A recent University of Michigan study has revealed ground-breaking news about the bone-destroying nature of bisphosphonates, the most commonly prescribed class of osteoporosis drugs. The research uncovers the mechanism by which bisphosphonates weaken the femoral neck, leading to atypical femur fractures.
Why isn’t this news being shouted from the rooftops? Shamefully, this study was covered up, never published in any of the major journals, and only revealed within the confines of the Orthopedic Research Society’s 2013 meeting.
Today, we’re going to analyze what the study reveals, and why it was covered up.
Atypical Femur Fractures: A Closer Look
An atypical femoral fracture is just that – not typical. It’s an unusual type of fracture that is characterized by the following features:
- Lack of traumatic injury (atypical fractures are spontaneous)
- Pain in the groin or thigh preceding the fracture
- Fracture is located in the femoral shaft or “subtrochanteric” (below the trochanter of the thigh bone)
- Cortical thickening
- Fracture is transverse, short oblique, or noncomminuted (typical femur fractures are spiral, comminuted, and other forms)
- Delayed healing
- History of bisphosphonate use1
This last point is notable – a history of bisphosphonate use is included in the official characteristics that define an atypical femur fracture.
The Connection Between Bisphosphonates And Femoral Fractures
For years, researchers have been exploring the apparent connection between long-term bisphosphonate use and the occurrence of atypical femoral fractures.
In 2010, a task force reported that:
“…recent observations suggest that the risk [of atypical femoral fractures] rises with increasing duration of exposure, and there is concern that lack of awareness and underreporting may mask the true incidence of the problem.”2
And a 2012 study entitled, “Increasing Occurrence of Atypical Femoral Fractures Associated With Bisphosphonate Use” begins with this background statement:
“Current evidence suggests that there is an association between bisphosphonate therapy and atypical femoral fractures, but the extent of this risk remains unclear.”3
The study, which was published in the prestigious Archives of Internal Medicine Journal, which forms part of the JAMA network, concludes that:
“Atypical femoral fractures were associated with bisphosphonate use; longer duration of treatment resulted in augmented risk. The incidence of atypical fractures increased over a 12-year period, but the absolute number of such fractures is very small.”3
Notice the caveat that the “absolute number” of such fractures is small, which deflects from the point entirely. The point is that drugs intended to make bones stronger have the opposite effect, and the longer they are used, the greater the chance that those deleterious effects will actualize.
Another comprehensive review of atypical femoral fractures noted that:
“…current epidemiologic evidence suggests that long-term bisphosphonate use may be an important risk factor for atypical fractures. Long-term bisphosphonate users must be monitored for biochemical markers of bone turnover and evidence of stress fractures in the proximal femur.”1
While this report gets closer to directly implicating bisphosphonate use with atypical femoral fractures, like other studies, reviews, and reports, the information remains vague, sprinkled with caveats like the one above, or language about how bisphosphonate use “has been shown to increase bone mineral density and to reduce…fracture risk.”3
All of these studies failed to uncover the mechanism by which bisphosphonates set the stage for fractures. Even more disturbing, some research ignores what should be a logical conclusion, deflecting the direction of the evidence away from the mechanism by which bisphosphonates increase fracture risk.
For example, a meta-analysis, first published online in 2014, that explored the “increasing occurrence of atypical femoral fractures associated with bisphosphonate use” lays out the mechanism by which alendronate (Fosamax) “works”:
“ALN [alendronate] belongs to the third generation of bisphosphonate drugs that could inhibit the activity of osteoclasts by physicochemically combining with the bone matrix and subsequently blocking the action of osteoclasts by inducing the secretion of a variety of cytokines.”4
Taken to its logical conclusion, and coupled with a rudimentary understanding of how natural bone remodeling works, one can easily see how this cellular manipulation could result in weakened bone and increased fracture risk. The analysis goes on to note that slightly more than 82% of atypical fracture sufferers had been treated with bisphosphonates, yet concludes that:
“…this meta-analysis suggests that patients undergoing long-term treatment using ALN may be at an increased risk of AFF [atypical femoral fractures].”4 (emphasis mine)
Vague language like this gives the Medical Establishment leeway to continue prescribing these drugs; after all, it’s easy to ignore inconclusive evidence and instead blame the patient’s genetics or other factors when atypical femur fractures occur during bisphosphonate therapy.
