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Journal of Nutritional Medicine (1991) 2, 165-178


The Importance of Magnesium in the Management of Primary Postmenopausal Osteoporosis


Optimox Corporation, 2720 Monterey Street, Suite 406, Torrance, CA 90503, USA

Data are presented which support the theory that most cases of primary postmenopausal osteoporosis (PPMO) are not caused by calcium deficiency. The commonly applied therapy of continuous supplementation solely with large doses of calcium is unlikely, therefore, to be of help. It is furthermore suggested that magnesium deficiency has a significant role in PPMO: magnesium is involved in calcium metabolism and in the synthesis of vitamin D, and in maintaining bone integrity. The results of a clinical evaluation of a dietary programme involving magnesium supplementation are also presented.

Keywords: magnesium, osteoporosis, calcium, postmenopause, primary postmenopausal osteoporosis.


During the last National Institute of Health (NIH) Workshop on Osteoporosis, the panel of experts recommended that 1500 mg of calcium should be ingested daily by postmenopausal women to prevent bone loss from primary postmenopausal osteoporosis (PPMO) [1], reiterating advice by others since 1981 [2-5]. The bone loss occurring during the first decade following menopause is predominantly at the expense of the trabecular bone with 50% loss whereas only 5% of the cortical bone is lost during the same time interval [6]. Evidence has been presented that calcium supplements of 660-3000 mg per day had no significant effect on trabecular bone loss in postmenopausal women [7, 8], and caused hypercalcemia and hypercalciuria in 24% of women receiving 1000-3000 mg per day [9]. Presented here are data supporting the concept that PPMO in most cases is not caused by calcium deficiency, and that it is not preventable by calcium megadosing. Furthermore, data will be presented suggesting that magnesium deficiency plays an important role in PPMO and adequate magnesium intake and reserve may be the most efficient, safe and cost-effective approach to the prevention and management of PPMO.



The bone loss, without change in bone structure, of osteoporosis leads to high susceptibility to bone fracture [10, 11]. When it is caused by excess glucocorticoids [12], immobilization [13] or weightlessness [14, 15], it is termed secondary osteoporosis. When it develops in both sexes over 70 years of age, it is termed primary senile osteoporosis, and is characterized by loss of both cortical and trabecular bone. In postmenopausal women, it is termed primary postmenopausal osteoporosis (PPMO), which is characterized by radiologically manifest loss, predominantly of trabecular bone, occurring during the first decade after menopause [16, 17] (Fig. 1).

Guy Abraham Figure 1

Dietary Calcium and Magnesium Intakes, Possibly Related to Spontaneous PPMO

Although bones contain 99% of the total body calcium, (Table 1) there is a poor correlation between bone density and calcium intake [18-22]. The lowest hip fracture rates in postmenopausal women are found in populations with the lowest calcium intakes (400-500 mg per day) [23]. In premenopausal Caucasian women, lifetime calcium intakes averaging 500-800 mg per day was associated with optimal mass of both cortical and trabecular bone, that was not greater in those with calcium intakes above 800 mg per day [24]. During the first five years following menopause, calcium supplementation has no effect on either trabecular or cortical bone even when calcium intake from food was as low as 400 mg per day [25]. After five years postmenopause, calcium supplementation using 500 mg of the citrate salt has a positive effect on trabecular bone when intake of calcium from food was below 400 mg. This effect was not present when calcium carbonate was used.

Guy Abraham Table 1

Vegetarian postmenopausal women, who consume less calcium, but twice as much magnesium as omnivorous women [26, 27], have greater mean density of cortical bone [27, 29]. The difference is significant after the fifth decade of life [27], usually the first decade after menopause. When the bone mineral densities (BMD) of the hip, spine and forearm were correlated with the intake of 14 nutrients in 159 Caucasian women [30], no significant correlation was found between calcium intake and bone mass at any site. Zinc correlated positively to forearm BMD in premenopausal women only whereas, iron and magnesium were significant predictors of forearm BMD in pre menopausal and postmenopausal women. In many rural areas, cereals and potatoes provide more than 70% of the energy consumed [31]. These staple foods contain much more magnesium than calcium (Table 2), and can provide as much as 1000 mg per day of magnesium with consumption of 2000 kcal from these sources (almost four times more magnesium than the most recent recommended dietary allowance (RDA) for magnesium for women—280 mg per day [32]. Such a diet would provide less than 50% of the RDA for calcium.

