Alpha-Lipoic Acid Lowers Oxidative Stress and Bone Loss

Bone loss often begins in our late 30’s. This is long before a woman looses most of her estrogen at menopause or a man begins to decline in testosterone levels at andropause. So what gives? Both estrogen and testosterone ARE important for bone health but there must be something else going on if bone loss begins before these hormones begin to decline. And you are right, there is. It is called oxidative stress (OS).

The term OS is used to define the unhealthy state in the body where it is unable to neutralize free radicals such as reactive oxygen species (ROS). In other words, when it is being overrun by free radicals. Without adequate antioxidant mechanisms to neutralize ROS, progressive cellular damage results and the body is placed at a much greater risk for disease.

Normally, the body can adequately neutralize ROS. But pollution, heavy metal toxicity, chronic physiological stress, and gastrointestinal dysfunction can, and often does, place the body into overwhelming oxidative stress.

For bone, this can lead to insufficient production of bone-forming osteoblasts and the hyper-stimulation of bone-degrading osteoclasts. Oxidative stress, therefore, is a critical contributor to accelerated aging of bone and muscle.

In 2007 Grassi, et al., reported that there is a rise in ROS in bone marrow when estrogen levels are low. This excess ROS increases white blood cell and T cell activity fivefold. The T cells then begin releasing copious amounts of RANKL, the potent signaling molecule that stimulates the formation and activation of osteoclasts. This is why we see a dramatic rise in bone loss for at least 5 years past menopause.

So how can women and men reduce their risk of osteoporosis during these critical years? One way is by neutralizing excess ROS production by eating a healthy vegetable-rich low-inflammatory diet. Another is to supplement with antioxidants such as alpha-lipoic acid (ALA). (Our OsteoStim contains 300 mg ALA.) ALA protects against oxidative damage and since it is both water and fat soluble it is capable of going EVERYWHERE in the body. This is important because it can get into the fat-infiltrated bone marrow we often see in osteoporotic individuals. ALA can also help decrease excess blood glucose levels (a risk factor for increased fracture risk) and it is an essential cofactor for mitochondrial activity and energy production.

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C-Reactive Protein: Its Relationship to Fracture Risk and Bone Density

We have known for years that low-grade chronic systemic inflammation is associated with higher fracture risk. In my book, The Whole Body Approach to Osteoporosis, I explain this relationship in full. But what we do not fully understand is how this inflammation relates to bone mineral density (BMD).

This is exactly the question researchers from Norway set out to explore. In a study of 1902 women and 1648 men between the ages of 55 and 74, researchers tested the relationship of inflammation, as indicated by a biomarker called C-reactive protein (hs-CRP), to bone density and non-vertebral fractures.

The study showed an inverse relationship between hs-CRP and bone density in men (but not women). The higher the hs-CRP in men, the lower was their bone density. They also determined that elevated hs-CRP predicted increased fracture risk for both men and women. The authors concluded that inflammation influences fracture risk in both men and women.

So what can you do to lower chronic inflammation and reduce your fracture risk? A low-inflammatory diet rich in vegetables is a great way to start. Then try OsteoStim. This OsteoNaturals product is a potent blend of antioxidants, vitamins and medicinal herbs designed to limit the adverse effects of chronic inflammation on bone and encourage normal bone metabolism (as seen through the reduction in NTX, CTX, and/or DPD -- biomarkers that reflect the activity level of bone-resorbing osteoteoclasts).

One of the ingredients in OsteoStim is alpha-lipoic acid (ALA). This powerful antioxidant is an essential co-factor for cellular energy production. ALA also helps reduce the damaging effects of pro-inflammatory cytokines (Il-1, Il-6, TNF alpha, and NF-KB) and their tendency to spur on aggressive osteoclastic bone-resorbing activity.

In a recent article published in the European Journal of Pharmacology, researchers evaluated the protective effect of ALA on rat bone metabolism. They monitored pro-inflammatory cytokines (Il-1, IL-6, and TNF) to observe the inflammation process and how it was affected by ALA. The researchers concluded that "ALA had a protective effect on both senile and postmenopausal osteoporosis." "...ALA may be a candidate for radical osteoporosis treatment both in senile and postmenopausal types..."

Dahl, K., et al. 2014. High-sensitivity c-reactive protein is an independent risk factor for non-vertebral fractures in women and men: the Tromso Study. Bone Nov. 20. 

