Bone Drugs: Are they worthwhile?

Conflicting advice on bone drugs — what does the evidence say?

It’s no secret that I’m no fan of bone drugs in general. I’ve found the arguments for their use deeply unconvincing for decades. And now, European researchers looking at the accumulated evidence about the various drugs’ long-term effects are starting to come to the same conclusion:

Except in extreme cases, bone drugs don’t offer enough benefit in reducing the risk of fractures to be worth the price paid in terms of both short- and long-term side effects.

A European/Canadian research group reviewed the evidence on bisphosphonates like:

  • alendronate (Fosamax),
  • ibandronate (Boniva) and zoledronic acid (Zometa or Reclast)
  • teriparatide (Forteo)
  • denosumab (Prolia)
  • two treatments not used in the U.S.: calcitonins and strontium ranelate

Their findings struck me as good general “lessons” for all of us to learn.

‘Denser’ bones are not always stronger bones

The review found that the majority of osteoporotic fractures happened in those who did not have “osteoporotic bone density.” This helps confirm: Bone density alone cannot predict fracture risk.

Other recent studies show a large percentage of people who fracture have only osteopenia or even normal bone density. Many people with an osteoporotic bone density never fracture.

Not all fractures are created equal

When it comes to assessing bone drugs’ effects, a painless vertebral fracture or a toe fracture (painful, but not life-altering) shouldn’t be considered as clinically important as a hip fracture, which is life-changing.

Yet many drug trials either focus on vertebral fractures or on “non-vertebral” fractures as an endpoint. The stubbed toe becomes equivalent to a hip fracture in determining how effective the drugs are in fracture prevention.

Not surprisingly, when hip fractures are looked at specifically as the endpoint of choice, the researchers discover something different. They found that the data on less serious fractures of toes, wrists and so forth obscure the fact that the drugs don’t do much to prevent the most serious and dangerous osteoporotic fractures.

Bone drugs’ benefits remain inconclusive

The benefits of taking a bone drug must outweigh the costs for it to be worth recommending. And even in high-risk older adults, such benefits have not been shown conclusively.

In weighing the risk-benefits of bone drugs, researchers took a hard line on the importance of evaluating all costs. “Clinical trials evaluating harm-benefit balance in osteoporosis or fracture prevention should be well-powered long-term studies that include hard endpoints,” they note. “Total mortality, total serious adverse events, hip fractures, and functional status are essential outcomes.”

New U.S. osteoporosis guidelines miss the mark

What’s frustrating to me is that experts in the U.S. still focus uncritically on the flawed studies that the review critiques. They glibly parrot the ideas that bone density is the same thing as fracture risk and that drugs offer protection from fractures.

Case in point: The American College of Physicians’ latest osteoporosis guidelines, which were published virtually simultaneously with the European review. They make a “strong recommendation” for the use of bisphosphonate drugs “to reduce the risk of hip and vertebral fractures.” Most galling to me, they openly equate bone mineral density with fracture risk: “most women with normal DXA scores” it notes, “do not progress to osteoporosis within 15 years.”

To which I respond with the European review’s first lesson: Denser bones ≠ stronger bones.

Erviti J, Gorricho J, Saiz LC, Perry T, Wright JA. Rethinking the Appraisal and Approval of Drugs for Fracture Prevention. Front Pharmacol. 15 May 2017 |

Qaseem A, Forciea MA, McLean RM, Denberg TD, for the Clinical Guidelines Committee of the American College of Physicians. Treatment of Low Bone Density or Osteoporosis to Prevent Fractures in Men and Women: A Clinical Practice Guideline Update From the American College of Physicians. Ann Intern Med. 2017;166:818–839.

Can Strontium Build Bone?

Strontium: bone drug or nutrient?

Quite frequently women write me to ask: What is strontium and why do you include it in your Better Bones Builder?

Well, there’s a short answer and a long answer to that question. Here’s the short answer: Strontium is an element very much like calcium and naturally present in our food and water. If you are eating a typical diet, you might getting anywhere from 1 mg to more than 10 mg of strontium per day. The reason it’s in the Better Bones Builder is that the elemental form (that is to say, the non-radioactive version found in nature) has been shown to promote formation of healthy teeth and bones. So it makes sense to include dietary doses of strontium in comprehensive bone-building formulas such as our Better Bones Builder because low-dose strontium is a companion nutrient that works with calcium and other minerals to promote bone health.

Low-dose vs. high-dose strontium

Now let’s get to the long answer. Where confusion sets in is when people hear about strontium being used by itself to build bone. What most people don’t realize when they read about strontium as “the solution” for bone health is that such talk isn’t referring to dietary doses of elemental strontium — rather, it’s referring to the extremely high-dose strontium that has been developed and patented as a drug therapy for osteoporosis in Europe. This drug, known as Protelos®, contains 680 mg of elemental strontium and two grams of strontium ranelate, a synthetic salt that combines strontium with ranelic acid.