In laboratory animals, experimental calcium deficiency induces osteomalacia [22], whereas magnesium deficiency induces osteoporosis [33].

Guy Abraham Table 2

Physiological Factors, Involving Magnesium, that Affect Calcium Metabolism and Bone Density

Magnesium, inadequacy of which is common in the occidental diet [26, 34, 35, 36], plays important roles in calcium metabolism, through its requirements for normal activity of the hormones controlling calcium utilization and for maintenance of normal bone structure.

Adequate magnesium intake and reserve is required for the synthesis of calcitriol, the active dihydroxy metabolite of vitamin D [37]. Magnesium deficiency causes abnormal calcium utilization, extending to hypocalcemia, by impairing parathyroid hormone (PTH) secretion, release and interfering with end-organ response to PTH [37-40]. This effect of magnesium on PTH secretion and action could be explained by the requirement of magnesium for the activity of adenylate cyclase in parathyroid tissue [41], kidney [42], and in bone [43].

Balance studies suggest that man can adapt to relatively low calcium intake by increasing its absorption and decreasing its renal excretion [44]. Decreasing the calcium intake from 1000 mg to 500 mg per day resulted in a negative calcium balance during the first months, but after eight months, the balance became positive [45]. The loss of calcium during this time was 8-10 g, which is less than 1% of total bone. The hormonal response to this adaptation mechanism was present one week after switching from 2000 to 300 mg per day calcium in nine normal women [46]. No efficient mechanism has been found for rapid adaptation to low magnesium intake [47].

Adaptation to low calcium intake entails synthesis of the hormone, 1,25-(OH)2D3 (calcitriol) [48], by ingestion of foods containing vitamin D3, or synthesizing it from a cholesterol derivative in the skin, by its 25-hydroxylation in the liver, and by its 1-alpha-hydroxylation to 1,25-(OH)2D3 (calcitriol) in the kidneys [48-50]. Decreased calcitriol levels have been reported in PPMO [51] and small doses of calcitriol normalize calcium absorption in PPMO [52]. The enzyme involved in the renal hydroxylation step, that activates vitamin D, is magnesium-dependent [37], and is inhibited by intramitochondrial accumulation of calcium and phosphate [48], which is magnesium-dependent [53]. Clinical evidence that magnesium deficiency, which is common in women with PPMO [54, 55], contributes to poor responsiveness to vitamin D has long been recognized with the therapeutic effect of vitamin D on intestinal calcium absorption and hypocalcemia being not fully achieved in the absence of adequate magnesium [56, 57].

Sodium intake induces urinary calcium losses [58, 59]. In young subjects, there is a compensatory mechanism which is magnesium-dependent that increases absorption of calcium by PTH-induced 1,25-(OH)2D3 synthesis [58]. This adaptation mechanism is impaired in postmenopausal women [59], probably due to magnesium deficiency.

Since potassium enhances 1-hydroxylation of 25-(OH)D3 [60], it is conceivable that potassium depletion could impair synthesis of 1,25-(OH)2D3 and predispose to PPMO. In cases of magnesium deficiency, the cells cannot retain potassium because of a defective potassium pump. In such cases, potassium supplementation will be ineffective unless magnesium deficiency is also corrected.

PTH and calcitonin (CT), the second and third hormones that play important roles in calcium metabolism and bone density [61], are also influenced by magnesium so as to inhibit calcium removal from bone, and deter its deposition in soft tissues. The major skeletal effect of PTH is to increase bone resorption by stimulating osteoclasts, thereby mobilizing bone calcium. It also favors soft tissue calcium uptake and phosphate renal excretion. CT conversely increases calcium deposition in bone matrix and blocks soft tissue calcium uptake.

Increased serum magnesium and serum ionized calcium stimulate CT and suppress PTH secretion. Hyperparathyroidism increases in frequency at and after the menopause [62, 63], and PPMO is more severe in hyperparathyroid than in hypoparathyroid women [64]. In most women with PPMO, however, PTH is the same or lower than in normal postmenopausal women 65-67]; CT is not lower [68]. Since serum magnesium is normal [69] or low [55], with evidence of low bone magnesium [54] in women with PPMO, but albumin-adjusted serum calcium is elevated [68], the pattern of PTH and CT in PPMO may reflect the elevated serum calcium resulting from bone mineral mobilization.