Polat, B., et al. 2013. The effect of alpha-lipoic acid in ovariectomy and inflammation-mediated osteoporosis on the skeletal status of rat bone. European Journal of Pharmacology 718(1-3):469-74.

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Happy Thanksgiving

Every time I compete, I am reminded of how lucky I am to still be able to toe the line. Having osteoporosis, experiencing the collapse of my inner boney core, was not just tough on my capacity to engage in physical activity but it also undermined my self-confidence (at least temporarily). So during this Thanksgiving holiday week, I gave thanks. Thanks that I have been able to come back from those dark days. Not just come back to a level of health where I no longer break bones, but to a level necessary to train hard and compete in races. This weekend it was the Talking Turkey Race, a 6-miler in Holyoke, MA.

Steve Jones (left) and Keith at the 2014 Talking Turkey Race.

The race was special for me this year because I ran with my younger son and was also fortunate to win my age group. In addition, I had the pleasure of talking with Steve Jones before the race. Steve is the best marathon runner to ever come out of Britain. When Steve was in his prime he not only won several of the world's most prestigious marathons (Chicago, London, New York, Toronto) but in 1984 he held the world record (2:08:05) for the marathon (26.2 miles). Steve now lives in Boulder, Colorado and came by to watch the race and cheer runners on.

So yes, no doubt I have been lucky, or at least extremely fortunate in my battle against osteoporosis. But it has also taken considerable effort over the past 15 years to make my skeleton healthier and stronger. I did things like drastically improve my diet, supplement with the best nutrients possible (you guessed it...all the stuff we put in our OsteoNaturals, of course), exercise (I always did that), and have the best attitude possible. Being able to compete again is an extraordinary gift that I don't take for granted--especially on race day! I hope you all had a very Happy Thanksgiving!

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Are You Taking Medications That Could Cause Osteoporosis?

Unfortunately, some medications can actually CAUSE disease. In a recent review article published in Therapeutic Advances in Musculoskeletal Diseases, Panday, Gona, and Humphrey discuss common medications that can cause bone loss. The authors emphasize the importance of being aware of this often over-looked, drug-induced, adverse side effect. Why?...Because many doctors (although they know that aging, menopause, and chronic illness can lead to osteoporosis) fail to realize that certain drugs, even ones they may be prescribed to YOU, can also lead to severe bone loss. In other words...be aware of the "adverse effects" linked to any medication that you might be taking.

Commonly prescribed drugs known to cause bone loss and increase fracture risk:  
- glucocorticoids (GC)
- proton pump inhibitors (PPIs)
- selective serotonin receptor  
  inhibitors (SSRIs)
- thiazolidinediones (TZDs)
- anticonvulsants
- medroxyprogesterone acetate
  (MPA)
- hormone deprivation therapy
- calcineurin inhibitors
- chemotherapies
- anticoagulants

You may not realize it but your skeleton is very much alive. Bones are metabolically active and can be adversely affected by foreign chemicals such as the medications you are taking. Medications, although they can be extremely helpful, are foreign to the body and can cause adverse effects such as a loss of bone.

For bones to remain strong and healthy throughout your life they must undergo a constant renewal process called remodeling. At any one time, 5% of your skeleton is being remodeled and over the period of several years your whole skeleton will be completely renewed due to this process. When bone is stressed during normal daily activities it incurs small cracks called microfractures. Over time, if these cracks were not removed and strong new bone put in their place, the bone's microarchitecture would weaken leading to increased fracture risk. To prevent this, special cells called osteoclasts eat away the weakened bone with cracks, then other cells, the osteoblasts, come to the site and form new bone. This remodeling process is vital for continued bone health and is overseen by a third type of bone cell called the osteocyte. The problem with certain medications is that they can interfere with normal osteoclast, osteoblast, and osteocyte activity thus disrupting the remodeling process and causing bone loss.

Glucocorticoids

Of all the drugs that cause bone loss GCs are the most aggressive robber of bone density and structural strength. They are also some of the most widely used medications. Physicians use GCs (almost like candy, unfortunately) to treat autoimmune diseases, inflammation, dermatological and respiratory diseases, malignancies, and organ transplants.

GCs adversely affect bone by altering the activity of all three of the bone cell types (osteoclasts, osteoblasts, and osteocytes). When the cells are disrupted, the remodeling process becomes uncoupled leading to a loss of bone density and microarchitectural integrity. GCs have both direct and indirect effects on bone.

