Calcium and Bone Health

By Lynn Keegan, RN, PhD, HNC-BC, FAAN Director, Holistic Nursing Consultants, Port Angeles, WA. Dr. Keegan reports no consultant, stockholder, speaker's bureau, research, or other financial relationships with companies having ties to this field of study.

Recent analyses from the women's health initiative have shed new light on the importance of adequate calcium and vitamin D intake to women's bone health. This is especially important considering that women's calcium requirements significantly increase not only with menopause, but also pregnancy, post-pregnancy, and lactation.1 Despite the dissemination of this important information, many women still do not comply with the calcium requirement recommendations.2

For example, an investigation in Taiwan found that 80.6% of young adult women (n = 265) were very likely to have accurate knowledge about osteoporosis but also typically had a low calcium intake (454 mg/d).3 The factors that most strongly affected the intake of calcium by women were knowledge, number of children, self-rated health score, body mass index, graduation from high school, experience of bone density examination, and family history. Findings from three studies conducted from 1994 to 2000 examining the determinants of calcium intake among women at midlife suggest that there is a high level of awareness among women that consuming an inadequate amount of calcium increases their risk of developing osteoporosis, but that this awareness is not being translated into long-lasting behavior change.4 Even when individuals are interested in increasing their calcium intake, perceived barriers often appear to prevent them from acting or lead to recidivism.

Mechanism of Action

During perimenopause, both the quantity and quality of bone decline rapidly, resulting in a dramatic increase in the risk of fracture in postmenopausal women.5 The osteoporosis that may occur as a result is a disorder in which loss of bone strength leads to fragility fractures. The fundamental pathogenetic mechanisms underlying this disorder include: (a) failure to achieve a skeleton of optimal strength during growth and development, (b) excessive bone resorption resulting in loss of bone mass and disruption of architecture, and (c) failure to replace lost bone due to defects in bone formation.6 Estrogen deficiency is known to play a critical role in the development of osteoporosis, while calcium and vitamin D deficiencies and secondary hyperparathyroidism also contribute. There are multiple mechanisms underlying the regulation of bone remodeling, and these involve not only the osteoblastic and osteoclastic cell lineages but also other marrow cells, in addition to the interaction of systemic hormones, local cytokines, growth factors, and transcription factors. Polymorphisms of a large number of genes have been associated with differences in bone mass and fragility. Bone loss with age and menopause are universal, but rates vary among individuals. Both peak bone mass and subsequent bone loss can be modified by environmental factors, such as nutrition, physical activity, and concomitant diseases and medications.7

Clinical Trials

Calcium supplementation appears to increase bone density. In one meta-analysis, calcium was shown to be more effective than placebo in reducing bone loss rates in postmenopausal women.8 There also was a trend toward improvement in vertebral fracture risk. A review of clinical trials found that increased calcium intake in postmenopausal women led to a slight decrease in fracture risk.9

Two U.S. national databases were used to assess the adequacy of calcium intake in patients with osteoporosis. Quantity of calcium intake, both from supplements and food, among individuals with osteoporosis (n = 38 men, n = 376 women) was estimated using the 1999-2002 National Health and Nutrition Examination Survey (NHANES).10 Physician visits for osteoporosis in the United States increased 4.5-fold between 1994 (1.3 million visits) and 2004 (5.8 million visits). During this time the proportion of osteoporosis visits in which bisphosphonates were prescribed increased from 14% to 81%, while reported calcium use fell from 43% to 23%. Among osteoporosis patients in NHANES, 64% reported using calcium-containing supplements. Reported median calcium intake was 433 mg/d for calcium supplement nonusers and 1,319 mg/d for calcium supplement users. Overall, only 40% of osteoporosis patients had calcium intake exceeding 1,200 mg/d. These researchers concluded that as osteoporosis increasingly is identified and treated with effective medications, calcium is being neglected as a component of osteoporosis management. Despite the fact that the efficacy of new osteoporosis medications depends on adequate calcium intake, reported calcium intake in osteoporosis patients is far below recommended levels.