Risks of high-dose strontium

Elemental strontium is different

Elemental strontium is a natural part of the earth’s crust and is very different from “strontium 90” which is a hazardous radioactive nuclear fallout product from aboveground nuclear testing. All strontium used in bone-building health products is elemental strontium.

One goal of Protelos® is for a small number of strontium atoms to displace calcium atoms in bone. For this effect it is necessary that the strontium drug be taken at least two hours apart from calcium. This separation of calcium from strontium is not necessary for low-dose strontium (22 mg) like that in my bone-building formula, which is used as a nutrient to aid the development of healthy bones. Unlike dietary strontium, the strontium drug has been found to have various adverse side effects including nausea, diarrhea, and, more rarely, memory problems, serious skin rashes, and venous clots. For the first 10 years of its use as an osteoporosis drug, however, more serious drug-induced problems were detected as the strontium drug (Protelos®) was found to substantially increase the risk of heart problems, including heart attack. In 2014, the European Medicines Agency Pharmacovigilance Risk Assessment Committee (PRAC) concluded that the risks of the strontium drug outweighed the benefits and they recommended suspension of its use.

Specifically, PRAC reported in 2014 that:

  • For every 1,000 patient years of use of the strontium drug (Protelos®) there were 4 more cases of serious heart problems and 4 more cases of blood clots or blockages of blood vessels than there were with the placebo.
  • As for benefits, the strontium drug had only a modest effect in osteoporosis, preventing 5 non-spinal fractures, 15 new spinal fractures, and 0.4 hip fractures for every 1,000 patient years.

Later in 2014 this same European committee revised its recommendation allowing the strontium drug to be used by patients who could not be treated for osteoporosis by other bone medicines, but requiring that patients using the strontium drug be carefully monitored. In addition, those with a history of heart or circulatory problems were not allowed to use this medication.

The high-dose strontium drug is not available in the U.S.

Keeping strontium in perspective

To avoid any confusion, let me be perfectly clear: In the U.S. the strontium drug Protelos® is not approved for use as a bone drug, and it is not available here for purchase. In the U.S. and Canada, however, one can purchase equally high dose natural forms of strontium as strontium citrate or strontium carbonate and some companies promote bone support formulas with 680 mg elemental strontium (the same strontium dose as in the Protelos® strontium drug formula). Keep in mind that this high-dose strontium, be it natural strontium as sold in the U.S. or synthetic as in Protelos®, is best viewed as a “bone drug,” and, as with all bone drugs, it should be used with great caution. While the synthetic strontium drug (Protelos®) has been shown to carry serious adverse effects, to date there have been no studies on the safety or efficacy of high-dose (680 mg) natural strontium as sold here in the U.S.

Here at the Center for Better Bones our mission is to explore the full human potential for natural, life-long bone health. We strive to work with nature and in accord with nature when at all possible. The Better Bones, Better Body program includes small low doses of supplemental strontium, while not generally recommending the use of high-dose strontium (680 mg) or conventional bone drugs.

I hope this helps clear up the confusion when it comes to strontium. I will be writing more on strontium in the future, so stay tuned!

Best wishes to everyone.



2014 European Medicines Agency. PRAC recommends suspending use of Protelos/Osseor (strontium ranelate),Jan 10. EMA/10206/2014

2014 European Medicines Agency. PRAC. Protelos/Osseor to remain available but with further restrictions. April 14, EMA 235924/2014


Strontium Ranelate

Strontium Ranelate


medications that cause bone loss

3 types of medications that cause bone loss

Are your medications dangerous to your bone health? While we all know that medications have some side effects, we may not recognize that certain medications, especially used long term, can seriously harm your bones.

Let’s look at the 3 most commonly used classes of medications known to increase fracture risk.

Which medications damage bone?

Corticosteroids. This class of drugs interferes with bone formation while simultaneously stimulating bone resorption, thus accelerating bone loss significantly.  At one point, scientists estimated that approximately 20% of all osteoporosis in the U.S. was the result of corticosteroid use, and it is estimated that up to 50% of patients using long-term oral corticosteroids will develop bone fractures.

While short-term, very occasional steroid use has less potential to weaken bone, longer-term use of oral and even inhaled steroids clearly jeopardize bone strength and increase fracture risk. Doses as low as 5 mg a day have been shown to increase fracture risk.

It is wise to seek alternatives to steroid therapy, use them when only truly necessary and for the shortest period  of time possible, and to fully support your bone health while using them to help offset the drug’s effects.

