Magnesium, Calcium and Osteoporosis


#7 Authors; Steidl L. Ditmar R.

Institution; Neurological Clinic, Palacky University, Olomouc, Czechoslovakia.

Title; Osteoporosis treated with magnesium lactate.

Source; Acta Universitatis Palackianae Olomucensis Facultatis Medicae. 129:99-106, 1991.


33 patients with senile, 18 patients with postmenopausal and 9 patients with medicamentous (corticosteroids) osteoporosis were treated with single therapy of Mg lactate (37 patients) and with the combined one of Mg lactate and Na fluoride (23 patients). They were evaluated in three periods of half a year, one year, two years. The better results were achieved with the single therapy than with the combined one and in the senile and postmenopausal osteoporosis than in the medicamentous one. Pain and restricted spine movement were influenced favorably. Kyphosis and x-ray findings were stabilized.


#8 Wallach is one of the earliest and the best of the best workers in the field.

Authors; Wallach S.

Institution; Medical Service, Veterans Administration Medical Center, Bay Pines, Fla.

Title; Effects of magnesium on skeletal metabolism. [Review] [107 refs]

Source; Magnesium & Trace Elements. 9(1):1-14, 1990.


Magnesium (Mg) makes up 0.5-1% of bone ash and is therefore not a trace element in the skeleton. Mg influences both mineral and matrix metabolism in bone by a combination of effects on hormones and other factors that regulate skeletal and mineral metabolism, and by direct effects on bone itself. The skeletal content of Mg is very variable both between and within species, and reported values range between 150 and 440 mmol/kg ash weight (AW). Dietary Mg has a direct influence and age an inverse influence on skeletal Mg content. It is unclear whether skeletal Mg content varies from region to region. In humans, reported values cluster around the 200 mmol/kg AW level, 30-40% lower than most rat data. Human iliac crest cortical bone has 10-20% less Mg per unit weight than iliac crest trabecular bone. Mg depletion adversely affects all phases of skeletal metabolism. In the rat, cessation of bone growth is noted with a decrease in both osteoblast and osteoblast activity, decreased bone formation, osteopenia, increased fragility and development of a form of ‘aplastic bone disease’. The epiphyseal growth plate is thinned and the percent ash weight of the growth plate is increased, possibly due to enhanced crystallization of bone salt under conditions of Mg depletion. In contrast, in chicks and in rats with severe Mg deficiency, these ‘antianabolic’ effects are not observed but instead, predominant inhibition of bone resorption occurs with increased cortical thickness rather than osteopenia, and \the occasional development of subperiosteal hyperplasia or of fibrous tumors of the periosteum. It is probable that this unusual response under conditions of severe Mg deficiency is in part an indirect effect secondary to a defect in secretion and/or skeletal responsiveness to parathyroid hormone (PTH) and vitamin D metabolites. Mg excess also has adverse biologic effects on bone. Crystallization of bone salt is severely impaired and an osteomalacia-like picture may be produced with decreased osteoblastic activity, widened growth plates, excessive osteoid seams and short, thickened bones. In some studies, especially in mice, Mg excess stimulates bone resorption, independently of PTH. The role of Mg deficiency and excess in human skeletal conditions requires more extensive investigation. Bone Mg is uniformly increased in renal insufficiency and may play a role in renal osteodystrophy since improvement has been noted in the osteomalacic component by normalizing the serum Mg. Decreased bone Mg has been reported in alcoholic patients, diabetes and in osteoporosis.(ABSTRACT TRUNCATED AT 400 WORDS) [References: 107]



Authors; Cohen L. Kitzes R.

Title; Infrared spectroscopy and magnesium content of bone mineral in osteoporotic women.

Source; Israel Journal of Medical Sciences. 17(12):1123-5, 1981 Dec.


Larger and more perfect crystals in bone mineral from osteoporotic women have been described using biophysical methods. In search of the cause of this change, both chemical analysis and infrared spectrophotometry were used on iliac crest bone biopsies from 19 postmenopausal osteoporotic women. These women had each had a vertebral crush fracture and had a urinary hydroxyproline: creatinine ratio greater than 0.012. Lower than normal trabecular bone magnesium content and larger and more perfect crystals in trabecular bone mineral identified on infrared spectrophotometry were found in 16 out

of the 19 women. Magnesium deficiency was confirmed by Thoren’s magnesium load test in this subgroup of 16. Higher than normal bone magnesium content and smaller and less perfect crystals in bone mineral were found in five postmenopausal uremic women tested.