For instance, a recently-published Japanese study goes to great lengths to point out the characteristics of those who suffer atypical fractures of the femur. Despite language clearly implicating the mechanism by which bisphosphonates weaken bone, the researchers still side-stepped the obvious conclusion.
“A reduction of the bone turnover by BP [bisphosphonate] treatment alters the bone mineral and matrix properties… BP therapy causes an increase in advanced glycation end products of the extracellular bone matrix, deteriorating the mechanical properties of the bone. …Prolonged BP therapy causes the accumulation of microdamage to bone and reduces the heterogeneity of the organic matrix and mineral properties.”5
Despite this evidence, the study then devotes a significant segment to an analysis of “Femoral geometry and biomechanical considerations of the lower limb” as risk factors for atypical fractures.5 It’s always easier to blame the patient.
Nonetheless, despite excuses and vague language, it’s getting harder and harder to cover up the evidence and minimize the risk associated with bisphosphonates that these studies reveal. Hence the push for new osteoporosis drugs to replace bisphosphonates.
Finally, an unflinching study was discovered that doesn’t side-step obvious conclusions, but instead observed the action of bisphosphonates on bone on the cellular level.
Revealed: The Mechanism Behind Bisphosphonate-Induced Bone Weakness
That’s where the revealing University of Michigan study comes in. While other research has hinted at the possibility of bisphosphonates causing atypical femoral fractures, this study analyzed just how bisphosphonates weaken bones on a cellular level.
The researchers in this study set out to find “the association between bisphosphonate therapy and atypical, low-energy subtrochanteric femoral fractures.”6
Their hypothesis was that:
“…microcracks and their surrounding osteocyte lacunae are particularly prone to direct bisphosphonate binding.”6
Lacunae are small, round cavities in cortical bone formed during the resorption phase of bone remodeling. Within these cavities are osteocytes, which form into bone cells that correspond with the type of bone (cortical bone cells, for instance, are more elongated in shape than trabecular bone cells).
Osteocytes mature and differentiate into various forms, with some ending the bone remodeling cycle as osteoblasts (bone-building cells) that are incorporated into the bone matrix. It’s important to bear this in mind as we look at the following study.
Testing The Hypothesis
To test the hypothesis noted above (“microcracks and their surrounding osteocyte lacunae are particularly prone to direct bisphosphonate binding”), researchers studied the forearms of mice. After undergoing cyclic loading, the mice were given the bisphosphonate pamidronate, in the form of Osteosense (far-red fluorescent pamidronate, or FRFP). After 24 hours’ recovery, the mice were euthanized and the bone cells of their forearms analyzed, with particular attention paid to areas of microdamage.
They found that:
“…bisphosphonates may interfere with targeted microdamage repair directly by binding to microcrack surfaces and interfering with osteoclast repair at the site that needs it the most.”6 (emphasis mine)
What’s more, bisphosphonates were found to interfere with the body’s targeted bone repair indirectly by “surrounding osteocyte lacunae” and thus interfering with a specific signal, called the apoptotic signal, by which the body induces targeted remodeling.6
In other words, bisphosphonates directly inhibit the body’s process of repairing microdamage that occurs with normal bone remodeling and everyday movement and exercise.
This explains why the longer the bisphosphonate use, the greater the risk of atypical fractures – bisphosphonates allow bone-weakening microdamage to accumulate, unchecked by the body’s natural repair mechanisms.