Common corticosteroids

    • Beclomethasone (inhaled)
    • Betamethasone (lotion or cream for skin)
    • Budesonide (oral capsule, inhaler and nasal spray)
    • Ciclesonide (inhaled)
    • Cortisone (oral, injection)
    • Dexamethasone (oral)
    • Ethamethasoneb (oral, injection)
    • Flunisolide (inhaled)
    • Fluticasone (inhaled)
    • Hydrocortisone (spray, liquid, lotion, gel, cream, ointment)
    • Methylprednisolone (oral)
    • Mometasone (inhaled)
    • Prednisolone (oral)
    • Prednisone (oral)
    • Triamcinolone (oral, injection



Antacids. Proton pump inhibitors such as esomeprazole (Nexium) and lansoprazole (Prevacid) are commonly used antacids. These antacid drugs powerfully reduce the production of stomach hydrochloric acid and thus likely weakened nutrient absorption.  Proton pump inhibitors have been repeatedly documented to increase the risk of hip, wrist, and spine fractures.

H2 receptor antagonist drugs like cimetidine (Tagamet) and ranitidine (Zantac) are also used to suppress acid production, which suggests that they might impair nutrient absorption similarly. However, studies have suggested that they do not seem to increase fracture risk as do proton pump inhibitors. One reason may be that they work by blocking the action of histamine — a chemical released in immune responses. Histamine tends to promote bone resorption. So these drugs are less likely, long term, to promote bone loss. Even so, there are studies showing that bone loss occurs in people taking H2 receptor antagonists if they do not have good intake of specific key bone nutrients, such as calcium and vitamin D.


Antidepressants. A specific class of antidepressant medications called selective serotonin reuptake inhibitors (SSRIs) is associated with a significant increase in fracture risk. One study noted that there are some indicators that the medications have direct effects on bone, but they’re not well determined. However, the impact of SSRIs on balance and alertness are well established.

What it boils down to is this: if you take SSRIs, it’s important to look carefully at your bone health. Even in the absence of a direct effect on bones, falling is the primary cause of fracture in those with weakened bones.

Take action!

I realize that it’s not always possible to avoid these medications, but there often exist dietary and lifestyle changes and alternative medical approaches that go to the root of the disorder and reduce the need for bone-damaging medications.  Also, once you know your medication may harm your bones, you can take steps to protect your skeleton. Plus, by knowing what the medications are, you can talk with your practitioner to determine whether there are less bone-damaging alternatives and support your body’s natural healing processes as much as possible.

Halpern MT, Schmier JK, Van Kerkhove MD, et al. Impact of long term inhaled corticosteroid therapy on bone mineral density results of a meta-analysis. Ann Allergy Asthma Immunol 2004;92:201-207.

Hodgson SF. Corticosteroid-induced osteoporosis. Endocrinol Metab Clin North Am 1990;19: 95-111.

Jones A, Fay JK, Burr M, et al. Inhaled corticosteroid effects on bone metabolism in asthma and chronic obstructive pulmonary disease. Cochrane Database Syst Rev 1, 2006.
Low Dose Steroids Can Increase Fracture Risk. Medsafe, NewZealand Medicines and Medical Devices Safety authority, 2017

Vestergaard P, Rejnmark L, Mosekilde L. Proton pump inhibitors, histamine H2 receptor antagonists, and other antacid medications and the risk of fracture. Calcif Tissue Int. 2006 Aug;79(2):76-83. Epub 2006 Aug 15.

Warden SJ, Fuchs RK. Do Selective Serotonin Reuptake Inhibitors (SSRIs) Cause Fractures? Curr Osteoporos Rep. 2016 Oct;14(5):211-8. doi: 10.1007/s11914-016-0322-3.

Wiercigroch M, Folwarczna J. [Histamine in regulation of bone remodeling processes]. Postepy Hig Med Dosw (Online). 2013 Aug 26;67:887-95.

Yu EW, Bauer SR, Bain PA, Bauer DC. Proton pump inhibitors and risk of fractures: a meta-analysis of 11 international studies. Am J Med. 2011 Jun; 124(6): 519-526.doi: 10.1016/j.amjmed.2011.01.007

Yu EW, Blackwell T, Ensrud KE, Hillier TA, Lane NE, Orwoll E, Bauer DC. Acid-suppressive medications and risk of bone loss and fracture in older adults. Calcif Tissue Int. 2008 Oct;83(4):251-9. doi: 10.1007/s00223-008-9170-1. Epub 2008 Sep 24.

Zhou B, Huang Y, Li H, Sun W, Liu J. Proton-pump inhibitors and risk of fractures: an update meta-analysis. Osteoporos Int. 2016 Jan;27(1):339-347.


All you need to know about the latest bone drug

The next big bone drug: big bang or little whimper? 5 questions to ask

The next big new bone drug is about to hit your doctor’s office. Impressive claims that the drug reduces fractures by 73% are being tossed around. But bisphosphonates were once touted in similar terms and are falling out of favor due to side effects and limited efficacy.

Do the stats in these studies mean anything real?

Whenever I hear about a new bone drug, I look at the research and ask a set of key questions to see whether there is any good news. I’m sharing them with you so you have tools to help you assess what you hear.

Question #1: What’s the nature and action of the drug? What will its long-term effects be?