     The direct effects:

       -  prolonged osteoclastic survival time thus more bone area being resorbed than
           the osteoblasts are capable of replacing

       -  limit in the number of osteoblast cells formed, therefore a reduction in new
           bone formation

      -  premature death of osteocyte cells which causes bone fragility even before there
          is a detectible loss of bone mineral density. (This means that people taking GCs
          can be at increased fracture risk even before a bone density (DXA) examination
          shows a loss of mineral density.

     The indirect effects:

       -  decrease in calcium absorption, suppression of growth hormone, altered
           sex hormones, and abnormal release of parathormone.

Fracture risk increases as the daily dose of GCs increases. For example, studies have shown that taking a daily dose of 7.5 mg can increase fracture risk five fold. Taking 10 mg/day for 90 days can lead to a 17-fold increase in fractures. Even the low dose of 2.5 mg prednisone can increase fracture risk.  A major problem with monitoring fracture risk of patients who take GCs is that their risk increases even BEFORE changes in bone mineral density can be detected.

Proton Pump Inhibitors

PPIs cause a moderate increase in fracture risk. While the mechanism by which PPIs increase fracture risk is not fully understood, it is thought that their action in suppressing digestive acids leads to reduced calcium (as well as other nutrients) absorption. Studies indicate that PPI use for as short as one year can increase hip fracture risk 20 to 60% and spine fracture risk 40 to 60%.  Several studies have indicated that patients taking bisphosphonate medications for osteoporosis who also take PPIs are at a further increased risk of fracture.

Antiepileptic drugs

AEDs are not only used to control seizures in epileptic patients but they are also used to treat migraines, psychiatric disorders, chronic pain, and neuropathy. AEDs cause bone loss by interfering with vitamin D and the bodies ability to absorb calcium. They also prevent osteoblast proliferation and the production of osteocalcin, a glue-like compound necessary for strong healthy new bone. The most commonly used AEDs known to increase fracture risk are: carbamazepine, clonazepam, gabapentin, phenobarbital, and phenytoin.

Medroxyprogesterone acetate

MPA, a contraceptive and medication for the treatment of endometriosis, suppresses estrogen production and can lead to substantial bone loss especially during the first two years of use. Although this bone loss is often reversible when MPA is discontinued, increased fracture risk may remain.

Aromatase Inhibitors

The AIs letrozole, anastrozole, and exemestane are used to treat estrogen-receptor-positive breast cancer in postmenopausal women by reducing estrogen levels. With the production of estrogen falling below normal menopause levels, bone loss occurs even more rapidly. Because of this, all women starting AI therapy should receive a bone density (DXA) examination and be encouraged to obtain adequate calcium and vitamin D intake.

Gonadotropin-releasing hormone agonists and androgen-deprivation therapy

GnRHs for the treatment of polycystic ovary syndromes, endometriosis, uterine myomas, and breast and prostate cancer, and ADT for the treatment of prostate cancer, can lead to bone loss and increased fracture risk. All patients receiving these medications should receive a DXA examination as well as extra calcium and vitamin D supplementation.

Selective serotonin reuptake inhibitors

SSRIs are commonly used medications for the treatment of depression, anxiety disorders, premenstrual syndrome, peripheral neuropathy, fibromyalgia, and chronic musculoskeletal pain. Although the exact mechanism for SSRIs adverse effects on bone are not completely understood, studies indicate these medications lead to reduced bone mineral density and increased fracture risk.

Thiazolidinediones

The TZDs rosiglitazone and pioglitazone are used to treat type 2 diabetes mellitus.  TZDs reduce bone density and increase fracture risk by stimulating osteoclast bone resorption, impairing the development of bone-building osteoblast cells, and causing a build-up of fat within bone marrow.

Calcineurin inhibitors

These drugs are used as immunosuppression agents to prevent organ transplant rejection and for the treatment of certain autoimmune disorders. The extent to which this group of medications can contribute to bone loss and fracture risk has not been fully studied.

Anticoagulants

Long-term use of the anticoagulant heparin (used in the treatment of venous thromboembolism) leads to loss of bone mineral density and an increased fracture risk. Although the bone loss associated with heparin is usually reversible, studies indicate substantial bone loss and increased fracture risk can occur within 6 months of starting heparin therapy.  The anticoagulant, warfarin, may also reduce bone density but its full impact on bone health and fracture risk is still under study.


Panday, K., Gona, A., and Humphrey, M.B. 2014. Medication-induced osteoporosis: screening and treatment strategies. Therapeutic Advances in Musculoskeletal Disease 6(5):185-202.