Authors; Cohen L. Laor A. Kitzes R.

Title; Lymphocyte and bone magnesium in alcohol-associated osteoporosis.

Source; Magnesium. 4(2-3):148-52, 1985.


Serum, lymphocyte and bone magnesium concentrations were determined in 5 alcoholic patients in order to assess their total body magnesium status. Decreased values confirmed the existence of magnesium deficiency in chronic alcoholism. Spinal osteoporosis on X-rays, together with magnesium deficiency and decreased bone magnesium concentration in alcohol-associated osteoporosis match similar findings in involutional osteoporosis.



Authors; Cohen L.

Title; Recent data on magnesium and osteoporosis. [Review] [22 refs]

Source; Magnesium Research. 1(1-2):85-7, 1988 Jul., Scott Library subscribes; check Library holdings for details.


Larger and more perfect bone mineral crystals and decreased bone magnesium concentration were found in postmenopausal osteoporosis, senile osteoporosis, alcoholic osteoporosis and osteoporosis associated with thalassanemia. The decreased bone magnesium concentration and the increased retention of magnesium in the magnesium load test suggest magnesium deficiency in post-menopausal osteoporosis, probably caused by magnesium malabsorption. [References: 22]



Authors; Cohen L. Bitterman H. Froom P. Aghai E.

Title; Decreased bone magnesium in beta thalassemia with spinal osteoporosis.

Source; Magnesium. 5(1):43-6, 1986.


Low bone Mg concentration was found in a case of beta thalassemia associated with osteoporosis. In the absence of endocrine abnormalities and congestive heart failure, this low bone Mg suggests Mg depletion in uncomplicated beta thalassemia.



Authors;Lee SJ. Kanis JA.

Title; An association between osteoporosis and premenstrual symptoms and postmenopausal symptoms.

Source; Bone & Mineral. 24(2):127-34, 1994 Feb.


This study examined the relationship of premenstrual and postmenopausal symptoms with vertebral osteoporosis by means of a retrospective case control questionnaire in patients with vertebral osteoporosis and control patients. Seventy-five postmenopausal women aged 55-70 years with vertebral osteoporosis and 77 age-matched controls were interviewed at the outpatient clinics of the Royal Hallamshire Hospital, Sheffield, UK to establish the past history of premenstrual symptoms, and present and past history of postmenopausal vasomotor symptoms. The risk of vertebral osteoporosis was significantly greater in women with a history of premenstrual symptoms (RR = 1.86) or oligomenorrhea (absent of menses) (RR = 3.08). Significantly more patients with osteoporosis than controls recalled vasomotor symptoms at the time of the menopause (RR = 1.35). Patients were more likely than controls to describe their symptoms as severe (RR = 1.43) or persistent (RR = 2.19). We conclude that the relative risk of vertebral osteoporosis is increased in women with a history of premenstrual symptoms, irregular periods, and with severe and/or persistent menopausal vasomotor symptoms.

NOTE: While this one may be #13, it is probable the single most significant medical report of all of these, because of the untreated woman who has MgD induced PMS, which is ‘curable’, prevented with Mg and will most likely also prevent osteoporosis.



