Osteoporosis Treatment: Much More Than Calcium



The scourge of many elderly women and men, osteoporosis and other bone loss conditions account for more than 1.3 million fractures and $6 billion in losses annually in the United States.( 1-5) In 1990, an estimated 24 million Americans suffer from osteoporosis, although only 10 million have been diagnosed, and 7 million treated.( 6)

Furthermore, all indicators point to increased numbers of osteoporosis cases for all industrialized countries. Befitting a health problem of this magnitude, and enormous research effort has been applied to find effective treatments. Enough data has accumulated to allow consensus conferences to set guidelines on calcium intake of 1,500 mg daily.( 1, 4)

In spite of an intense effort to treat osteoporosis, the most effective management to date can only slightly increase cortical bone mass.( 1-6) However, primary postmenopausal osteoporosis is mostly demineralization of trabecular bone. Combinations of high calcium intake, estrogen, vitamin D metabolites, fluoride and other hormones have simply been unable to significantly affect trabecular bone mass, even in studies lasting several years.( 7)

While this management may become effective for prevention of osteoporosis in younger postmenopausal women, it does not address current and future cases of osteoporosis that have lost significant bone mass. A 5% increase of cortical bone mass typically seen from the most successful calcium-oriented studies cannot be thought of as a successful reversal of bone loss when 20-50% of trabecular bone mass has already been lost.

Perhaps we can shed some light on reversing bone loss.

Osteoporosis -- Calcium Is Not The Answer

At present, it is heretical to suggest that supplemental calcium will not be beneficial to bone health. While it is clear that a long-term, deficient intake of calcium (which happens to be the average status for American women) is definitely associated with osteoporosis, it is now apparent that increased calcium intake will not reverse osteoporosis and may only partially prevent its incidence. This finding is echoed by current editorials.( 7, 8)

Also of interest is the fact that many primitive cultures have excellent bone health with little or no osteoporosis and low calcium intakes.( 9) In fact, the World Health Organization recognizes a practical allowance of 400-500 mg of calcium daily,( 10) a value far below the current U.S. Recommended Daily Allowance of 800-1,200 mg of calcium daily. How does the rest of the world maintain bone mass without large intakes of calcium?

Trace Minerals and Osteoporsis -- The Missing Link?

Insufficient calcium intake causes osteoporosis, yet treatment with calcium does not fully ameliorate it. How can these conflicting findings be reconciled? The answer is simple: Osteoporosis is not just a calcium deficiency, but an accumulation of insults from multiple deficiencies of minerals. Thus, it is scientifically accurate to say that lack of calcium is associated with osteoporosis, but it is not the only cause.

When calcium intake is low, it is highly likely that intake of other essential trace minerals is also low. This is seen repeatedly in dietary intake studies.( 11) In fact, intakes of magnesium, zinc, manganese and copper are all marginal or deficient (below the RDA safety limits) for the majority of American women of all ages.( 11) Table 1 lists the major nutrients that are associated with osteoporosis when deficient.

Why are trace minerals important to bone health? Each mineral participates in key steps of bone synthesis. Magnesium and zinc are needed for the function of many enzymes and hormones used by osteoblasts to make bone. Manganese and cooper are required for activity of enzymes that make the organic part of bone (osteoid).

Notice that if osteoid is not synthesized correctly, then bone mineralization cannot occur, no matter how much calcium is available. If osteoid formation is only delayed by marginal trace mineral intakes, then an imbalance between bone resorption and bone resynthesis occurs, leading to a net loss of bone. This imbalance happens to be a definition of osteoporosis.

More support for the role of trace minerals in osteoporosis comes from well-known effects of deficiencies in animals and humans. When an organism is made frankly deficient for a short time period, or marginally deficient for long time periods, in only one trace mineral, then bone loss and skeletal abnormalities are always a primary finding.( 12, 14) Whether the mineral is magnesium, zinc, copper or manganese is inconsequential. In fact, very recent findings in osteoporotic humans have found decreased levels of magnesium, zinc, manganese and copper in serum and/or bone.( 14, 17)

Another example of multiple trace mineral deficiencies leading to bone loss is the case of Bill Walton, an outstanding professional basketball player whose career was plagued and shortened by numerous injuries. After calcium supplements did not help his bone loss, his blood was analyzed for trace minerals.( 14) He was found to have no manganese and very low levels of other trace minerals. Supplementation with trace minerals allowed him to recover sufficiently and resume professional play for several more years.