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Kefir: "Has the Potential to Prevent or Treat Osteoporosis"

Kefir, a fermented milk product, "has the potential to be utilized as an alternative treatment for postmenopausal osteoporosis". That is according to research published by Chen, et al. in the latest issue of Osteoporosis International. Kefir's amazing bone-health-promoting effects come not only from its high calcium content but also from its abundance of bio-active proteins. When milk is cultured with yeast and bacteria unique peptides are formed that enhance calcium absorption, boost the immune system, prevent blood clots, and ward off bacterial infections. Adding kefir to your daily diet can be a great boost to your over-all health.

By studying ovariectomized rats, Chen and colleagues determined that kefir, given daily over a 12 week period not only reduced CTX (a bone resorption marker indicative of osteoclast bone resorbing activity) but also actually prevented bone loss. The kefir improved bone mineral density as well as trabecular strength properties as measured through micro-CT scanning.

The authors concluded that kefir "may have the potential to prevent or treat osteoporosis in humans resulting from estrogen deficiency."

Chen, H.L., et al. 2014. Kefir improves bone mass and microarchitecture in an ovariectomized rat model of postmenopausal osteoporosis. Osteoporosis Int  DOI 10.1007/s00198-014-2908-x.

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Fall Season (2,926 icons)

Fall Season as of October 1st:

[Full] [Fall]  |  [Torrent]

tfw icons

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Soda Intake Increases Risk of Hip Fractures

A recent analysis published in The American Journal of Clinical Nutrition found an association of soda intake with an increased risk of hip fractures in postmenopausal women. Using the Nurses' Health Study cohort, this questionnaire-based analysis found that for every additional soda there was a 14% increase in risk of hip fracture. This higher risk was for all types of sodas not just colas as indicated by prior studies.

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70.3 Ironman Triathlon World Championships

This weekend I competed in the 70.3 Ironman TriathlonWorld Championships in Mont Tremblant, Quebec, Canada. Mont Tremblant was a fantastic venue to hold this event and the Canadians were incredible hosts. While driving to Canada from Massachusetts we passed through Montreal which was a real treat for me. I hadn't visited this city since 1976 when I participated in the Olympic Games.

The beautiful hamlet of Mont Tremblant is almost magical. No cars are allowed in the cozy pedestrian village itself and getting around is fun and easy via its cobble-stoned walkways and "over-the-village" ski-lift. The people of Mont Tremblant are extremely welcoming and there were lots of fun activities to do such as swimming, bungee jumping, miniature golf, and luge to keep my mind off the upcoming race.

Race day came and the weather was perfect. I started off with a good 1.2 mile swim being 4th out of the water in my age group. The 56 mile bike was challenging with some headwinds and lots of hills but I felt good up to around 40 miles...then I started to fall apart. The weeks leading up to the race hadn't been the best for training. I'd been pretty sick 4 weeks before the race and am still plagued by a nasty lingering cough. Then the day before the race (possibly from eating some smoked salmon) I developed plumbing issues that may have dehydrated me a bit. I'm not trying to make excuses (oh yes, and don't forget the mild concussion and pulmonary contusion from my bike crash 3 weeks ago...) but the bottom line is that when I got off the bike and headed out for the final 13.1 mile run portion of the race...I was toast. I had nothing left in the tank. End result...I finished 12th in my age group. Oh well...there is always next year...right? I am just grateful to be able to compete at this level. It was lots of fun but there is also lots of room for improvement.

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Tennis: A Great Exercise for Warding Off Osteoporosis: Report from the U.S. Tennis Open 2014

The nice thing about tennis is that you can do it year round (indoor and ourdoor tennis courts abound), you can play competitively or non-competitively as you like, and as long as you can stand up without falling over you can play well into your 70's, 80's, or even 90's. Now THAT is a GREAT sport!

It is always an honor to watch elite athletes in action no matter what sport. So when I got the opportunity to attend a match at the US Tennis Open in New York I was extremely excited even though I don't play tennis and barely know how to keep score. Today was the quarterfinals match between Victoria Azarenka and Ekaterina Makarova and I was totally in awe as that ball blasted back and forth at speeds exceeding 100 m.p.h.! Such amazing athletes...so powerful, so agile, and extremely competitive. Makarova from Russia won 4-6, 2-6 and will take on Serena Williams in the semi-finals in two days.

