Monday, July 14, 2014

Second Chances...Yes, it is Possible for Bone Health

2014 Northeast Champ: Olympic Distance Triathlon
Second chances in life don't just have to make them happen. When it comes to second chances in health, this can become a little more unpredictable but we still need to "make it happen." When I was diagnosed with severe osteoporosis 15 years ago I not only knew very little about the disease but I was also totally floored because I THOUGHT I was already doing pretty much everything right as far as eating and life style choices were concerned. So WHY would I have poor bone health?

After immersing myself in the study of osteoporosis I quickly realized that there was A LOT I could do to help myself. Now, 15 years later and 60 years old, I feel so much stronger, so much healthier. I'm thankful to have made that second chance happen. Winning the Northeast Championships in triathlon this weekend makes me thank my lucky stars that second chances are possible...but they don't come without work.

You can make it happen too! It is NOT too late. That second chance is there for the taking...but it won't wait until tomorrow. Start making that second chance happen TODAY!

Thursday, July 10, 2014

Osteoporosis: Bone Mineral Density (DXA) Exam vs Risk Factors

Clinical risk factors* for osteopenia and osteoporosis include:

   - Loss of height
   - Low body weight
   - Advanced age
   - Late age at menarche
   - Menopausal
   - Time since menopause
   - Smoking
   - Calcium intake
   - Alcohol intake
   - Medications
   - Inflammatory conditions
   - Prior fragility fracture

But: Risk factor assessment is NOT a substitute for having a bone mineral density examination (DXA). Research shows that 50% of patients with osteoporosis do not have risk factors and 50% of patients with risk factors do not have osteoporosis as per a DXA exam** (T score of -2.5 or worse).

So: Make sure you get a bone density examination (DXA)! Please do not rely on risk factors because they DO NOT predict your chances of having osteoporosis.

*Riggs B.L. and Melton L.J., NEJM. 1986;314:1676-1686.
**Delmas, P.D. et al. Impact Trial, JBMR. 2005; 20:557-563.

Tuesday, July 8, 2014

Exercise and Osteoporosis...Make it a Priority

As I was cruising to the finish line in a recent triathlon (finishing 1st in my age group [60-64] and 4th overall), a surge of great pleasure ran through me. "This is who I am...someone who uses his body to the max." I ABSOLUTELY love it. I love being an athlete. It really IS WHO I AM! The interesting byline here is that I also have--or at least HAD-- severe osteoporosis. I would be miserable if I couldn't train and compete hard.

That brought to mind a recent posting on an osteoporosis chat line where a woman wrote "I have advanced osteoporosis and it is an exercise limitation." She went on to explain that there were many things that she could not do because of her bone loss and increased fracture risk.

This not only saddened me but reminded me of the dreaded fear of "breaking" that the diagnosis of osteoporosis carries with it. My initial diagnosis at the age of 45 seems like eons ago. My T-score was -4.3 and I experienced a lot of fractures. The fear of ongoing fracturing was HUGE, but thankfully none of that seemed to stop me. The key here is that from the very beginning I was in a fighting mode. I never let the diagnosis stop me. I fought back. Of course most of you know by now that OsteoNaturals is the result of this fight and the ingredients in our products are what turned things around for me. I now have my bone health under control and, thankfully, OsteoNaturals has become an integral weapon for others in their fight to reclaim skeletal health. The really great thing is that these people are winning too.  Onward!

Thursday, July 3, 2014

More on Prolia (denosumab) for the Treatment of Osteoporosis

Back in 2012 I wrote a post on Prolia (denosumab), a drug that had recently been introduced for the treatment of osteoporosis. (I have included the article here in case you missed it and/or would like to refresh your memory as to how it works.) Prolia has proved to be effective for the treatment of osteoporosis but has three major drawbacks. One: once you start taking this medication you have to stay on it...forever. It has the unfortunate drawback of causing a rebound effect that actually increases a person's bone loss if they should discontinue its use. Two: there are quite a few adverse effects associated with Prolia, the most common ones being low blood calcium levels, back pain, muscle and bone pain, rashes, and painful urination. And three: Prolia is extremely expensive.

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 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. 

Over time, we have learned that there are adverse effects that need to be considered when using these medications. For instance, bisphosphonates have a high affinity for bone and are sequestered or held within calcium crystals, posing both beneficial and detrimental effects. Beneficial because bisphosphonates continue to suppress osteoclastic bone resorption long after a patient has discontinued their use. Detrimental because long-term suppression of osteoclasts can lead to low bone-turnover disorders such as osteonecrosis of the jaw and increased bone fragility with a heightened risk for atypical femur fractures. Stopping use of these drugs does nothing to help rectify these situations because of sequestered drug levels.
With new medication always comes new hope. 
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.)
Unlike bisphosphonates, denosumab is not sequestered in bone and therefore does not have the same long-lasting effects after treatment has been discontinued. However, even with such a short track record, we are already beginning to see that denosumab has a dark side with long-term use.  So hopes for denosumab, like all medications, must be kept in perspective. We need to use medications to our benefit, but always be aware that they can carry risks. Here is what we have so far:
  • 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.
According to a review article in Therapeutics and Clinical Risk Management by Anastasilakis et al., when denosumab is discontinued "bone markers rise to above pretreatment levels within 12 months." In other words, if you stop using denosumab you quickly loose the density that was accrued. Not only that, but you loose it at a rate faster than that seen before treatment was initiated. This "rebound," or hyper-increase-in-bone-loss effect, lasts for approximately two years. Clinical studies have not determined the full implications of this rebound effect but when a person elects to begin treatment with denosumab they probably shouldn't stop. Any "drug holiday," such as that which is becoming common after 3 to 5 years of bisphosphonate therapy, may actually escalate fracture risk to a level even higher than that which the individual had before denosumab treatment was initiated. 
Anastasilakis et al. concluded "denosumab is reasonably safe for all subgroups of patients with postmenopausal osteoporosis, with the exception of those with hepatic or stage 5 renal insufficiency. However, given the lack of pharmacovigilance data for this agent as yet and its brief post-marketing period, it would be prudent to be vigilant for adverse events related to the putative effect of RANKL inhibition in tissues other than bone, as well as those related to bone turnover oversuppression."
Bottom line:  Osteoporosis medication should be used only when absolutely necessary – when fracture risk is moderately or severely elevated.
Anastasilakis et al., 2012. Long-term treatment of osteoporosis: safety and efficacy appraisal of denosumab. Therapeutics and Clinical Risk Management, 8:295-306.
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