Osteoporosis and Nutrition -- What to Do

Obviously, intake of trace minerals needs to be increased, along with adequate calcium intake. Interestingly, calcium carbonate, dairy products and iron in supplements all depress uptake of trace minerals, especially manganese.( 18) Thus, the very recommendations of consensus conferences to increase dairy and calcium intake may exacerbate trace mineral deficiencies. This may help to explain why countries with highest dairy intakes have highest rates of osteoporosis.

Is calcium supplementation necessary? Yes. Calcium provides the raw material for structural integrity of bone. If it is not present in adequate amounts, then even marginal status of one or more other essential nutrients will prevent proper use of calcium. However, if plenty of calcium is available, but other essential nutrients are deficient, calcium use is improper, and cannot fully restore bone synthesis. The key is to have enough of everything that bones need to resynthesize matrix.

Which type of calcium is ideal? So far, the organic acid forms of calcium are documented to be absorbed to a higher degree by more persons, especially those with low stomach acidity.( 19-21) These forms include calcium citrate, calcium citrate/malate and calcium lactate. Calcium citrate, which has been studied most extensively, has been shown to have the highest uptake of calcium from any source, including bone meal (microcrystalline hydroxyapatite).( 19-21) In addition, organic acid forms of calcium counteract metabolic acidosis, another risk factor for osteoporosis.

Phosphate is the major mineral component of bone. Phosphate supplementation is not generally recommended for osteoporosis for several reasons. First, Americans consume twice the RDA for phosphorus in typical diets.( 11) Second, phosphate forms insoluable complexes with calcium and other trace minerals, preventing proper uptake of minerals needed for bone synthesis. Third, phosphate causes excess excretion, or removal, of minerals from the body via urine.( 2)

How can trace minerals be supplied by the diet? The simplest and surest answer to provide adequate trace mineral intakes is supplementation.

Pitfalls of figuring out which foods have what levels of trace minerals, and whether the plants were grown in mineral-depleted soils are avoided by trace mineral supplements.

Organic chelate forms of trace minerals have better uptake and less interactions between each other than inorganic forms. An example is to choose zinc gluconate or picolinate over zinc sulfate.

When animals deficient in one or more trace minerals are repleted, bone loss can be fully reversed, and bone mass normalized.( 22, 24) Human infants with bone loss from mineral deficiencies (especially copper) quickly return to normal bone mass upon repletion of the deficient mineral.( 11)

Two recent studies of humans given magnesium has given exciting support for emphasis on trace minerals rather than calcium. A Czechoslovakian study administered only oral magnesium lactate supplements to 37 elderly osteoporotics and found "very favourable" results.( 25)

Researchers from the Woman's Life Care Clinic in Anaheim, Calif., administered a multiple vitamin/mineral product containing 500 mg of calcium (as citrate), 600 mg of magnesium (as oxide) and substantial amounts of zinc, manganese, iron and copper daily to 19 postmenopausal women on hormonal therapy.( 26) After one year, an 11% increase in bone mass was found a remarkable finding, while seven controls showed no change.

Another study found that 3 mg of boron supplemented to elderly women improved retention of calcium and magnesium, as well as improving the status of steroid hormones (estrogen and testosterone) known to prevent osteoporosis.( 27)

Thus, the hypothesis that trace mineral repletion may reverse osteoporosis has only just begun to be tested in animals or humans. So far, the initial results are encouraging and support the hypothesis that treatment of osteoporosis is more than calcium.