So if you are looking for a new challenge and you want to get some exercise to help build up your muscles and bones...you might want to check out tennis. You don't have to be US Open material...you just have to hold a racket and get yourself out onto a court. Looked like a lot of fun to me!

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A Face-Plant at Twenty-Five M.P.H.

Last weekend while competing in a triathlon (swim, bike, run), I experienced an unscheduled strength test of my skeleton that was somewhat unorthodox…I crashed. And just to make sure that you all understand…having a bone mineral density examination is certainly a MUCH safer way to determine fracture risk…but then again, I’m not one to always follow the rules.

As many of you know, the reason I became so interested in osteoporosis was because I myself was diagnosed with this disease 15 years ago. A T-score of -4.3 plus 12 fragility fractures were the impetus for my delving so head long into the study of osteoporosis. My goals were to uncover the cause of my extreme bone fragility and then to find ways to make those bones stronger and healthier. Taking this then one step further by helping others deal with an osteoporosis diagnosis was just the right thing to do. *

I have been an athlete my whole life and I’ve tried to never let osteoporosis impede my activity level, even back in the days when I was frequently breaking bones. (Maybe that’s a clue into why I broke so many bones...hmmm….) I’m now 60 years old and because I continue to race in triathlons I realize the danger quotient is escalating. Traveling at high speeds on my bike, up to 50+ mph down hills, has the potential to cause considerable damage to the skeleton should I crash. I don’t know if any of you have ever raced bicycles but sometimes there can be some unforeseen entanglements with other riders especially when the aggressive factor of racing is high. Such was the case in this race.

The first part of the race, the swim, went well even though my 4% body fat lost the battle against the 60-degree water. Even with my wet suit I was a bit chilly. I exited the water in first place and clipped into my bike for the second leg of the race. I hadn’t gone but two or so miles when it started to rain lightly. I sensed the road getting slick but pushed on at top speed hitting about 40 mph on a moderate downhill. I had driven the course the day before and knew there was a turn after going through a narrow, one-lane, tunnel-like under-pass at about mile 6…but I hadn’t really paid enough attention to the acute sharpness of the turn. As I was coming out of the tunnel I could see just how sharp the turn was and tried desperately to slow down. As I applied my brakes the rear wheel immediately began to fishtail. (I felt like Joseba Beloki in the 2003 Tour de France as I struggled to stay in control.) Four times in quick succession I applied my rear brake and 4 times I fishtailed. Only through sheer luck was I able to keep the bike up-right but, still going 20+ mph, I careened down off the road and into a gravel driveway. Finally I skidded to a stop 30 feet off the road. (Whew…that was close!) I quickly pushed my bike back up the hill, jumped on my bike and started to crank hard, anxious to gain back lost time. The rain continued and the road was becoming slicker, more dangerous.

On the second lap I made it through the tunnel safely but this time, on a straight stretch of road, things got really

squirrely. As I fast approached two slower athletes that I was about to lap, one of them pulled out to the left to pass. I swerved hard to avoid hitting him, crossed the centerline and hit a really bad patch of pot-holed road. At 25 mph I totally lost control and flew off the side of the road. My bike flipped flinging me headlong and performing a perfect face-plant into the road-side vegetation. I hit hard on my forehead and the right side of my chest. The helmet (see photo) saved me I’m sure. I wasn’t knocked out but certainly dazed and lay there for x amount of time. Another competitor stopped to ask if he should call for an ambulance but I said no and got up slowly…looked for my bike (which I couldn’t find at first because it was 10 feet away and under a lot of vegetation)…thanked the blurred racer (I can only barely remember that “being” standing there)…and hopped on my bike. (For any of you bikers out there reading this and worrying more about my bike than you are about me….No, my bike was not damaged…thank goodness!!!)

On the third and final lap with my head and chest a bit sore (but my vision improved) I thought I better slow down and not push my luck. I had already lost at least 3 minutes and I knew that there had to have been a few other competitors that had passed me while I was lounging around on the side of the road in the underbrush. So with first place surely gone…and probably a top five finish for that matter…I just started to relax and enjoy the rest of the race.

As I approached T2 (the transition between the bike and the run) the rain stopped and the sun came out just in time to warm up the run course. I racked my bike, threw on my running shoes and headed out for the final leg of the race, a 6.5 mile run. Since I had backed off on the final lap of the bike portion of the race I felt pretty good heading out on the run. Other than some back spasms as a result of the crash, I was able to keep a steady pace all the way into the finish line.

