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Bone Health

Bone fractures in people over fifty years of age cause significant disability, not only temporarily during the period of healing, but also over the long term – many people never regain their prior level of function following a fracture.  There is also a two- to four- fold increased risk of death in people over 50 with fractures.  Prevention of fractures is therefore important in increasing longevity and promoting healthy aging.

Bone is a dynamic structure, constantly being remodeled by cells that remove it (resorption by osteoclasts) and renew it (formation by osteoblasts).  In childhood the latter process predominates to support skeletal growth.  Once adulthood is reached, these two processes achieve relative balance, but over time the removal process typically predominates, particularly as hormone production declines around mid-life.  Predominance of resorption results in low bone mineralization and low bone density on DXA scanning, a diagnostic procedure in which the penetration through bone of a pair of xray beams is assessed.  DXA scans yield measurements of bone density, with results characterized as normal, low (osteopenia), or severely low (osteoporosis).  These results are used to predict fracture risk.

Although DXA scanning is the best method we have to predict fracture risk, it has a number of limitations:

As a result, only about half of fractures in women and one quarter of fractures in men over the age of fifty are associated with low bone density.  Better predictions can be made by entering information into the online calculator (FRAX) that has been developed to include a variety of historical factors into the prediction algorithm.

It is common for patients to undergo DXA scanning, be told that their bone density is low, or that it is declining based on serial scans, and that as a result prescription medications are recommended to reverse the process of bone loss.  Although for some patients this may be appropriate – as when the risk of fracture is very high – for others it may not be for several reasons:

It is common for patients with low bone density to look for a non-medication approach to reducing fracture risk.  There are some studies that show that a couple of mineral supplementation regimens increase bone density, and in the past we have recommended nutrient supplementation with magnesium, calcium, Vitamin K2, Vitamin D3, strontium citrate, boron, and melatonin.  Of these, only three nutrients have been shown to not simply improve bone density but also to reduce the incidence of fractures; when used in combination, the reduction in vertebral fractures is as much as 60% and non-vertebral fractures by as much as 76%:

The role of strontium has been controversial.  In Europe, strontium ranelate is approved for treatment of osteoporosis, but in the US it has not been approved as it has potential for adverse cardiovascular effects. Instead, strontium citrate—which has not been associated with cardiovascular risk—has been recommended at a dose of 680 mg per day (taken hours apart from other mineral supplements).  Although the citrate form has been shown to increase bone density, there are no controlled studies showing its impact on fracture incidence.  Strontium has both weak anti-resorptive (bisphosphonate-like) and stronger bone formative (PTH/Forteo-like) effects.

In addition to nutrient supplementation, several other interventions are important in reducing fracture occurrence:

Given the limitations of bone density screening, and the fact that it is recommended only at two year intervals, there has been interest in using blood testing to assess the balance of bone resorption and bone formation in between DXAs.  Two tests are currently used for that purpose – the C Telopeptide (CTP) which is a resorption marker and the procollagen type 1 N-propeptide (P1NP) which is a formation marker.  The use of these tests has not been studied as an adjunct to treatment to reduce fracture incidence.

Helpful resources are:

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