Clinical Diabetes 20:153-157, 2002

Title; Osteoporosis and Diabetes

Diane L. Chau, MD and Steven V. Edelman, MD

Osteoporosis is a bone condition defined by low bone mass, increased fragility, decreased bone quality, and an increased fracture risk.1 It is the most prevalent metabolic bone disease in the United States. Using World Health Organization (WHO) criteria, the third National Health and Nutrition Examination Survey (NHANES III, 1988–1991) reported that 34–50% of postmenopausal white women have osteopenia (T score –1–2.49) and ~17–20% have osteoporosis (T score <=–2.5).2 Both low bone mass conditions increase fracture risks, with osteoporosis having the greater impact, osteoporotic fractures to be $13.8 billion, an amount that is expected to double over the next 25 years because of the increasing elderly population. 3. Iindividuals of either sex and all ethnic groups.diagnosed with osteoporosis despite presenting with a fracture. Any fracture (unrelated to motor vehicle accidents) sustained between the ages of 20 and 50 years is associated with a 74% increase in the future risk of fractures after the age of 50 years.4 Thus, the true occurrence of osteoporosis may be significantly underestimated because many women who suffer minimal trauma fractures still are not being evaluated for osteoporosis. 5. The incidence of fractures increases with age, and this is associated with an increased mortality rate and an overall functional decline. During the first year following a hip fracture, the mortality rate is 36% for men and 21% for women. 6. In certain patient groups, such as those with psychiatric disorders, the mortality rate has been reported to be >50%. 7. If patients survive their fractures, they face greater risks of having a permanent disability and often require long-term nursing home care. The degree of recovery after a fracture is age- and disease-dependent. Those who are younger or healthier have better outcomes. Osteoporosis is a major public health problem because of its associated fractures. Thus, identifying and evaluating populations at increased risk of developing osteoporosis is critical to disease prevention and management. Although osteoporosis traditionally has not been listed as a complication of diabetes, patients with either type 1 or type 2 diabetes are among those at increased risk for this disease. In this article, we review this important relationship.

NOTE: There is a link between diabetes and Mg, there also must be a link between Mg, diabetes and Osteo. The following is a link to the complete article on line.



Authors; Basso LE. Ubbink JB. Delport R. Spies J. Vermaak WJ.

Title; Effect of magnesium supplementation on the fractional intestinal absorption of 45CaCl2 in women with a low erythrocyte magnesium concentration.

Source; Metabolism: Clinical & Experimental. 49(8):1092-6, 2000 Aug., Scott Library subscribes; check Library holdings for details.


The cosupplementation of magnesium with calcium has been suggested to be beneficial in the prevention of osteoporosis. We investigated the effect of magnesium supplementation on parameters of bone resorption and fractional 45Ca absorption. Twenty apparently healthy women with a mean age of 39.2 +/- 9.2 years and an erythrocyte magnesium concentration less than 1.97 mmol/L were recruited into a controlled magnesium supplementation trial. During weeks 1 to 4, they received a daily control preparation, potassium/sodium citrate malate (PSCM). During weeks 5 to 8, the subjects received magnesium citrate malate (MCM) equivalent to 250 mg magnesium per day. During the fourth and eighth weeks, blood was collected for measurement of the serum intact parathyroid hormone (PTH) concentration and serum and erythrocyte magnesium concentration. Urine was collected for measurement of calcium, magnesium, creatinine, and deoxypyridinoline excretion. On the final day of each treatment period, 5 microCi45CaCl2 was administered orally, and the isotope was traced in the blood and urine over 7 hours. Urinary calcium, 45Ca, and deoxypyridinoline excretion, as well as serum intact PTH levels, showed no statistically significant changes as a result of magnesium supplementation. However, urinary magnesium excretion increased by 31.1% (P < .005) while fractional 45Ca absorption decreased by 23.5% (P < .001) as a result of magnesium supplementation. It is concluded that magnesium supplementation does not result in changes in bone resorption, while the fractional intestinal absorption of 45Ca appears to decrease.



Authors; Haden ST. Glowacki J. Hurwitz S. Rosen C. LeBoff MS.

Institution; Endocrine-Hypertension Division, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School

Title; Effects of age on serum dehydroepiandrosterone sulfate, IGF-I, and IL-6 levels in women.

Source; Calcified Tissue International. 66(6):414-8, 2000 Jun., Scott Library subscribes; check Library holdings for details.