The whole reason for this long drawn out story is to say that I didn’t break any bones. Walking around after the race, feeling a bit sore in my back, a little confused from the concussion, spitting some blood from a laceration on my tongue, and coughing up some blood that was later diagnosed as a pulmonary contusion (bruised lungs) (a chest x-ray was negative for any real damage)…I was pretty darn happy that I didn’t break anything. I think that’s what makes a person with osteoporosis the happiest….not fracturing when they fall! Sounds a bit strange I know but every time I take a fall and don’t break…I just smile.

Oh…the final pièce de rèsistance after all this? I finished 2^nd overall and 1^stin my age group. A good day at the races for sure.

* If you would like to learn more about the comprehensive nutritional approach that changed my life, visit www.osteonaturals.com.

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

2014 Northeast Champ: Olympic Distance Triathlon

Second chances in life don't just happen...you 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!

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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.

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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!

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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 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. 

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:

PROS

• 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.

CONS

• 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.

UNKNOWNS

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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Summer Season (2,865 icons)

Summer Season V2 as of July 10th:

[Full] [Summer]  |  [Torrent]

Kill me.

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Bisphosphonates and Osteonecrosis of the Jaw

Osteonecrosis of the jaw (ONJ) (a painful, refractory condition where a portion of the jaw bone dies and becomes exposed) has been linked to bisphosphonate therapy in the treatment of osteoporosis. Numerous studies over the past ten years have been unsatisfactory in demonstrating the actual incidence of oral bisphosphonate-related ONJ and therefore the level of risk remains controversial. A new study out of Australia may bring us closer to understanding this association. Gorromeo, et al. showed a "strong, significant association between oral bisphosphonate use and delayed dental healing and jaw osteonecrosis."*

"The most significant finding of this study was the 13-fold increased odds of developing delayed dental healing in individuals on oral bisphosphonate therapy (11.6-fold after adjusting for smoking)." "There was no association of bisphosphonate exposure with osteonecrosis risk independently of a predisposing dental intervention, thereby highlighting the importance of a thorough dental assessment at the outset of bisphosphonate therapy."

Other studies have shown smoking and diabetes to increase the risk for ONJ in patients being treated with bisphosphonates.

*Delayed dental healing is defined as a failure to heal within 6 weeks. This condition is considered a precursor to ONJ. ONJ is defined as exposed jaw bone of greater than 8 weeks duration. 

Borromeo, G.L. et al. 2014. A large case-control study reveals a positive association between bisphosphonate use and delayed dental healing and osteonecrosis of the jaw. J Bone and Mineral Res 29(6):1363-1368.

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Our New Supply of OsteoNaturals Products is Here

Our new products are here. Thank you all for your patience. OsteoSustain, OsteoMineralBoost, and OsteoStim had been back ordered for way too long...but they are all now available!

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Boston Marathon

This has been a fun April for me in the sporting world. Two weeks ago I took first in my age division in the 70.3 Texas Ironman, in Galveston. Placing first in a time of 4:54 qualified me for the 70.3 World Championships to be held in Mount Tremblant, Canada in September. Then yesterday I ran in the Boston Marathon. It was SO much fun. The crowds were spectacular as they carried me and the rest of the 36,000 runners all the way from the start at Hopkinton to the finish, 26.2 miles later, on Boylston Street in Boston. I've never run a race with so many cheering spectators lining the course. The race was truly magical and my time of 3:22 was satisfying. Such an awesome day! Thank you..I truly appreciate all of your support.

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Magnesium Intake Affects Vitamin D Status

If you feel like you're ingesting bucket loads of vitamin D capsules yet your blood levels remain lower than you would like...make sure you're getting enough magnesium. Research conducted by Deng et al. and published in BMC Medicine concludes that magnesium intake can affect vitamin D status.

Magnesium is vital for a whole host of biochemical reactions in the body--at least two of which are critical for bone health. Magnesium is necessary for the parathyroid glands to produce

parathormone (PTH), a hormone that regulates blood calcium levels. If blood calcium levels are too low, the release of PTH activates osteoclastic degradation of bone to help raise blood calcium levels back to normal. Normal levels of PTH are important for bone remodeling activity and the maintenance of healthy bones.

Magnesium is also involved in vitamin D production. As it turns out, magnesium is necessary for the production of three enzymes that are key to the production of 25(OH)D (vitamin D) and its active form, 1,25(OH)2D. Without optimal blood levels of vitamin D (40 to 80 ng/ml) we are unable to absorb calcium from the gut (among other things) which is critical for optimal bone health.