In premenopausal women, estrogens suppress the PTH-mediated mobilization of bone minerals. The protective effect of estrogen on bone may be explained by its inhibiting effects both on PTH release [70] and on PTH-demineralizing effect on bone [71, 72]. Serum and urine magnesium levels are higher in postmenopausal women than in premenopausal women; estrogen administration in postmenopausal women abolishes the change in serum and urine magnesium after the menopause [73, 74] probably by blocking mobilization of bone magnesium. Therefore another possible mechanism of estrogen action on bone is maintenance of bone magnesium reserve.

Although only 17% of total bone mass is trabecular bone [75], more than twice as much trabecular as cortical bone loss occurs during the decade after menopause; as much as half the trabecular bone is lost, versus 5% of cortical bone [6]. During that time, there is a sharp decrease in bone magnesium [76] whereas liver magnesium remains constant (Fig. 2). As indicated by serum and erythrocyte magnesium levels, it seems that in women with PPMO, mobilization of trabecular bone magnesium is insufficient to maintain blood and soft tissue magnesium levels [54, 55, 69]. In contrast to the depressed trabecular magnesium, bone calcium levels are normal [54].

Guy Abraham Figure 2



Because of its availability and low cost, calcium carbonate from oyster shell is the most commonly promoted calcium supplement [77]. However, it has a propensity for formation of uroliths [78] and interferes with iron absorption [and it has relatively poor bioavailability [79]. The citrate salt of calcium is less likely to cause urolithiasis [75], is more bioavailable [80], and because of its acidity is less likely to interfere with absorption of iron.

A recent prospective study suggests that moderately increased calcium intake may lower the incidence of hip fracture of senile osteoporotic patients [81]. However, when patients with severe PPMO were given massive doses of calcium, they developed positive calcium balance, but without radiographic evidence of improvement in the osteoporotic process [82, 83, 84]. Since experimental excess calcium has long been associated with soft tissue calcinosis, especially in the presence of magnesium deficiency [71], and high dosage calcium treatment of patients with osteopathies has interfered with magnesium retention [85, 86], megadosing PPMO patients with calcium may present a risk of abnormal calcium deposition [53]. As much as 10% of calcium in the elderly is extraskeletal [87].

Excess calcium may also predispose to luteal deficiency in premenopausal women, 1 mM calcium chloride having been found to decrease luteal hormone (LH) binding to the plasma membrane of the corpus luteum and causing luteolysis [88]. It also increases synthesis of prostaglandin F2x, which is luteolytic [88, 89]. There is no evidence that calcium supplementation in excess of 500 mg prevents or reverses PPMO [7, 8, 25]. For the above reasons, 500 mg of calcium in the form of citrate is recommended.

Vitamin D

High doses of vitamin D have caused soft tissue calcification in experimental animals, and have been implicated in renal and other comparable lesions in humans [71]. An extensive review of vitamin D intake in the USA has disclosed that the average American may unwittingly consume several thousand units of vitamin D from fortified foods [90]. This overdosage with vitamin D can increase the risk of soft tissue calcification from excess calcium. Since the depressed calcitriol levels of patients with PPMO have not been related to vitamin D deficiency, but to its decreased synthesis, contributed to by magnesium deficiency, there is no justification to administer more than the recommended daily dose of 400 IU of vitamin D to postmenopausal women.


Dalderup, in The Netherlands [91], was the first to suggest that magnesium supplementation might be beneficial in the management of osteoporosis, and warned against the risk of soft tissue calcification from excess calcium and vitamin D treatment. This is a particular problem for the American postmenopausal woman, whose vitamin D intake is likely to be high, who is urged to consume more calcium, and whose magnesium intake is likely to be low. Surveys have shown that 39% of American women between 15 and 50 years of age receive less than 70% of the RDA for magnesium (at 300 mg per day) [35, 36]. A review of the literature indicates that the magnesium content of the food supply in North America and Europe provides about 72-161 mg less than the 300 mg magnesium RDA [26]. The most recent US RDA is 280 mg per day. In the USSR, the magnesium RDA for women is 500-1250 mg, depending on physiological factors [92]. Since the US RDA is largely based on short-term balance studies, the most recent of which are in stress-free metabolic ward conditions (which decrease magnesium needs), the US RDA may reflect the minimum daily requirement, without allowance for increased needs of anabolism, nutrient and hormonal imbalances, and stress [93].