The experimental bone drug I mentioned is a monoclonal antibody called romosozumab that inhibits action of a protein in the body known as sclerostin. Some time ago, it was discovered that sclerostin deficiency causes a rare genetic disorder characterized by high bone mass and resistance to fracture, so the pharmaceutical industry decided to make a drug to block this protein and see if it could reduce bone breakdown and enhance bone buildup.

Now Romosozumab is a drug that tinkers with both bone breakdown and bone formation in a whole new way, and its discoverers claim that “the risk of new vertebral fracture was 73% lower in those who took the drug.” Pretty impressive, if it’s true. So let’s take a closer look and continue asking questions.

To begin with, an important unanswered question is, “What are the many roles that sclerostin plays in the body, and what will be the long-term impact of suppressing this protein?” The current study does not address the issue of long-term impact or safety, and it often takes 10+ years to see the full effects of such tinkering with human physiology. For now, we know roughly how the drug acts, but we do not know what its long-term effects are.

Question #2: How many people participated in the study, and how were they selected?

This study looked at 7180 postmenopausal women ages 55 to 90 with a hip bone density T score between -2.5 and -3.5. The group was divided into two subgroups — 3325 who took the drug, 3327 who were given a placebo. So on the surface, this is a strong study — it includes a large sample of individuals who are similar in age, gender, and baseline bone density, and the groups are equivalent in size.

But a closer look shows that those at higher risk of fracture were excluded from the study. That includes women with a hip T score worse than -3.5, a history of hip fracture, or even one severe or more than two moderate vertebral fractures; those with a vitamin D below 20 ng; women with high or low blood or calcium as well as those with bone diseases or conditions affecting bone metabolism.

In other words, they chose participants based on low bone density rather than fracture risk (and if you’ve read my blogs, you know that the two aren’t necessarily the same).

Question #3: How long was the study?

Study subjects were only given the new drug, romosozumab, for 12 months and then switched to another monoclonal antibody bone drug, denosumab (Prolia®), in the second year. While researchers do not explain why they switched to another drug, I suspect they feared extended use of this new drug would result in serious longer-term adverse effects. This is not unlike the case with the drug teriparatide (Forteo®), the use of which is limited to two years due to potential life-threatening impacts.

Question #4: What is the real-life fracture-reduction benefit?

The length of the study is important because the short-term fracture reduction benefits may be very different from the long-term ones. In this case, all we have is a 1-year study with romosozumab and then another year-long study switching all study subjects (those on placebo and those on romosozumab) to the denosumab (Prolia®) bone drug. This makes the study a little confusing, but I’ll try to clarify the findings:

  • Only a few vertebral fractures were prevented by using either of the two drugs. The study had a total of 6,652 women, all of whom had a pretty low fracture risk to begin with. In the first year of the study using romosozumab versus placebo more than twice as many women (59) in the placebo group experienced vertebral fractures than the women in the romosozumab group (16). So when you look at how many women were spared from a vertebral fracture by taking the new drug (that is, 59 – 16 = 43 women), you realize that for every 1 woman who benefited, there were 76 others in the drug group who took the medication and got nothing out of it. If your doctor told you he had to treat 3,327 women to prevent just 43 vertebral fractures, you might look into other ways to strengthen your spine.
  • Both drugs put together had very little benefit on vertebral fracture. Among the 3,327 women who received placebo the first year and then were put on denosumab in the second year, there were 84 new vertebral fractures, whereas the women who took romosozumab the first year had only 21. Overall, then, 63 women out of 6652 were saved from having a fracture by taking bone drugs for both years. That’s not even 1% of the total number of participants.
  • The new drug had almost no impact on non-vertebral fractures. Vertebral fractures often cause no symptoms in those who have them, but others — like fractures in the wrist, collar, arm or hip — can be more serious and painful. Such fractures occurred in 56 patients on the new drug and 75 in the placebo group. That means the drug helped prevent only 19 of the 3,327 women avoid non-vertebral fractures with over 1 year of treatment. So you’d have to treat 175 women to save just 1 woman from fracturing a hip. And when you take the second year into account, when all the participants took bone drugs, you find no significant difference in risk between the romosozumab group and the placebo group. So if you were looking to prevent fractures of the hip, wrist, collarbone, arm, or other non-vertebral fracture, the new drug was no help at all.

Question #5: What are the reported and potential adverse effects of the drugs?

In this 1-year trial of romosozumab, adverse effects included the following: hypersensitivity to the injection; 2 cases of osteonecrosis of the jaw; 1 atypical femur fracture; a high incidence of anti-romosozumab antibodies (the impact of this on the immune system is yet unknown); and lowered serum calcium levels in those using romosozumab. These are all fairly serious problems.

Is there a better way to reduce needless fractures?

From my nearly 3 decades of clinical practice and bone health research, I confidently say yes, there is a better way! And that better way is one that builds Better Bones and a Better Body naturally, without the many risks of bone drugs.