By analyzing data from the National Health and Nutrition Examination Survey (NHANES: 2001 to 2006), Deng et al. concluded that "magnesium was independently associated with significantly reduced risks of vitamin D deficiency and insufficiency respectively. Intake of magnesium significantly interacted with intake of vitamin D in relation to risk of both vitamin D deficiency and insufficiency." They concluded that "it is possible that magnesium intake alone or its interaction with vitamin D intake may contribute to vitamin D status."

Although magnesium is derived from foods such as legumes, whole grains, broccoli, green leafy vegetables, seeds, and nuts, deficiency is common. Ever wonder why you get muscle cramps, twitching of the skin below your eye, constipation, fatigue, rapid heart rate...these could be signs of low magnesium. The best lab test for assessing magnesium status is to have your doctor order a red blood cell magnesium. The standard serum magnesium test is not ideal.

To ensure adequate magnesium intake, make sure you are getting a total of 500 to 700 mg between food and supplements. When supplementing with magnesium, I prefer the forms of magnesium bisglycinate chelate, dimagnesium malate, and magnesium citrate (all of which can be found in our OsteoNaturals products OsteoSustain and OsteoMineralBoost) over what may be less bioavailable forms such as magnesium oxide and magnesium carbonate.  

Deng, X, et al. 2013. Magnesium, vitamin D status and mortality: results from US National Health and Nutrition Examination Survey (NHANES) 2001 to 2006 and NHANES III. BMC Medicine 11:187.

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Diabetes and Fracture Risk

Your skeletal health is only as deep as its microarchitecture. With almost 50% of women and 20% of men predicted to sustain an osteoporosis-related fracture in their lifetime, the possibility of fragile bones is always something everyone should be aware of. With the diabetic individual, he or she will need to take extra vigilance as they have greater fracture risk.

Diabetes has reached epidemic proportions in the United States. Over 25% of adults have diabetes and this population—especially that developing type 2 diabetes (T2D)—is growing. With medical advances, people with type 1 diabetes (T1D) are living longer and into an age where osteoporosis becomes of greater concern.

How much greater is the fracture risk for diabetic individuals?

Compared to non-diabetic individuals, the bone mineral density (BMD) of type 1 diabetic patients is only slightly lower on average than non-diabetic individuals, so one might expect only a slightly higher fracture risk. But the risk level is much greater: individuals with T1D are 12 times more likely to fracture a hip according to data from the Iowa Women’s Study.¹

In contrast to T1D, individuals with T2D are often overweight and have higher than average BMD. With higher weight and increased bone density one would expect lower fracture risk. But T2D also carries an increase in fracture risk: 40% to 70% increase in risk for hip fracture and over 20% increased risk for all fractures.

It is clear that both T1D and T2D carry increased risk for spinal and hip fractures, yet BMD T scores and FRAX analysis underestimate their fracture risk. The bottom line: middle-aged and elderly diabetics are suffering a decrease in bone strength that is not measurable by current methods. Diabetes-related fracture risk is linked to reduced microarchitectural bone quality. Of course, an increase in falls due to hypoglycemic episodes, poor balance from diabetic neuropathy, and retinopathy-induced visual impairment may also be factors.

Why is the bone quality of diabetic individuals so poor?

Diabetes may affect bone in a number of ways:

1.     Chronic elevations in blood glucose weakens skeletal microarchitecture through the formation of advanced glycation end-products (AGEs) (such as carboxy-methyl-lysine and pentosidine) in both the bone-matrix collagen and the non-collagenous protein, osteocalcin².  This non-enzymatic glycation is a spontaneous reaction that lowers bone biomechanical competence. AGE induced collagen cross-links between reducing sugars and proteins stiffen collagen, making bone less pliable and less resistant to fracture.

2.     Hyperglycemia affects bone cells leading to low bone turnover osteoporosis.

3.     Reduced osteocyte function and higher sclerostin levels may inhibit bone formation by osteoblasts.³

4.     Reduced osteoblast bone formation and increased cortical porosity may explain accelerated bone loss at the hip in T2D.

