day and a risk of developing
metastasized prostate cancer that was more than four times greater (53). Similar results were
observed in a case-control study in Sweden, which compared the calcium consumption of 526
men diagnosed with prostate cancer to that of 536 controls (54). Neither study found calcium
intake to be associated with an increased risk of total prostate cancer or non-advanced prostate
cancer. More recently, another prospective study of U.S. physicians found that increased intake
of calcium from dairy foods was associated with an increased risk of prostate cancer (55).
Although this study did not examine supplement use, each 500 mg/day increase in calcium
intake from dairy foods was associated with a 16% increase in the risk of prostate cancer
(advanced and non-advanced, combined). Most recently, a prospective study in a cohort of
29,133 male smokers, followed for 17 years, found that high calcium consumption (> 1,000
mg/day) was associated with an increased risk for prostate cancer (56). The physiologic
mechanisms underlying the relationship between calcium intake and prostate cancer are not yet
clear. High levels of dietary calcium may lead to decreased circulating levels of calcitriol, the
active form of vitamin D. In experimental studies conducted in prostate cancer cell lines and
animal models, calcitriol was found to have protective effects. However, the findings of studies
conducted in humans on serum calcitriol levels and prostate cancer risk have been much less
consistent.

Not all epidemiological studies have demonstrated an association between calcium intake and
prostate cancer. One review reported that seven out of 14 case-control studies and five out of
nine prospective cohort studies found statistically significant positive associations between
prostate cancer and some measure of dairy product consumption. Of those studies that examined
calcium intake, three out of six case-control studies and two out of four cohort studies reported
statistically significant associations between prostate cancer and calcium intake (57). However,
one Serbian case-control study found increased calcium intake to be associated with a decreased
risk of prostate cancer (58). In a meta-analysis of six prospective studies, Gao et al. reported that
men with higher daily calcium intakes had a 39% increased risk of developing prostate cancer
compared to those with lower intakes; men with higher dairy product intakes had a 11% higher
risk of prostate cancer compared to those with lower dairy product intakes (59). However, only
half of the distinct studies included in this meta-analysis reported an association between higher
calcium intakes and prostate cancer. More recently, a prospective study in 14,642 men
participating in the Melbourne Collaborative Cohort Study found that calcium intake was not
associated with prostate cancer risk (60). Gao et al. repeated their meta-analysis (59) to include
this most recently published study. They found that those with higher calcium intakes had a 32%
increased risk of prostate cancer; however, meta-analysis of all seven studies revealed that dairy
intake was no longer associated with a significantly increased risk of prostate cancer (60). The
lack of agreement among studies suggests complex interactions among the risk factors for
prostate cancer and may also reflect the difficulties associated with assessing calcium intake in
free living humans. Until the relationship between calcium and prostate cancer is clarified, it is
reasonable for men to consume a total of 1,000 to 1,200 mg/day of calcium (diet and
supplements combined), which is recommended by the Food and Nutrition Board of the Institute
of Medicine (see RDA).

Drug Interactions

Taking calcium supplements in combination with thiazide diuretics (e.g., hydrochlorthiazide)

increases the risk of developing hypercalcemia due to increased reabsorption of calcium in the
kidneys. High doses of supplemental calcium could increase the likelihood of abnormal heart
rhythms in people taking digitalis (digoxin) for heart failure (61). Calcium, when provided
intravenously, may decrease the efficacy of calcium channel blockers (62). However, dietary and
oral supplemental calcium do not appear to affect the action of calcium channel blockers (63).
Calcium may decrease the absorption of tetracycline, quinolone class antibiotics,
bisphosphonates, and levothyroxine; therefore, it is advisable to separate doses of these
medications and calcium rich foods or supplements by two hours. Use of H2 blockers (e.g.,
cimetidine) and proton pump inhibitors (e.g., omeprazole) may decrease the absorption of
calcium carbonate and calcium phosphate (50, 64).

Calcium-Nutrient Interactions

The presence of calcium decreases iron absorption from nonheme sources (i.e., most
supplements and food sources other than meat). However, calcium supplementation up to 12
weeks has not been found to change iron nutritional status, probably due to a compensatory
increase in iron absorption. Individuals taking iron supplements should take them two hours
apart from calcium-rich foods or supplements to maximize iron absorption. High calcium intakes
in rats have produced relative magnesium deficiencies, but calcium intake was not found to
affect magnesium retention in humans (1). Although a number of studies did not find high
calcium intakes to affect zinc absorption or zinc nutritional status, a study in ten men and women
indicated that 600 mg of calcium consumed with a meal decreased the absorption of zinc from
that meal by 50% (65).

Recent Research

Calcium and weight loss

Diets with higher calcium density (calcium per total calories) have been associated with a
reduced incidence of being overweight or obese in some studies. These studies were not
designed to examine the effect of calcium on obesity or body fat, and their significance was
unclear until recent studies in cell culture and animal models indicated that low calcium intakes
could result in hormonal and metabolic changes that increase the tendency of fat cells to
accumulate fat (66). In a two-year exercise trial, higher dietary calcium intakes were associated
with weight loss whether participants were in the exercise group or the control group (67). A
placebo-controlled calcium supplementation trial found significantly greater weight loss in
elderly women supplemented with 1,200 mg of calcium/day compared to a control group (68).
More recently, a 1-year dairy product intervention (1,000 to 1,400 mg of calcium/day) in healthy
young women did not alter body weight or fat mass compared to the control group (< 800 mg of
calcium/day) (69); however, a slight reduction in body fat mass was observed in the high-dairy
group (1,300 to 1,400 mg of calcium/day) at the 6-month follow-up (70). Controlled feeding
studies where calories remain fixed are needed to quantify the likely small effect of calcium, if
any, on body fat and body weight. Such studies are currently underway.

Linus Pauling Institute Recommendation

The Linus Pauling Institute supports the recommended dietary intake (RDA) levels set by the
Food and Nutrition Board of the Institute of Medicine. Following these recommendations should
provide adequate calcium to promote skeletal health and may also decrease the risks of some
chronic diseases.

Children and adolescents (9-18 years)

To promote the attainment of maximal peak bone mass, children and adolescents should
consume a total (diet plus supplements) of 1,300 mg/day of calcium.

Adults (women aged 19-50 years, men aged 19-70 years)

After adult height has been reached, the skeleton continues to accumulate bone until the third
decade of life when peak bone mass is attained. To promote the attainment of maximal peak
bone mass and to minimize bone loss later in life, adult women (50 years of age and younger)
and adult men (70 years of age and younger) should consume a total (diet plus supplements) of
1,000 mg/day of calcium.

Older women (51 years and older)

To minimize bone loss, postmenopausal women should consume a total (diet plus supplements)
of 1,200 mg/day of calcium. Taking a multivitamin/multimineral supplement containing at least
10 mcg (400 IU)/day of vitamin D will help to ensure adequate calcium absorption (see Vitamin
D).

Older men (71 years and older)

To minimize bone loss, older men should consume a total (diet plus supplements) of 1,200
mg/day of calcium. Taking a multivitamin/multimineral supplement containing at least 10 mcg
(400 IU)/day of vitamin D will help to ensure adequate calcium absorption (see Vitamin D).

Pregnant and breast-feeding women

Pregnant and breast-feeding adolescents (under 19 years of age) should consume a total of 1,300
mg/day of calcium, while pregnant and breast-feeding adults (19 years and older) should
consume a total of 1,000 mg/day of calcium.