Approaches like my Better Bones Program enhance health, vitality, and fitness while reducing fracture risk. Why not take a few minutes to review the steps to the Better Bones, Better Body Program and get started strengthening your bones today?


Cosman, Felicia et al., Romosozumab treatment in postmenopausal women with osteoporosis. New England Journal of Medicine 2016;375:1532-1543.

What's wrong with standard osteoporosis treatment?

6 ways standard osteoporosis treatment is dead wrong: Part 2


I’ve written recently about two of my top six concerns about the standard approach to bone health.  And now, here are two more that emphasize how women are often being misled about how to best protect their bones:

3. Contemporary osteoporosis management treats bone as if it were separate and isolated from the rest of the body

It’s tempting to look at the body the way we look at cars — as a collection of independent parts, each with a specific job. But that’s not what the body is! It’s a set of dynamic, interconnected systems that are constantly changing in response to what goes on around us and inside us.

While most people lose some bone as they age, bones don’t just “wear out” over time, the way a car’s parts do. If bones are weak or rapidly become thin, it’s nearly always because of a larger systemic problem in the body. The most effective approach in this situation is a big-picture perspective that looks at bone health as an indicator of overall health — it’s been shown that older adults who experience a hip fracture have lower baseline health-related quality of life than those who don’t.

But the standard approach is to focus on the mechanics of bone breakdown and interfere with them. Most bone drugs work by targeting the cells that break bone down and stopping them from doing their job. Doing this doesn’t actually solve the problem — it just masks the effects.

Enduring bone health requires rebuilding strength and vitality. That’s why it makes sense to look at the complete body system — circulation, bone, acid-base balance — to find the places where something isn’t working right to cause bone loss, rather than focus in on halting bone loss itself, which is most often an effect of a larger problem.

4. High-dose calcium is still considered the first-line treatment, yet it does not prevent fracture, and may be harmful

Speaking of “larger problems,” let’s take a look at what happens when you try to address fracture risk with calcium supplements. There is tremendous controversy about calcium and bones, but now it’s becoming clear that high-dose calcium supplementation is not the solution.

Multiple studies show that calcium does not decrease fracture risk except in those with a very low calcium intake — and some studies suggest that taking high-dose calcium supplements can lead to an increase in arterial calcification, stroke, kidney stones.  In my own research, it’s quite clear that while adequate calcium is needed for healthy bones, using high doses is counterproductive.

It seems wise to obtain the total 1,200 milligrams of calcium daily from diet and supplements as recommended by the National Institute of Health. At the same time, we recommend you also learn about the other key bone nutrients and make sure you obtain adequate doses of all these essential bone builders.

Stay tuned for next week’s blog for my final two reasons the standard approach to bone health doesn’t make sense. And as you’ll see, are far less effective and far more risky than commonly thought!

See Part 1 here.



Randall, AG et al., Deterioration in quality of life following hip fracture; a prospective study osteoporosis international 2000, 11(5);460-6.

Bischoff-Ferrari HA, et al., Calcium intake and hip fracture risk in men and women: a meta-analysis of prospective cohort studies and randomized controlled trials. Am J Clin Nutr. 2007

Bolland MJ, Leung W, Tai V, Bastin S, Gamble GD, Grey A, Reid IR. Calcium intake and risk of fracture: systematic review. BMJ. 2015;351:h4580. doi: 10.1136/bmj.h4580.
Bolland MJ, Grey A, Reid IR. Calcium supplements and cardiovascular risk: 5 years on. Ther Adv Drug Saf. 2013 Oct;4(5):199-210. doi: 10.1177/2042098613499790

* Information presented here is not intended to cure, diagnose, prevent or treat any health concerns or condition, nor is it to serve as a substitute professional medical care.

6 ways standard osteoporosis treatment is dead wrong: Part 3

In my previous two blogs, I’ve given you 4 important reasons why I don’t believe standard osteoporosis treatment is effective. In this final blog of the series, I want to emphasize that there is no magic bullet for optimal bone health – despite what you may have heard about calcium or bone drugs.  Here’s why:

5.    The calcium-centered focus has distracted us from the fact that at least 20 nutrients are essential for bone health

I’ve pointed out that calcium doesn’t reduce fracture risk and excessive calcium intake holds increased risk of cardiac problems. But if calcium isn’t the “magic bullet” for bones, what is? Well for one thing, adequate vitamin D levels are essential, and  a lot of doctors are finally realizing how important vitamin D is for bone health.

Yet too little attention is still paid to other essential bone nutrients — especially vitamin K, which makes a major contribution to bone health and supports many other systems as well, but also zinc, magnesium copper, boron, folate, manganese and vitamin C.

6.    Bone drugs are far less effective and far more risky than commonly thought

Here’s where it really becomes frustrating. Our health system pushes high-dose calcium (which doesn’t work) as the solution to low bone density (which is not necessarily the problem). Then when there’s no improvement in bone density from overloading the body with calcium, the typical next step is to prescribe a bone drug.