Given the ground-breaking nature of this discovery, it would make sense for bisphosphonates to be pulled from the market. But instead, studies not-so-coincidentally published in 2013 recommend a “bisphosphonate drug holiday” and tailoring the duration of bisphosphonate treatment to the individual patient.7, 8
Meanwhile the University of Michigan study presented at the 2013 Orthopedic Research Society meeting has since remained within its own confines, unpublished by any major scientific or medical journal.
Why The Cover-Up?
The answer is that it all comes down to a disturbing collaboration between the Medical Establishment and Big Pharma…all in the interest of protecting the blockbuster drugs – and the billions of dollars they generate to Big Pharma. There are a few exceptions, but the vast majority of scientists are afraid to present research that might undermine Big Pharma’s massive profits.
The good news is such information is getting harder to cover up. While the Medical Establishment and Big Pharma continue their desperate search for a non-bisphosphonate alternative drug, here at the Save Institute, we’re continuing to do our part to inform and empower as many people as possible with the truth about osteoporosis drugs.
And the truth is that there are many evidence-backed reasons to avoid osteoporosis drugs. The Osteoporosis Reversal Program is a safe, drug-free alternative to increasing bone density and boosting the body’s natural bone repair, instead of impairing it as osteoporosis drugs do.
Stop Worrying About Your Bone Loss
Join thousands of Savers from around the world who have reversed or prevented their bone loss naturally and scientifically with the Osteoporosis Reversal Program.
The Program explains exactly which nutrients your bones need (Foundation Supplements) and the foods that contain them (Foundation Foods), and why. It also explains the importance of a pH-balanced diet, of exercise in maintaining and building bone, delves into the benefits of stress relief in rejuvenating bone, and much more.
As you can see, the Osteoporosis Reversal Program is a comprehensive lifestyle and nutritional plan to show you how to build your bones without dangerous and toxic osteoporosis drugs.
Now you have yet another weapon in your fight against osteoporosis: the truth!
Till next time,
1 Donnelly, Eve, et al. “Atypical Femoral Fractures: Epidemiology, Etiology, and Patient Management.” Curr Opin Support Palliat Care. 6. 3. (2012): 348-354. Web. April 30, 2016. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4556525/
2 Shane, E., et al. “Atypical subtrochanteric and diapheseal femoral fractures: report of a task force of the American Society for Bone and Mineral Research.” J Bone Miner Res. 25. 11. (2010): 2267-94. Doi: 10.1002/jbmr.253. Web. April 30, 2016. https://www.ncbi.nlm.nih.gov/pubmed/20842676
3 Meier, Raphael, P.H., M.D., et al. “Increasinng Occurrence of Atypical Femoral Fractures Associated With Bisphosphonate Use.” Arch Intern Med. 172. 12. (2012): 930-936. Web. April 30, 2016. Web. https://archinte.jamanetwork.com/article.aspx?articleid=1160667
4 Liu, Lu, et al. “Association between alendronate and atypical femur fractures: a meta-analysis.” 4. Z. (2015): 58-64. Doi: 10.1530/EC-14-0120. Web. April 30, 2016. https://www.endocrineconnections.com/content/4/1/58.full
5 Saita, Yoshitomo, Ishijima, Mueaki, and Kaneko, Kazuo. “Atypical femoral fractures and bisphosphonate use: current evidence and clinical implications.” Ther Adv Chronic Dis. 6. 4. (2015): 185-193. Web. April 30, 2016. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4480549/
6 Davis, M.S., et al. “Visualization of bisphosphonate binding to bone microcracks and surrounding osteocyte lacunae using near-infrared optical imaging.” University of Michigan. 2013. https://www.ors.org/Transactions/59/007/0042.html
7 Diab, D.L., et al. “Bisphosphonate drug holiday: who, when and how long.” Ther Adv Musculoskelet Dis. 2013 Jun; 5(3): 107–111. doi: 10.1177/1759720X13477714
8 Ro, C. MD et al. “Bisphosphonate drug holiday: chosing appropriate candidates.” Curr Osteoporos Rep. 2013 Mar; 11(1): 45–51.doi: 10.1007/s11914-012-0129-9