Non-essential trace elements that affect bone health in a positive manner include boron and silicon.( 16) Deficiencies of folate, vitamins B( 6), C, D and K can also cause bone loss.( 16) Another nutrient with potential application for bone resynthesis is chondroitin sulfate.

This glycosaminoglycan found in connective tissues is a component of bone osterod. In vitro, chondroitin sulfates can stimulate formation of connective tissues (osteoid), and they have been used successfully for many years to fill and remineralize osseous defects in animals and humans.( 30-32) One German study found unspecified benefits for nine of 16 osteoporotics given injectable chondroitin sulfates.( 33) Exercise and sunlight are very important lifestyle factors that aid in the maintenance of bone mass.( 1-5) Moderation seems to be vital for these factors to enhance bone mass. Other factors may increase bone loss and should be reduced.( 1-5) These include diets rich in animal protein and fats. Bone minerals are used to buffer metabolic acidosis from these diets.


When enough medical researchers finally initiate long-term studies of calcium plus trace minerals plus adjunct nutrient supplementation for osteoporotics, it is likely that a reversal of osteoporosis may be achieved (see Table 2).

Fortunately, many products incorporating guidelines in this article have been marketed, resulting in a wide choice of nutritional supplements to improve bone health. Rather than wait many years for conclusive demonstration of a strong hypothesis that already had preliminary support, it seems prudent to recommend nutritional supplements containing effective doses of calcium, trace minerals and adjunct nutrients to patients with bone loss, or those at risk of developing osteoporosis.

(1.) Avioli, L.V., "Osteoporosis: Consensus Conference," JAMA 252(6):799-802, 1984.

(2.) Dawson-Hughes B., "Osteoporosis and Aging: Gastrointestinal Aspects," J Am Coll Nutr 5:393-398, 1986.

(3.) Riggs, B.L., and Melton, L.J., "Involutional Osteoporosis," N Engl J Med 314(26):1676-1686, 1986.

(4.) Spencer, H., and Kramer L., "NIH Consensus Conference: Osteoporosis -- Factors Contributing to Osteoporosis," J. Nutr 116:316-319, 1986.

(5.) Resnick, N.M., and Greenspan, S.L., "'Senile' Osteoporosis Reconsidered," JAMA 261(7):1025-1029, 1989.

(6.) Cusamano, L.M., and Jack, W., Osteoporosis: A Tough Market to Crack," Pharm Exec, May, 1989, pp. 64-70.

(7.) Genant, H.K., ed., Osteoporosis Update, San Francisco: Radiology Research and Education Foundation, 1987.

(8.) Lindsay, R., "Fluoride and Bone -- Quantity Versus Quality," N Engl J Med 322(12):845-846, 1990.

(9.) Solomon, L., "Bone Density in Ageing Caucasian and African Populations," Lancet 2:1326-1330, 1979.

(10.) Kanis, J.A., and Passmore, R., "Calcium Supplementation of the Diet, I and II," Br Med J 298:137, 205, 1989.

(11.) Pennington, J.A.T., Young, B.E., Wilson, D.B., Johnson, R.D., and Vanderveen, J.E., "Mineral Content of Foods and Total Diets: The Selected Minerals in Foods Survey, 1982 to 1984," J Am Diet Assoc 86:876-891, 1986.

(12.) Shils, M.E., and Young, V.R., eds., Modern Nutrition in Health and Disease, 7th Ed., Philadelphia: Lea & Febiger, 1988.

(13.) Allen, T.M., Manoli, A., and LaMont, R.L., "Skeletal Changes Associated With Copper Deficiency," Clin Orthop 168:206-210, 1982.

(14.) Strause L, and Saltman, P., "Role of Manganese in Bone Metabolism," In: Kies, C, ed., Nutritional Bioavailability of Manganese, Washington, D.C.: American Chemical Society, 1987, pp. 46-55.

(15.) Cohen, L., and Kitzes,R., "Infrared Spectroscopy and Magnesium Content of Bone Mineral in Osteoporotic Women," Isr J Med Sci 17(12):1123-1125, 1981.