I’ve always maintained that such medications should be used only as a last resort, for very severe cases where drastic measures are needed — for instance, a person experiencing low-impact fractures or excessive, uncontrollable bone loss. This is not the situation for most people who have relatively low bone density .

With that in mind, it shouldn’t be surprising that the results of bone drug therapy are often  very disappointing. Even worse, the evidence suggests no benefit from bisphosphonate bone drugs on real-world hip fracture incidence. Nor do these drugs benefit people 80 years old and older — which is, of course, the group most likely to fracture a hip!

What it all boils down to is this: If we’re to really help people to live long, healthy lives free from the fear of bone fractures, we don’t need more bone drugs.  Instead, we need to change our approach by:

  • Carefully assessing each individual case to identify whether excessive bone loss or weakness exists;
  • Detecting and correcting both obvious and hidden causes of excessive bone weakening;
  • Broad-spectrum, whole-body support with nutrition, exercise, neuroendocrine and hormonal balance, stress reduction, and resilience enhancement.

Such an approach would limit bone drugs to the few specific situations where obvious bone weakness cannot be offset by natural means and requires heavy-duty intervention.

Missed the previous blogs?  Read more.

Part 1

Part 2

* Information presented here is not intended to cure, diagnose, prevent or treat any health concerns or condition, nor is it to serve as a substitute professional medical care.

6 ways standard osteoporosis treatment is dead wrong: Part 1


It’s no secret that I’m not a fan of the way bone drugs like Prolia® and Fosamax® are used these days. But people sometimes misinterpret my thinking as being “anti-drug” — yet it’s not just the drugs I object to. It’s how medicine in general approaches bone health and fracture risk.

I have at least 6 major objections to the standard approach, but for the sake of brevity, we’ll look at them two at a time over the next three weeks.

1.    Treatment is based on bone mineral density — but bone mineral density does not predict fracture

Having a low-side bone density isn’t actually a health problem. It doesn’t hurt or limit mobility — it doesn’t even necessarily mean the bones aren’t strong! It’s only when you fracture a bone that you have a health problem — and more, you cannot predict fracture by bone density alone. In fact, the majority of people whose bones are so fragile they experience a low-trauma fracture do not have an “osteoporotic” bone density.

That’s why treating low bone density bones as a “disorder” that “needs to be addressed” with heavy-duty medications makes no sense. Weak bones, on the other hand, need intervention. And, as far as weak bones go, there’s almost always an underlying problem causing the depletion of bone strength — whether it be nutritional, hormonal, bone-damaging medications, or some other hidden health condition or lifestyle factor. Properly detected and corrected these underlying causes can greatly reduce the risk of fracture. This is why a real fracture risk assessment and an assessment of underlying causes are so critical to developing a comprehensive bone-building program.

2.    The standard medical approach to osteoporosis is fear-based — and fear actually damages bone

Given that a low-side bone density does not necessarily indicate weak bones, why do you suppose doctors are so adamant that people with a low-side bone density need treatment? They’re afraid their patient will have a serious fracture.

But fear of fractures is itself bone damaging and can be a self-fulfilling prophecy — literally, as studies have linked higher levels of stress and the stress hormone cortisol with osteoporosis and increased fracture risk. A recent Danish study, for example, showed that just the perception of stress — seeing yourself as stressed — increases risk of osteoporotic fracture by 68%. It is bad enough that we have so many reasons to fall into stress and worry, we really do not need our health professional piling on more stress with unfounded fears of fracture. Again, what’s needed is a fracture risk assessment leading to a comprehensive bone building program — one that includes stress reduction and hope.

It’s interesting to note that Traditional Chinese Medicine holds that bone health is determined by the “kidney energy” and that fear is the emotion that disrupts the kidney energetic system. (And even Western medicine links osteoporosis with renal disease because the kidneys play such a central role in vitamin D metabolism, mineral reabsorption, and acid-base balance. (As I have discussed before, when kidneys can’t adequately buffer metabolic acids, calcium from bones is called upon to rescue essential pH homeostasis.) The ancient Chinese wisdom tradition suggests that the kidneys control bone and fear damages the kidneys — and I have found this to be true. All in all, we need less fear and more hope and bone-building solutions.

This isn’t all of course. Look for my post next week giving two more problems with the standard approach to bone health!



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Stone, K. L., D. G. Seeley, L. Y. Lui, J. A. Cauley, K. Ensrud, W. S. Browner, M. C. Nevitt, S. R. Cummings, and Osteoporosis Fractures Research Group. 2003. BMD at multiple sites and risk of fracture of multiple types: Long-term results from the Study of Osteoporotic Fractures. Journal of Bone and Mineral Research 18(11):1947–1954.

Fosamax® is a registered trademark of Merck Sharp & Dohme Corp., a subsidiary of Merck & Co., Inc.

Prolia® is a registered trademark of Amgen Inc.

