The reason why Prolia works is that it interferes with the inflammatory cascade involving the protein
RANKL, a key signaling molecule that promotes osteoclastic bone resorption. Except in desperate situations (which are rare), I have never understood why anyone would choose to go on this medication especially when there are ways to reduce RANKL naturally. For example (and this is the BEST example you are going to find), our OsteoNaturals product OsteoStim has been formulated to help reduce RANKL and normalize the bone remodeling cycle (plus there are no side effects and it is inexpensive). OsteoStim includes therapeutic amounts of alpha-lipoic acid, berberine, and milk thistle that have been shown to help balance RANKL signaling and reduce osteoclast bone resorption. It also contains vitamin D to increase calcium absorption, vitamin K2 (MK4 and MK7) to promote bone crystal formation, and milk basic protein and N-acetyl cysteine to promote osteoblast bone formation.
If you ask any doctor how they can tell if Prolia is working to reduce fracture risk, they will tell you that on repeat testing of bone resorption markers (NTX, CTX or DPD) (for more info on these test please check out page 34 in my book, The Whole Body Approach to Osteoporosis) there will be a drop in the amount of bone-collagen cross-links after antiresorptive treatment is initiated. This is standard for monitoring the effectiveness of bisphosphonates or Prolia in the treatment of osteoporosis patients.
I use similar monitoring when I recommend OsteoStim to my patients with bone loss. I get a baseline NTX, CTX or DPD (you don’t have to get all three…one is suffice) and then after four months of being on OsteoStim, plus a calcium/magnesium supplement (for example our OsteoSustain and/or OsteoMineralBoost), and improving the person’s diet (lots of fruits and vegetables) and implementing an exercise program, we repeat the test. Time and time again I find that we can avoid the pitfalls of taking harsh medications such as Prolia. OsteoStim helps to normalize bone remodeling and this is reflected in the lowering of bone resorption markers on repeat testing. Also, by implementing a whole treatment program that emphasizes diet and life-style changes, the person feels WAY better! To me, it just makes total sense to try this more natural approach BEFORE resorting to drug therapy.
Here is my prior blog on Prolia:
For more than 10 years, the use of bisphosphonate therapy has been the “osteoporosis treatment of choice” when medication is absolutely necessary. You have likely heard of the names alendronate (Fosamax®), residronate (Actonel®), ibandronate (Boniva®), and the most recent zoledronic acid (Reclast® approved in 2007). When the bone remodeling process has gone awry due to to chronic systemic inflammation, too much resorptive activity (bone degrading) by osteoclasts and too little bone formation by osteoblasts create the perfect storm for osteoporosis. When bisphosphonates are used for therapy, they eliminate existing osteoclasts, thereby slowing bone loss and improving bone density.
Denosumab (Prolia®) was introduced for the treatment of osteoporosis in 2010, two years ago. Like bisphosphonates, this new medication limits the bone degrading activity of osteoclasts, but it uses a different mechanism. Denosumab is an antibody to RANKL, a natural signaling molecule in the body. When produced in normal amounts RANKL keeps the immune and skeletal systems functioning normally. But in excess (seen when the immune system gets out of balance), RANKL can cause havoc, spilling into the bone marrow and hyper-stimulating osteoclast cell formation/activation. Over time, this hyper-stimulation of osteoclastic bone resorption leads to osteoporosis. Being an antibody to RANKL, denosumab prevents bone loss by grabbing RANKL, neutralizing it, and preventing it from activating osteoclasts. (Note: If you want to learn more about RANKL and its involvement in bone loss, I give a more in-depth explanation in my book, The Whole-Body Approach to Osteoporosis.)
- Denosumab is administered subcutaneously every 6 months (better than having to take bisphosphonates orally or through infusions).
- It works. Osteoclastic bone resorption is profoundly suppressed by denosumab and results in similar increases in bone mineral density when compared to bisphosphonates. (Spine: 3% 5% after 1 year; 6% to 7% after two years; 8% to 10% after 3 years, 13% after 5 years) ( Hip: 1% to 3% after 1 year, 3% to 5% after 2 years, 5% to 6% after 3 years, 7% after 5 years)
- Denosumab significantly reduces vertebral and nonvertebral fractures (similar to the rates of bisphosphonates).
- Effective in patients with impaired kidney function.
- Denosumab may disturb immune function and increase susceptibility to infections although in a two-year extension of the FREEDOM trial (a total treatment duration of seven years) researchers did not see an increase in infectious events.
- There are concerns that denosumab may increase the risks of cancer. Anastasilakis et al. state, “numerically more cases of neoplasms, including those of the breast, ovary and gastrointestinal tract, have been reported.” But since other trials have “failed to detect a statistically significant difference” with denosumab use compared to placebo, “long-term use of denosumab in a large post-marketing base would clarify this putative risk.”
- There is a significant risk of developing cutaneous allergic and inflammatory hypersensitivity skin reactions including eczema, dermatitis, and rashes.
- There is a significant risk (7%) of developing high blood cholesterol levels.
- Possible increased risk of vascular calcification and cardiovascular disease.
- Increased risk for low blood calcium (hypocalcemia).
- Because denosumab is such a potent suppressor of osteoclastic bone resorption and bone remodeling in general, it carries similar concerns of “frozen bone” types of adverse effects as the bisphosphonates. Atypical fractures of the femur and osteonecrosis of the jaw are of concern. In fact, Health Canada has just released a health advisory alerting the public of the association of Prolia with the increased risk of atypical femoral fractures.