Low magnesium intake may increase vulnerability to PPMO [53]. The only three therapies of PPMO that show a significant and positive effect on trabecular bone are fluoride, 1,25-(OH)2D3 [94] and estrogens [7]. Fluoride increases the incorporation of magnesium in bone and the proper F+/Mg2+ ratio is important for bone integrity [95]. Side-effects and poor response to fluoride therapy may be due to magnesium deficiency. A recent study suggests that supplementation of the diet with 400-600 mg of magnesium daily reduced significantly (p < 0.0l) the side-effects of fluoride therapy in postmenopausal women with PPMO [96]. As previously discussed, synthesis of 1,25- (OH)2D3 is impaired in magnesium deficiency [37]. Estrogen increases bone uptake and retention of magnesium [71].

This author recommends supplementation of magnesium to reach a total daily intake of 1000 mg, and has supplemented the diet with up to 600 mg per day of magnesium as the oxide without gastrointestinal side effects or loose stools [97].

The above recommendations for magnesium should be part of a total dietary program since several nutrients besides magnesium and calcium are important for bone integrity and some of those nutrients have been reported to be lower in serum and bone of women with PPMO than normal controls [98]. Since food items high in magnesium are also high in these nutrients found to be important for bone integrity [99], a magnesium-emphasized dietary program would also increase the intake of micronutrients which are important for the well being and bone integrity of the postmenopausal woman.


The magnesium-emphasized program was implemented for six to 12 months in 19 postmenopausal women receiving hormonal replacement therapy. Seven postmenopausal women on hormonal replacement therapy served as controls. Trabecular bone density was assessed with single photon densitometry of the calcaneous bone with a 3% error [100].

The vertebral body contains 70%-80% trabecular bone [101] and the calcaneous bone is 95% trabecular [102]. Bone mineral density (BMD) of the spine correlates very well with calcaneous BMD [100]. For measuring rate of bone loss at a single site calcaneous BMD compares well to other techniques with regard to the relationship between reproducibility and the anticipated rate of change [103]. Ross et al. [100] found that calcaneous BMD correlates with fracture risk and calculated the fracture threshold at which the fracture risk doubles relative to premenopausal women. This fracture threshold was 0·32 g cm2.

Twenty-six postmenopausal women were recruited from a menopause clinic. All subjects were on hormonal replacement therapy, either estrogen alone in those with surgical menopause or cyclic progestogen superimposed on estrogen therapy in those with an intact uterus. All patients underwent BMD of the calcaneous bone with single photon absorptiometry, as described by Ross et al. [100], and were advised about the dietary program (Table 3). Micronutrients were supplied in the form of a complete multivitamin, multimineral supplement (Gynovite® Plus, Optimox Inc., Torrance, CA) containing 500 mg of calcium as the citrate salt and 600 mg of magnesium as the oxide (Table 4). Seven patients received dietary advice but chose not to take the supplement. Nineteen patients received dietary advice and ingested six tablets of the nutritional supplement daily. Therefore, the 19 patients received 50% of the recommended daily allowance (RDA) of calcium and 200% of the RDA of magnesium for women. In all 26 patients, BMD of the calcaneous bone was repeated at their return visit, 6-12 months later.

Guy Abraham Table 3

Guy Abraham Table 4

Comparing the two groups of patients, there was no significant difference in age, height, weight, years since menopause, duration of hormone therapy, baseline BMD or duration of follow-up (Table 5).

Guy Abraham Table 5

A non-significant increase of 0·7% in the mean BMD of the seven patients receiving hormonal therapy and dietary advice was observed as compared with a mean increase of 11% in the 19 women receiving the supplements (p < 0.01 by paired data analysis).

The effect of this magnesium-emphasized program on calcaneous bone density was 16 times greater than that of dietary advice alone in postmenopausal women on hormonal replacement therapy. Ross et al. [100] defines the spine fracture threshold as a BMD of 0·32 g cm-2 of the calcaneous bone. In 15 of the 19 women receiving the supplement the BMD was below the fracture threshold before treatment. Within a year after the program only seven patients had BMD values less than 0·32 g cm-2.

The positive effect of this magnesium-emphasized supplementation on the BMD was still present at two year follow-up (Fig. 3-5). Best results were obtained when this program was implemented soon after menopause. The results of this study suggest that the effect of the magnesium-emphasized total dietary program on calcaneous BMD is not short-term and temporary but long-term and persistent.

Guy Abraham Figure 3

Guy Abraham Figure 4

Guy Abraham Figure 5


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