Another study examined the association of exercise frequency and calcium intake with change in regional and total bone mineral density (BMD) in a group of postmenopausal women completing four years of progressive strength training.11 Researchers followed 167 calcium-supplemented (800 mg/d) sedentary women (56.1 ± 4.5 years) randomized to a progressive strength training exercise program or to control for four years. Fifty-four percent of the women were using hormone therapy at baseline. The final sample included 23 controls, 55 crossovers, and 89 randomized exercisers. The study showed a significant, positive, association between BMD change and exercise frequency, supporting the long-term usefulness of strength training exercise for the prevention of osteoporosis in postmenopausal women, especially hormone therapy users. The positive relationship of calcium intake to change in BMD among postmenopausal women not using hormone therapy has clinical implications in light of recent evidence of an increased health risk associated with hormone therapy.

A Japanese study compared BMDs among subjects in the same age ranges, but attained by different birth cohorts in 1990 or in 2000.12 The mean value of the lumbar spine BMD (L2-4) in women in the birth cohort of 1940-1949, when they reached the age stratum 50-59, was significantly higher than that of the cohort born in 1930-1939 when in the same age stratum (P < 0.05). The same tendency was observed in BMD at the femoral neck. The comparatively higher levels of BMD observed in women in the 1940-1949 birth cohort when they reached their fifties, may reflect nutritional improvements in Japan. The nationwide nutritional survey reports mean values of calcium intake as 253 mg/d in 1946, 338 mg/d in 1955, 465 mg/d in 1965, and 552 mg/d in 1975, a dramatic increase, although still low. Both men and women in later birth cohorts showed higher BMDs in middle-age, which may predict a future decrease in the incidence and prevalence of osteoporosis.

An Australian study assessed whether a lifestyle intervention delivered to mothers might impact osteoporosis preventive behaviors in their children.13 A two-year randomized controlled trial of individualized BMD feedback was done with either an osteoporosis information leaflet or small group education in a population-based sample of 354 mothers. Receiving small group education was associated with mothers' report of increasing children's calcium intake, as was low t-score feedback. Mothers who increased their own physical activity more often reported an increase in both physical activity and calcium intake in their children. Mothers who commenced calcium supplements more often reported increasing children's calcium intake but not physical activity. Both BMD feedback and small group education delivered to mothers are effective at inducing maternally reported osteoporosis preventive behavior change in their children. These results require confirmation by studies with objective outcome measures.

Safety and Cautions

Abnormally elevated blood calcium (hypercalcemia) resulting from the overconsumption 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 alkali).14 This condition was termed milk alkali syndrome, and has been reported at calcium supplement levels from 1.5-16.5 g/d for two days to 30 years. Since the treatment for peptic ulcers has changed, the incidence of this syndrome has decreased considerably.15

Although the risk of forming kidney stones is increased in individuals with abnormally elevated urinary calcium (hypercalciuria), this condition usually is not 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.16 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.

Dosage Recommendations

Based on the adverse effects above, as well as the potential for decreased absorption of other essential minerals, the Food and Nutrition Board of the Institute of Medicine set the tolerable upper level of intake for calcium in adults at 2,500 mg/d.15

As part of any osteoporosis treatment program, it is important to maintain adequate calcium and 25-hydroxy-vitamin D levels either through diet or supplementation. Among the available pharmacologic therapies, the bisphosphonates alendronate and risedronate have demonstrated the most robust fracture risk reductions—approximately 40-50% reduction in vertebral fracture risk, 30-40% in nonvertebral fracture risk, and 40-60% in hip fracture risk.17 Ibandronate, a new bisphosphonate, has demonstrated efficacy in reducing vertebral fracture risk. Salmon calcitonin nasal spray and raloxifene demonstrated significant reductions in vertebral fracture risk in pivotal studies. Teriparatide significantly reduced vertebral and nonvertebral fracture risk. Drugs on the horizon include strontium ranelate, which has been shown to reduce vertebral and nonvertebral fracture risk, and zoledronic acid, an injectable bisphosphonate that increased bone density with once-yearly administration. In essence, both pharmacological and nonpharmacological strategies need to be employed.18

Food Sources

Average dietary intakes of calcium in the United States are well below the adequate intake recommendation for every age and gender group, especially in females. Only about 25% of boys and 10% of girls ages 9-17 are estimated to meet the adequate intake 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.14,15

