Fracture Risk

“Osteoporosis and resultant fractures of the spine, hip and other sites are important public health problems with significant individual and societal costs. The risk for osteoporotic fracture is based upon low bone density and the presence of one or more clinical risk factors (see Table 1). A history of fracture during adulthood or falls are important clinical factors in determining the risk of future fracture; however, age is the most influential risk factor, such that middle-aged adults with other risk factors are likely to be at low absolute fracture risk in the medium term. Using these clinical risk factors and BMD when available, fracture risk assessment tools (based upon data collected from large prospective observational studies) have been developed to estimate the 5–10 year probability of hip fracture and other fractures in untreated patients. Clinicians should be aware that fracture risk can also be estimated using the FRAX or Garvan tools without BMD data. Chronic glucocorticoid use is an established risk factor for osteoporosis, with studies showing that use of glucocorticoids leads to accelerated bone loss and an increased risk of fracture. Other drugs are increasingly recognized as potential causes of bone loss and fracture, particularly amongst predisposed individuals….”

See the following link for more on other drugs that can cause bone loss and fractures:

http://strontiumforbones.blogspot.com/2015/01/adverse-skeletal-effects-of-drugs.html

Table 1.  Clinical risk factors for fracture

Advancing age

Previous fracture during adulthood

History of a fall or falls in the past 12 months

Glucocorticoid therapy

Parental history of hip fracture

Low body weight

Current cigarette smoking

Excessive alcohol consumption

Medical diseases (e.g. rheumatoid arthritis, hyperparathyroidism, coeliac disease, hypogonadism)

This introduction and table appeared in “Adverse Skeletal Effects of Drugs – Beyond Glucocorticoids,” Susannah O'Sullivan, Andrew Grey, Clin Endocrinol. 2015; 82(1):12-22. 

http://www.medscape.com/viewarticle/837369?src=wnl_edit_tpal&uac=127701PY

Adverse Skeletal Effects of Drugs

There is an expanding list of drugs for which there are concerns regarding adverse skeletal effects. The effect of long-term use of glucocorticoid drugs to cause accelerated bone loss and increase the risk of fracture is well recognized. For some drugs (TKIs, calcineurin inhibitors and loop diuretics), the available data are inconsistent and/or do not support a definite adverse skeletal effect. Patients receiving these drugs can be managed in line with guidelines for the general population (See table). Other drugs (SSRIs, antipsychotic drugs, AEDs and PPIs) do not seem to affect bone metabolism or BMD, but there is evidence for increased fracture risk. However, the evidence is limited to observational data, and any relationship may be attributable either to nonbone effects of the drug or effects of the underlying condition to increase fracture rate. In these patients, evaluation for other risk factors for fracture and management of these risk factors should be considered. In a third group (depot MPA, chemotherapy and ART), there is evidence for increased bone loss and/or fracture, but the patient population is generally at low risk for fracture. In these cases, patients may require an assessment of risk, but will rarely require specific treatment for fracture risk reduction. In the last group (aromatase inhibitors, GnRH agonists and thiazolidinediones), there is evidence of increased risk of bone loss and/or fracture, and the drugs are more frequently prescribed to individuals at higher baseline fracture risk. Patients receiving these drugs require risk assessment and those at high risk of fracture should receive alternative treatments (or "add-back" HRT in the case of GnRH agonists) or, if necessary, specific treatment for osteoporosis.

Table:  Summary of management recommendations
Example drugs	Evidence for risk	Management recommendations
Tyrosine kinase inhibitors    Calcineurin inhibitors    Loop diuretics	No adverse  skeletal effect  or data  inconsistent	Manage as per general population
Selective serotonin re-uptake inhibitors (SSRIs)    Antipsychotics    Anti-epileptic drugs    Proton pump inhibitors	Evidence for increased fracture risk but fracture risk seems to relate to nonbone effects of the drug or effects of the underlying condition	Evaluate for other risk factors for fracture and manage these risk factors
Depot medroxyprogesterone acetate    Chemotherapy    Antiretroviral therapy	Evidence for increased bone loss and/or  fracture, but low risk population	Assessment of fracture risk, but will rarely require specific treatment
Aromatase inhibitors    Gonadotrophin hormone-releasing hormone agonists    Thiazolidinediones	Evidence for increased risk of bone loss and/or fracture, and the drugs are more frequently prescribed to individuals at higher baseline fracture risk	Assessment of fracture risk and those at high risk should receive alternative treatments and/or specific treatment for osteoporosis.