New analysis looks at bone drug risks vs. benefits

Wouldn’t it be valuable if there was one study to answer the important questions about bone drugs, including:

  • How effective are bisphosphonates?
  • How well do they actually work to prevent hip fractures?
  • What’s the possibility of harm from these bone drugs?

Now, there is one — thanks to researchers who conducted a detailed systematic analysis of clinical trials using bisphosphonate drugs to treat osteoporosis and prevent hip fractures.

Benefits vs. risks of bisphosphonates

Here are two striking numbers researchers discovered when looking at how bisphosphonates help or hurt the women who take them:

  • 175 postmenopausal women with bone fragility had to be treated for three years to prevent one single hip fracture.
  • Treating 300 people with bisphosphonate drugs for three years will result in one person being harmed from serious side effects.

What’s more, researchers noted that hip fracture rates in developed countries are declining, yet sales of bisphosphonate drugs tripled between 2001 in 2008 and are forecast to exceed $11 billion in 2015.

Also, while 80 is the average age at hip fracture, the evidence suggests no benefit from bisphosphonate bone drugs for this age group.

“Pharmacotherapy (for hip fracture prevention) can achieve at best a marginal reduction of hip fractures at the cost of unnecessary psychological harms, serious medical adverse events, and forgone opportunities to have greater impacts on the health of older people,” said Dr. Barbara Mintzes, one of the study authors.

I really appreciate that they took into account the psychological impacts of osteoporosis overdiagnosis, which is something I see often in my work.

Listen: The trouble with bisphosphonates

You can listen to Dr. Mintzes detail more about the research findings in the first 13 minutes of this interview that aired on Australian national radio titled “The trouble with bisphosphonates” here.


Jarvinen, T.L., et al, Overdiagnosis of bone fragility in the quest to prevent hip fractures. BMJ 2015;350:h2088, 2015 May 26 (

Forteo — is this bone drug too good to be true?

Forteo™ (teriparatide) is a new and different drug on the scene as a treatment for osteoporosis. Other bone drugs, like Fosamax, Actonel, Boniva, or even estrogen work to halt bone breakdown. Forteo, on the other hand, works to increase new bone formation. Short-term studies, in fact, report a common 9% increase in lumbar spine bone density and a 2–3% increase in hip density accompanied by significant reductions in fracture incidence. Sound too good to be true? Sure does. So let’s take a second look and try to understand this new drug from what the manufacturer, Eli Lilly, tells us in their 2008 Forteo Product Monograph.

What exactly is Forteo?

Forteo is a man-made (well, E. coli-made) recombinant parathyroid hormone that has an amino acid sequence identical to part of the human parathyroid hormone (PTH). Forteo was approved by the US FDA in 2001 as an osteoporosis drug.

How does Forteo work?

In the body, natural parathyroid hormone serves to regulate bone metabolism in many ways. Chronic elevation of PTH, as in hyperparathyroidism, results in increased bone breakdown, a loss of calcium, and osteoporosis. On the other hand, daily injections of the PTH drug Forteo have the paradoxical effect of increasing bone mass and reducing osteoporosis. As scientists report, it seems to be that the pattern of exposure to parathyroid hormone determines its effect on the skeleton.

Through activation of various bone metabolic pathways, the PTH drug (Forteo) increases the number of active osteoblasts (bone-building cells), decreases the naturally programmed death of osteoblast cells, and recruits bone-lining cells as osteoblasts. This drug appears to act largely upon the bone-building osteoblast cells stimulating them to overactivity. Safety studies on this drug in rats, in fact, have shown findings of excessive new bone formation and bone cancer. Interestingly enough, the cancer this drug was found to cause in rat studies (osteosarcoma — I’ll say a little more about this shortly) is a cancer often associated with high osteoblast activity and rapid bone growth.

By how much does Forteo reduce fractures?

  • Reduction of spinal fracturesAmong 1637 postmenopausal women with severe osteoporosis and one or more vertebral fractures at baseline, the drug produced a 9.3% absolute fracture risk reduction over 19 months.
  • Reduction of hip, pelvis, wrist, rib, humerus, and other fracturesOver 19 months in these same high risk women, Forteo reduced nonvertebral fractures by an absolute 2.9% reduction in fractures.

So, overall, the short-term studies on Forteo reported above show this drug to reduce fracture risk substantially more than the bisphosphonate drugs like Fosamax. In addition, Forteo in these studies increased bone density more than the bisphosphonates.

Just how much does Forteo increase bone density?

In this same 19-month study of high risk osteoporotic women, Forteo increased bone density by an average 9.7% in the spine and 2.6% in total hip, while the wrist lost bone density and total body mineral content remained the same.

Why are there just short-term studies on Forteo, and is it safe?