Dairy products represent rich and absorbable sources of calcium, but certain vegetables and grains also provide calcium. However, the bioavailability of that calcium must be taken into consideration. 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.19

Although 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 in high concentrations in spinach and rhubarb and somewhat lower concentrations in sweet potato and dried beans. Phytic acid is a less potent inhibitor of calcium absorption than oxalate. Yeast possesses 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.14

Recommendations and Conclusion

Osteoporosis, a major public health problem and often the result of poor bone health, is becoming increasingly prevalent in our aging population. A skeletal disorder characterized by compromised bone strength, osteoporosis predisposes individuals to increased risk of fractures of the hip, spine, and other skeletal sites. The clinical consequences and economic burden of this disease suggest that we need measures to assess individuals who are at high risk to allow for appropriate intervention. Adequate calcium throughout a woman's life span is a critical step to achieving and improving bone health. The most critical time periods include adolescence, pregnancy, lactation, perimenopause, and menopause, in which adequate calcium intake is most important.


1. Weisman SM. The calcium connection to bone health across a woman's life span: A roundtable. J Reprod Med 2005;50(11 Suppl):879-884.

2. Gold DT. Elevated calcium requirements for women and unique approaches to improving calcium adherence. J Reprod Med 2005;50(11 Suppl):891-895.

3. Chang SF. A cross-sectional survey of calcium intake in relation to knowledge of osteoporosis and beliefs in young adult women. Int J Nurs Pract 2006;12:21-27.

4. Blalock SJ. Toward a better understanding of calcium intake: Behavioral change perspectives. J Reprod Med 2005;50(11 Suppl):901-906.

5. Delaney MF. Strategies for the prevention and treatment of osteoporosis during early postmenopause. Am J Obstet Gynecol 2006;194(2 Suppl):S12-S23.

6. Raisz LG. Pathogenesis of osteoporosis: Concepts, conflicts, and prospects. J Clin Invest 2005;115:3318-3325.

7. Cosman F. The prevention and treatment of osteoporosis: A review. MedGenMed 2005;7:73.

8. Shea B, et al. Calcium supplementation on bone loss in postmenopausal women. Cochrane Database Syst Rev 2004(1):CD004526.

9. Cumming RG, Nevitt MC. Calcium for prevention of osteoporotic fractures in postmenopausal women. J Bone Miner Res 1997;12:1321-1329.

10. Stafford RS, et al. National patterns of calcium use in osteoporosis in the United States. J Reprod Med 2005;50(11 Suppl):885-890.

11. Cussler EC, et al. Exercise frequency and calcium intake predict four-year bone changes in postmenopausal women. Osteoporos Int 2005;16:2129-2141. Epub 2005 Nov 10.

12. Yoshimura N, Oka H. [Osteoporosis and nutrition: trends of calcium intake and bone mineral densities]. Clin Calcium 2006;16:103-109.

13. Winzenberg TM, et al. A mother-based intervention trial for osteoporosis prevention in children. Prev Med 2006;42:21-26. Epub 2005 Dec 5.

14. Weaver CM, Heaney RP. Calcium. In: Shils M, et al. eds. Nutrition in Health and Disease. 9th ed. Baltimore: Williams & Wilkins; 1999:141-155.

15. Institute of Medicine. Food and Nutrition Board. Calcium. Dietary Reference Intakes: Calcium, Phosphorus, Magnesium, Vitamin D, and Fluoride. Washington, DC: National Academy Press; 1997:71-145.

16. Curhan GC, et al. Comparison of dietary calcium with supplemental calcium and other nutrients as factors affecting the risk for kidney stones in women. Ann Intern Med 1997;126:497-504.

17. Hamdy RC, et al. Review of treatment modalities for postmenopausal osteoporosis. South Med J 2005;98:1000-1014; quiz 1015-1017, 1048.

18. Wilkins CH, Birge SJ. Prevention of osteoporotic fractures in the elderly. Am J Med 2005;118:1190-1195.

19. Weaver CM, et al. Choices for achieving adequate dietary calcium with a vegetarian diet. Am J Clin Nutr 1999;70(3 Suppl):543S-548S.