(16.) Gaby, A.R, and Wright, J,V., Nutrients and Bone Health, Baltimore: Wright/Gaby Nutrition Institute, 1989.

(17.) Freudenheim, J. L., Johnson, N.E., and Smith E.L., "Relationships Between Usual Nutrient Intake and Bone-Mineral Content of Women 35-65 Years of Age: Longitudinal and Cross-Sectional Analysis," Am J Clin Nu tr 44:863-876, 1986.

(18.) Kies, C, ed., Nutritional Bioavailability of Manganese, Washington, D.C.: American Chemical Society, 1987.

(19.) Nicar, M.J., and Pak, C.Y.C., "Calcium Bioavailability From Calcium Carbonate and Calcium Citrate," J Clin Endocrinol Metab 61(2):391-393, 1985.

(20.) Reid, I.R., Hannan, S.F., Schooler, B.A., and Ibbertson, H.K., "The Acute Biochemical Effects of Four Proprietary Calcium Preparations," Aust NZ J Med 16:193-197, 1986.

(21.) Schuette, S.A., and Knowles, J.B., "Intestinal Absorption of Ca(H(2)PO(4))(2) and Ca Citrate Compared By Two Methods," Am J Clin Nutr 47:884-888, 1988.

(22.) Calhoun, N.R., Smith, J.C., and Becker K.L., "The Role of Zinc in Bone Metabolism," Clin Orthos 103: 212-234, 1974.

(23.) Strause, L., Saltman, P., and Glowacki, J.,"The Effect of Deficiencies of Manganese and Copper on Osteoinduction and on Resorption of Bone Particles," Calcif Tissue Int 41(3):135-150, 1987.

(24.) Ericsson, Y., Luoma, H., and Ekberg, O., "Effects of Calcium, Fluoride and Magnesium Supplementation on Tissue Mineralization in Calcium-and Magnesium-Deficient Rats," J Nutr 116(6):1018-1027, 1986.

(25.) Ditmar, R., and Steidl, L., "The Significance of Magnesium in Orthopedics. V. Magnesium in Osteoporosis," Act Chir Orthop Traumatol Cech 56(2):143-159, 1989.

(26.) Abraham, G.E., and Grewal, H.A., "Total Dietary Program Emphasizing Magnesium Instead of Calcium: Effect on the Mineral Density of Calcaneous Bone in Postmenopausal Women on Hormonal Therapy," J Reprod Med 35(5):503-507, 1990.

(27.) Nielsen, F.H., Hunt, C.D., Mullen, L.M., and Hunt, J.R., "Effect of Dietary Boron on Mineral, Estrogen and Testosterone Metabolism in Postmenopausal Women," FASEB J 1:394-397, 1987.

(28.) Hjerpe, A., and Engfeldt, B., "Glycosaminoglycans and Proteoglycans in Skeletal Tissues," In: Varma, R.S., and Varma, R., eds., Glycosaminoglycans and Proteoglycans in Physiological and Pathological Processes of Body Systems, Basel: Karger, pp. 252-263, 1982.

(29.) Bollet, A.J., "Stimulation of Progein-Chondroitin Sulfate Synthesis By Normal and Osteoarthritic Articular Cartilage," Arth Rheum 11: 663-673, 1986.

(30.) Bouget, P., and Guenaud, D., "Packing of a Preformed Bone Cavity with Biodegradable Material: Value of Chondroitin Sulfuric Acid in the Osteogenic Process," Inf Dent 63:19-27, 1981.

(31.) Herold, H.Z., and Tadmor, A., "Chondroitin Sulfate in Treatment of Experimental Bone Defects," Isr J Med Sci 5:425-427, 1969.

(32.) Skinner, R.A., Toto, P.D., and Gargiulo, A.W., "Xenogeneic Implants in Primates: Collagen and Chondroitin Sulfate," J Periodonto1 47 (4):196-202, '76

(33.) Wagenhauser, F.J., "Therapie Mit Knorpelknochenmarkextrakt," Therapiewoche 15:32-37, 1965.

Life University.


By Luke R. Bucci

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