5.     A reduction in trabecular microarchitectural quality as assessed through trabecular bone score (TBS) has been implicated as contributing to the increased fracture risk in T2D despite a higher than average BMD.⁴

6.     Altered bone marrow fat composition (higher saturated fat) is linked to fragility fractures and diabetes.⁵ Excessive marrow fat leads to reduced hematopoetic stem cells and increased adipocytokine production. This lowers bone turnover rate and allows for the development of “old bone” weakened by the accumulation of microfractures.

7.     Diabetes leads to lower “insulin-like growth factor 1” production. IGF-1 is a powerful natural anabolic peptide that stimulates both muscle and bone growth.

8.     The pharmacological treatment of T2D with thiazolidinediones (PPAR gamma agonists) promotes marrow stem cell differentiation into adipocytes rather than osteoblasts.

The typical medical approach to the treatment of T2D often includes medications. Although not all diabetes medications increase fracture risk, the thiazolidinediones (rosiglitazone and pioglitazone) can double the fracture risk of women (not men) with osteoporosis. These PPAR (peroxisome proliferator activator receptor) agonist medications stimulate adipogenisis in bone marrow and reduce bone formation.

Bisphosphonates are the current medications of choice for treating osteoporosis; they work by subduing osteoclast bone resorption and slowing overall bone remodeling (including bone formation) activity. The medical community has expressed concern about using bisphosphonate drugs to treat osteoporotic T2D’s patients because a further reduction in bone formation (bisphosphonates reduce both resorption and formation activity) through the use of bisphosphonate medications in the already bone-formation suppressed microenvironment of the type 2 diabetic, could increase bone fragility even further. This seems highly likely especially with atypical femur fractures already linked to long-term bisphosphonate use in non-diabetic individuals.

If you are diabetic, talk with your doctor about things you can do to improve your blood glucose levels naturally: 

·       Diet – You will benefit from a lower carbohydrate intake and increased quality protein, healthy fats, and vegetable intake.

·       Exercise – Try to exercise 45 minutes to an hour, five days a week, and reduce stress.

·       Supplementation – Talk to your doctor or nutritionist about what specific nutrients and therapeutic compounds you can take that work synergistically to decrease insulin resistance, lower inflammation, balance blood lipids, and improve liver function, while controlling their glucose levels and preventing glycation-induced damage. The following are some of the key components to consider using if you are diabetic: activated B-complex vitamins; vitamin D3; essential minerals (especially magnesium, zinc, chromium, and vanadium) and trace minerals; antiglycating agents such as alpha lipoic acid, L-Taurine, L-Carnosine and benfotiamine; herbal support including green tea extract (EGCG) and Gymnema sylvestre leaf extract.

·       Tracking – Make sure your blood glucose and hemoglobin A1C levels are monitored. Hb A1C levels above 7% are correlated with increased fracture risk. The American Diabetic Association (ADA) recommends that people with diabetes have the Hb A1C tested every 3 to 6 months depending upon glycemic control.

In addition to lowering your fracture risk, these strategies will also help lower your risk of diabetic-related comorbidity. Hypertension, coronary and peripheral artery disease, stroke, and even spinal degeneration are all common comorbidities of diabetes.

Current medical therapy for the diabetic osteoporotic patient is problematic and a more natural, conservative, approach using diet, supplements, and exercise can substantially improve the long-term outcome. If you are diabetic, you can reduce your risk of fractures and improve your over-all health by following the simple suggestions outlined above.

 

¹  Nicodemus, K.K. and A.R. Folsom. 2001. Iowa Women’s Health Study. Type 1 and type 2 diabetes and incident hip fractures in postmenopausal women. Diabetes Care24:1192-1197.

²  Sroga, G. and Vashishth, D. 2013. Glycated osteocalcin. ASBMR Symposium: Cutting Edge Discoveries in Muscle Biology, Disease and Therapeutics. ASBMR Annual Meeting: Oct 4-7. P024

³  Kim, J.Y., et al. 2013. Extendin-4 increases bone mineral density in type 2 diabetes OLETF rats potentially through the down-regulation of SOST/sclerostin in osteocytes. Life Sciences Mar 21;92(10):533-40.

⁴  Dhaliwal, R., J. Spadaro, C. Ghosh, J. Kelly, and A. Moses. 2013. ASBMR Symposium: Cutting Edge Discoveries in Muscle Biology, Disease and Therapeutics. ASBMR Annual Meeting: Oct 4-7. SA0304

⁵  Patsch, J.M., et al. 2013. Bone marrow fat composition as a novel imaging biomarker in postmenopausal women with prevalent fragility fractures. J Bone Miner ResAug;28(8):1721-8.

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