Postmenopausal osteoporosis is closely associated with genetic factors and lifestyle. Minerals in the diet influence both the development and treatment of osteoporosis.

Dietary magnesium directly affects skeletal magnesium content and magnesium deficiency affects all phases of bone metabolism

Results of retrospective studies indicate that dietary calcium, magnesium, and phosphorus are below the recommended daily allowances for many populations. Serum, erythrocyte and bone magnesium content are found to be lower than normal in some studies.

It is well known that serum magnesium levels decrease both in serum and bone in postmenopausal women. Furthermore, dietary magnesium content correlates with the development of osteoporosis

A tight control of magnesium homeostasis seems to be crucial for bone health. On the basis of experimental and epidemiological studies, both low and high magnesium have harmful effects on the bones. Magnesium deficiency contributes to osteoporosis directly by acting on crystal formation and on bone cells and indirectly by impacting on the secretion and the activity of parathyroid hormone and by promoting low-grade inflammation. Less is known about the mechanisms responsible for the mineralisation defects observed when magnesium is elevated. Overall, controlling and maintaining magnesium homeostasis represents a helpful intervention to maintain bone integrity.

Magnesium and the bone 

About 60% of total magnesium (Mg) is stored in the bone. One third of skeletal Mg resides on cortical bone either on the surface of hydroxyapatite or in the hydration shell around the crystal. It serves as a reservoir of exchangeable Mg useful to maintain physiological extracellular concentrations of the cation. Bone surface Mg levels are related to serum Mg.

Accordingly, surface bone Mg increases with Mg loading, as described in chronic renal disease. The larger fraction of bone Mg is probably deposited as an integral part of the apatite crystal and its release follows the resorption of bone. Apart from a structural role in the crystals, Mg is essential to all living cells, including osteoblasts and osteoclasts.

Intracellularly, Mg is vital for numerous physiological functions. It is fundamental for ATP, the main source of energy in the cells. Moreover, Mg is cofactor of hundreds of enzymes involved in lipid, protein and nucleic acid synthesis. Because of its positive charge, Mg stabilises cell membranes. It also antagonises calcium and functions as a signal transducer. It is therefore not surprising that alterations of Mg homeostasis impact on cell and tissue functions.

Apart from t effects on the structure and the cells of the skeleton, Mg deficiency impacts on the bone also indirectly by affecting the homeostasis of the two master regulators of calcium homeostasis, i.e., parathyroid hormone (PTH) and 1,25(OH)2-vitamin D, leading to hypocalcemia.

Aydinet alshowed that short-term oral magnesium supplementation raises serum levels ofosteocalcin, significantly decreases urinary deoxypyridinoline and serum iPTH and thereby possibly decreases bone loss. These results are in accordance with the results of Dimaiet al and Toba et al who have demonstrated that magnesium supplementation decreases bone turnover in healthy men and oophorectomised rats suggest that magnesium may have a therapeutic use.

Urinary DPD and serum osteocalcin are widely used bone turnover markers and are appropriate for the monitoring of osteoporosis treatment. Increased serum osteocalcinlevels and urine DPD levels are strongly associated with rapid bone loss. Increase durinary DPD levels are associated with a two-fold increase in hip fracture risk. There are a multitude of studies that have shown that bone turnover markers decrease with antiresorptive therapies. Although urine DPD levels are increased in postmenopausal subjects compared to premenopausal women, they decrease following magnesium supplementation. This indicates the antiresorptive effect of magnesium in osteoporosis.

Compared to premenopausal women, serum osteocalcin levels are higher in postmenopausal women. This is probably due to the increase in bone turnover during the postmenopausal period. In this study, basal serum osteocalcin levels were high only in two postmenopausal patients (one in each group). Thirty days of oral magnesium supplementation increased serum osteocalcin levels significantly compared to baseline.

Similar results were reported in previous studies, indicating increased bone formation along with decreased resorption in response to magnesium supplementation.

These results are in contrast to the findings of Doyle et al who studied 26 healthy young adult females and showed that oral magnesium supplementation for 28 days had no effect on either biochemical markers of bone resorption (urinary pyridinoline and deoxypyridinoline) or bone formation (serum osteocalcin and bone-specific alkaline phosphatase).

Since bone turnover increases after menopause and both serum osteocalcin and urinary DPD levels are higher compared to the premenopausal period, magnesium supplementation may have no effect on bone turnover in premenopausal women. Furthermore, the dose of magnesium used in the Doyle study is lower than the doses used in other studies.

Hormone therapy or bisphosphonate treatment suppresses both bone formation and bone resorption in postmenopausal women whose bone turnovers are hyper activated. However, the results of this study indicate a decrease in bone resorption and an increase in bone formation. This indicates different mechanisms operating the actions of magnesium deficiency.

Similar results have been reported in various magnesium-depleted conditions. A number of potential mechanisms may contribute to resorptive effect of magnesium deficiency. First is the way of cytokines in which magnesium deficiency causes an increase in substance P production that stimulates monocytes over which causes an increase in TNF-α and IL-1β production that induce bone resorption. Secondly, reactive oxygen species especially oxy-radicals increase in magnesium depletion in that they stimulate osteoclasts directly. The postmenopausal period is a well-known state of magnesium depletion. Besides known factors such as estrogen deficiency, increase in bone resorption markers in postmenopausal period can be partly attributed to magnesium depletion. Theoretically, it is not surprising to expect a decrease in bone resorption with magnesium supplementation. Various studies on magnesium-depleted conditions demonstrate both a decrease in osteoblastic function and osteoblast number. Increase in bone formation markers can be possible.

Many population-based studies prove the beneficial effects of calcium in postmenopausal osteoporosis and a daily dose of 1000-1500mg calcium intake is essential in the treatment of osteoporosis. Although many studies mark the importance of magnesium in pathogenesis and treatment of osteoporosis, lack of large, community-based studies decreases its impact to be universal in the treatment of osteoporosis, as does calcium. The interesting question is whether magnesium is more than or as effective as calcium. The answer is unknown since there is no study comparing them.


Oral magnesium supplementation in postmenopausal osteoporotic women increases serum osteocalcin levels and decreases urinary deoxypyridinoline levels indicating a reduction in bone turnover. Although long-term studies are needed, the role of magnesium in the treatment and prophylaxis of osteoporosis cannot be overlooked.