Data from animal and in vitro studies suggest that the growth-promoting effects of the adrenal androgen dehydroepiandrosterone sulfate (DHEAS) may be mediated by stimulation of insulin-like growth factor-I (IGF-I) and/or inhibition of interleukin 6 (IL-6), a cytokine mediator of bone resorption. This study tests the hypotheses that there are effects of age on serum DHEAS, IGF-I, and IL-6 levels, and that levels of IGF-I and IL-6 are related to DHEAS levels. The study included 102 women: 27 premenopausal and 75 postmenopausal, including 35 postmenopausal women with osteoporosis , as defined by bone mineral density scores by dual X-ray energy absorptiometry. DHEAS levels decreased significantly with age (r = -0.52, P < 0.0001) and IGF-I levels decreased significantly with age (r = -0.49, P < 0.0001). IL-6 levels increased significantly with age (r = 0.36, P = 0.008). IGF-I was positively correlated to DHEAS levels (r = 0.43, P < 0. 0001, n = 102) and IL-6 levels were negatively correlated to DHEAS levels (r = -0.32, P = 0.021, n = 54). Levels of DHEAS and IGF-I were correlated with T scores of the spine and some hip sites. In a multiple variable model to predict DHEAS, age was an important predictor (P < 0.001), but osteoporosis status, IGF-I, and IL-6 were not. The median DHEAS level was lower in the postmenopausal osteoporotic women (67 microg/dl, n = 35) than in the nonosteoporotic postmenopausal women (106.3 microg/dl, n = 40, P = 0. 03), but this was not significant after correction for age. Age accounted for 32% of the variance in DHEAS levels. In summary, DHEAS levels decreased with age and had a positive association with IGF-I levels and a negative association with IL-6 levels. DHEA deficiency may contribute to age-related bone loss through anabolic (IGF-I) and anti-osteolytic (IL-6) mechanisms.

NOTE; It is well established that IL-6 is released in magnesium deficiency. HCMJr



NOTE: Vit C and Osteoporosis a review

Authors;Schaafsma A. de Vries PJ. Saris WH.

Title; Delay of natural bone loss by higher intakes of specific minerals and vitamins.


For early prevention or inhibition of postmenopausal and age-related bone loss, nutritional interventions might be a first choice. For some vitamins and minerals an important role in bone metabolism is known or suggested. Calcium and vitamin D support bone mineral density and are basic components in most preventive strategies. Magnesium is involved in a number of activities supporting bone strength, preservation, and remodeling. Fluorine and strontium have bone-forming effects. However, high amounts of both elements may reduce bone strength. Boron is especially effective in case of vitamin D, magnesium, and potassium deficiency. Vitamin K is essential for the activation of osteocalcin. Vitamin C is an important stimulus for osteoblast-derived proteins. Increasing the recommended amounts (US RDA 1989), adequate intakes (US DRI 1997), or assumed normal intakes of mentioned food components may lead to a considerable reduction or even prevention of bone loss, especially in late postmenopausal women and the elderly. [References: 205]



Authors; Herzberg M. Lusky A. Blonder J. Frenkel Y.

Institution; Institute of Clinical Biochemistry, Chaim Sheba Medical Center, Tel Hashomer, Israel.

Title; The effect of estrogen replacement therapy on zinc in serum and urine.

Source; Obstetrics & Gynecology. 87(6):1035-40, 1996 Jun., Scott Library subscribes; check Library holdings for details.


OBJECTIVE: To ascertain the influence of estrogen replacement therapy (ERT) on blood and urinary zinc in postmenopausal women. METHODS: Thirty-seven postmenopausal women aged 53.2 +/- 3.7 years were examined. All were treated with conjugated estrogens 0.625 mg and medroxyprogesterone acetate 5 mg. Zinc, magnesium, calcium, phosphate, and alkaline phosphatase levels in blood were measured before and after 6 and 12 months of treatment. Urinary excretion of zinc, magnesium , calcium, phosphate, and hydroxyproline were evaluated before and after 3, 6, and 12 months of therapy. Bone mineral density was examined before treatment and after 1.7 +/- 0.3 years of ERT. Subjects were classified by 1) initial bone mineral density values (osteoporotics less than 0.850 g/cm2) and 2) zinc excretion as elevated (greater than 600 micrograms/g creatinine). RESULTS: At baseline, the values of most markers of bone turnover were higher in the osteoporotic women (Hotelling test, P = .06). After 1 year of treatment, a higher decrease of most indices was observed in the osteoporotic patients, and no statistical difference was found between the osteoporotic and the normal groups (Hotelling test, P = .31). A consistent negative association was observed between changes in bone mineral density and urinary zinc excretion in the osteoporosis group. Estrogen replacement therapy reduced excretion of zinc, magnesium, and hydroxyproline in the elevated zinc excretion group. Zinc excretion decreased 35% after 3 months and 26% after 1 year of treatment. The serum tests, with the exception of alkaline phosphatase, showed only negligible changes during ERT. A significant decrease in zinc excretion was observed after 3 months of ERT. This change was more pronounced in women with osteoporosis and elevated zinc excretion. Because zinc excretion is almost uninfluenced by variation in diet, it may be used as an additional marker of changes in bone metabolism.

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