Written by Jessica Patella, ND. Of the 20 participating menopausal women, those who took magnesium citrate for 30 days had a significant 43.7% increase in osteocalcin, an indicator of bone formation. 

Osteoporosis is a disease where weakening of the bones leads to reduced bone strength and an increased risk for fracture (1). Osteoporosis is a major public health concern because 55% of Americans over the age of 50 have been diagnosed with osteoporosis and 24% of those, that fracture a hip, will die within one year (1, 2). Natural supplementation with magnesium has been shown to increase bone mineral density in osteoporosis. Recent research examined how magnesium improved bone density (3).

The research included 20 postmenopausal women with osteoporosis. The women were randomly assigned to one of two groups. The magnesium group (n=10) received a daily dose of 1,830 mg magnesium citrate (contains 290 mg elemental magnesium) for 30-days, while the control group (n=10) was not given any supplementation or placebo (2). The women in the magnesium group took the magnesium 2 hours away from eating food, to avoid any interference of magnesium absorption by food.

Blood levels of osteocalcin are used to measure bone turnover and monitor osteoporosis. Increased levels of osteocalcin are associated with increased bone formation (3, 4). After the 30-day trial, blood levels of osteocalcin increased by 43.7% in the magnesium supplemented group and decreased by 5.0% in the unsupplemented group (p<0.001). These findings indicate increased bone formation with magnesium supplementation (3).

Urinary levels of deoxypyridinoline (DPD) are also used to monitor osteoporosis and bone breakdown. Increased urinary DPD levels are associated with an increase in hip fracture risk (5). After the 30-day trial, the urinary levels of DPD decreased significantly by 40.5% in the magnesium supplemented group (p<0.05) and did not change significantly in the unsupplemented group (3).

Blood levels of intact parathyroid hormone (iPTH) increase when calcium is too low and therefore is a regulator in bone and mineral metabolism. Blood levels of iPTH decreased significantly by 32.1% in the magnesium-supplemented group (p<0.05) and did not change significantly in the unsupplemented group (3). This decrease indicates a decrease in bone loss (3).

Interestingly, the results of the study show magnesium both decreased bone loss and increased bone formation. While, hormone therapy and bisphosphonate* treatments decrease both bone formation and bone loss (3,6).

In this study, oral magnesium in postmenopausal women was associated with decreases bone loss and increases bone formation. This was the first study of its kind to show magnesium supplementation, was associated with increases osteocalcin levels and decreases DPD and iPTH levels, indicating reduction in bone loss.

Source: Aydın, Hasan, et al. “Short-term oral magnesium supplementation suppresses bone turnover in postmenopausal osteoporotic women.” Biological trace element research 133.2 (2010): 136-143.

© Humana Press Inc. 2009,  © 2017 Springer International Publishing AG. Part of Springer Nature.

Posted December 22, 2011. mk/r

*Bisphonate-A member of a class of drugs that prevents bone decomposition.

References:

  1. Plawecki K and Chapman-Novakofski K.  Bone Health Nutrition Issues in Aging. Nutrients 2010, 2, 1086-1105; doi:10.3390/nu2111086.
  2. Osteoporosis Fast Facts.  National Osteoporosis Foundation website.
  3. Aydin H, et al. Short-term Oral Magnesium Supplementation Suppresses Bone Turnover in Postmenopausal Osteoporotic Women.  Biol Trace Elem Res (2010) 133: 136-143.
  4. Delmas PD.  Biochemical markers of bone turnover.  J Bone Miner Res 1993 8S: 549-555.
  5. Chapurlat RD, et al.  Serum estradiol and sex hormone binding globulin and the risk of hip fracture. 2000 J Bone Miner Res 15 (9): 1835-41.
  6. Clifford RJ, et al. The predictive value of biochemical markers of bone turnover for bone mineral density in early postmenopausal women treated with hormone replacement or calcium supplementation.1997 J Clin Endo Metab 82 (6):1904-10.
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