As the manufacturer reports, the longest studies on the safety and efficacy of Forteo were of only a two-year duration. Why are there only short-term studies on this new drug? There are only short-term studies because in the animal safety studies, Forteo was shown to cause a high incidence of osteosarcoma (a rare malignant, often fatal, bone tumor), as well as osteoblastoma (abnormal mass of tissue in bone) and osteoma(small benign bone lesions). As with all drug safety tests, the drug doses tested were from 3-, 20-, and at times, 60-fold higher than those used in human medications. Notably, bone tumors were observed at all Forteo doses, with the incidence reaching 40–50% in the higher-dose groups.

Given this major safety concern, human trials with this drug were terminated early and guidelines were set to limit the duration of its use in humans. In fact, as the manufacturer specifically states, “The safety and efficacy of Forteo have not been evaluated beyond two years (median 19 months in women and 10 months in men). Consequently, the maximum lifetime exposure to Forteo for an individual patient is 18 months.” Also, given the cancer-causing effect of the drug, the FDA required a “black box” label warning, clearly stating the increased cancer risk shown in rat studies.

Expensive, experimental, possibly cancer-causing, and inconvenient

As near as I can calculate, since its development, studies on this drug have included only 1943 patients. According to the manufacturer, a study of one year is considered “long term,” while the maximum length of any study was only two years. Thus, not only is Forteo relatively new, but it is also experimental and, I would say, inadequately tested. In addition, it is very expensive — the drug costs upwards of $600–$700 per month! Further, it is inconvenient to use as it must be given as a daily self-administered injection. Most importantly, since this drug has shown to cause cancer in rat safety studies, its use by humans is limited to two years or less. While there may be significant bone density gains while using Forteo, the research is clear that these gains are lost once the drug is stopped. To maintain bone density gains, antiresorptive drugs such as Fosamax must be used after stopping Forteo.

Is there a better way?

This is the question I constantly ask myself — is there a better way to increase bone strength and reduce needless osteoporotic fractures? Is there a way that does not run the risk of causing cancer, or lead to excessive new bone formation — a way that is not only safe, but also good for the entire body? Yes, in most cases there is another way, and that way is through a comprehensive, life-supporting bone-building program that enlivens natural human healing and the body’s regenerative capacity.

To learn more on the topic of osteoporosis and bone loss, read our additional articles here:

Bisphosphonate bone drugs caught in compromising position


While you may not think to turn to The Journal of Clinical Endocrinology & Metabolism for breaking scandals, I recently saw troubling news about bisphosphonate bone drugs that I believe deserves some big headlines.

A new study shows that the popular bone drug therapy — Fosamax, Actonel, Boniva and Reclast — actually blocks the effectiveness of two natural bone builders.

Specifically, a team of international researchers showed there’s a vicious circle effect when it comes to the relationship between nitrogen – bisphosphonates and the levels of coenzyme Q10 (CoQ10) and vitamin E. In the case of CoQ10, the drugs compromise the metabolic pathways essential for its synthesis, resulting in lower levels in those using drugs. Plus, researchers suggested that the lack of the needed CoQ10 places additional demands on vitamin E, resulting in significantly reduced levels of that key antioxidant too!

If you don’t have the proper levels of CoQ10 and vitamin E in your body, here’s what your body is missing:

Benefits of vitamin E:

  • Protects essential lipids from oxidative damage body-wide.
  • Works synergistically with vitamin C for halting spinal bone loss in elderly women.
  • Low levels are associated with osteoporosis and low spinal bone density in early postmenopausal women.

Benefits of CoQ10:

  • Enhances immunity, and protects the heart and skeletal muscles.
  • Known to play a key role in cellular energy production and is found in nearly all cell membranes.
  • Works in conjunction with vitamin E to protect against free radical damage.
  • Inhibits the development of osteoclast bone-breakdown cells.

Remember that my intention #4 for 2014 is Sharing the truth about bone drugs. The more you know about bone drugs, the more you are empowered to make the right decision for your individual situation.



Kalyan, S, et al. Nitrogen – bisphosphonate therapy is linked to compromise coenzyme Q 10 and vitamin E status in postmenopausal women. Jr Clin Endocrin, Jan 13, 2014 me

Xu. Et al. Vitamin E Stimulates trabecular bone formation and alters epiphyseal cartilage morphometry. Calcif Tissue Int. 1995 Oct; 54(4):293-300.

Chuin A, et al., Effect of antioxidants combined resistance training on BMD in elderly women: A pilot study.Osteoporosis Int., 2009, Jul; (20 (7):1253-8

Mata-Granados JM, et al. Lower vitamin E serum levels are associated with osteoporosis in early postmenopausal women: a cross-sectional study, J Bone Miner Metab 2013, Mar 28

Moon, H-J, et al., Coenzyme Q10 regulates osteoclast and osteoblast differentiation. Jr of Food Science, Vol. 78, issue 5, May 2013: H785-H791. DOI: Moon, H-j et al. Antioxidants, like CQ 10, selenite and curcumin inhibit osteoclast differentiation by suppressing reactive oxygen species generation. Biochem and Biophys Res. Comm. Vol 418, issue 2, Feb 10, 2012:247-253.