 The conclusions and table are from a longer article, “Adverse Skeletal Effects of Drugs – Beyond Glucocorticoids,” by Susannah O'Sullivan and Andrew Grey, Clin Endocrinol. 2015;82(1):12-22. 

http://www.medscape.com/viewarticle/837369_1

My DXA Scan Results Look Great After Strontium Citrate

My first DXA scan was in May, 2007 (diagnosed with osteoporosis):

Spine from L1-L4 T-score -3.0

Left hip (total) T-score -2.2

Left femoral neck T-score -2.8

My second DXA scan was in July, 2009 (After 6 months on Fosamax once weekly and 18 months on strontium citrate, 680 mg strontium daily, still at osteoporosis, but scores improved):

Spine (total) T-score -2.7

Left hip (total) T-score -1.7

Left hip (neck) T-score -2.6

My third DXA scan was in August, 2013 (After 5 ½ years on strontium citrate, scan results were at the osteopenia stage; I was probably at the osteopenia stage before this, but I did not have a DXA scan in 2011):

Spine from L1-L4 T-score -1.6

Left hip (total) T-score -1.4

Left hip (neck) T-score -1.4

Osteopenia is defined as T-scores < -1.0 and -2.5.

Strontium Minerals Come from Mexico

Strontium (Sr) occurs in nature as mineral deposits of celestine (celestite) (strontium sulfate) and strontianite (strontium carbonate). Citric acid and citrate also occur in nature. The chelate strontium citrate (as provided in supplemental form) is made synthetically from strontium minerals and citrate.

http://www.jarrow.com/eMarketing/StrontiumFAQ_Dec9.pdf

Celestite is the most commonly used strontium mineral. The strontium compounds in the government report referenced below are strontium oxide, sr. hydroxide, sr. peroxide, sr. nitrate, and sr. carbonate.  

Import Sources (2009–12): Strontium minerals: Mexico, 100%. Strontium compounds: Mexico, 80%; Germany, 12%; China, 7%; and other, 1%. Total imports: Mexico, 87%; Germany, 8%; China, 4%; and other, 1%.

http://minerals.usgs.gov/minerals/pubs/commodity/strontium/mcs-2014-stron.pdf

One hundred percent (100 %) of the strontium minerals imported into the U.S. come from Mexico. None of the strontium minerals imported into the U.S. come from China.

Some time ago, I wrote to Doctor’s Best and asked if its Strontium Bone Maker, a product I take, comes from China. A representative from the company said, “No, our product is U.S.-made.”  Well, that answer was true to a point. Doctor’s Best probably buys strontium citrate from another company that imports celestite from Mexico to make strontium citrate in the U.S. I had to do a lot of sleuthing on the internet to find this information.

I keep hearing from people concerned that the strontium they take, or are considering taking, comes from China. I’ve also read posts on osteoporosis forums from so-called “experts” who keep repeating false information about strontium coming from China. For these reasons, I decided to post this information, citing a U.S. government publication for import sources.

It would be possible for a company to import strontium compounds (sr. carbonate, sr. nitrate) manufactured in China and then make sr. citrate from those, but it is unlikely when the mineral, celestite (strontium sulfate), is available from Mexico. A mine in China is believed to be the only developed strontianite deposit in the world per Hong, Wei, 1993, Celestite & strontianite—Review of ore processing and exploration: Industrial Minerals, no. 309, June, p. 55, as cited in “Strontium” by Joyce A. Ober.

http://minerals.usgs.gov/minerals/pubs/commodity/strontium/850400.pdf

As already stated, the U.S. is not importing strontium minerals from China.

Other than the natural occurrence as mineral, strontium carbonate is prepared synthetically in one of two manners. First of which is from naturally occurring celestine also known as strontium sulfate (SrSO₄) or by using soluble strontium salts by the reaction in solution with a soluble carbonate salt (usually sodium or ammonium carbonates). For example if sodium carbonate was used in solution with strontium nitrate:

Sr(NO₃)_{2 (aq)} + Na₂CO_{3 (aq)} → SrCO_{3 (s)} + 2 NaNO_{3 (aq)}.

http://en.wikipedia.org/wiki/Strontium_carbonate

 

Since 100% of the strontium minerals imported into the U.S. come from Mexico, and only 7% of the strontium compounds come from China, there is only a small chance the strontium in your strontium citrate supplement came from China.