Denosumab (aka Prolia, Xgeva) – Even Worse than the Bisphosphonates?

Treatment / March 23, 2012

Author: Lara Pizzorno, MDIV, MA, LMT

Lara Pizzorno is the author of “Your Bones: How You Can Prevent Osteoporosis and Have Strong Bones for Life – Naturally” and a member of the American Medical Writers Association with 29 years of experience specializing in bone health . Lara is the Editor of Longevity Medicine Review ( as well as a Senior Medical Editor for SaluGenecists Inc., and Integrative Medicine Advisors, LLC  

Like the bisphosphonates, denosumab (trade names Prolia, Xgeva)(1) also prevents osteoclasts from removing old, damaged or worn out bone. It just does so via a different action than the bisphosphonates — an action that may turn out to have even more harmful side-effects. Instead of poisoning already mature osteoclasts (which is what the bisphosphonates do), denosumab prevents the precursor cells for osteoclasts from ever developing into osteoclasts.

Mechanism of Action — How Denosumab Works

Denosumab (Prolia, Xgeva) does this by binding to and thus blocking off the RANK ligand (RANKL). RANKL is a protein whose job is to bind to a cell receptor called RANK that is found on several different cell types, just one of which is osteoclast precursor cells.  RANK (an acronym that stands for “receptor activator of nuclear factor-kappa B”) is activated by the RANK-Ligand (RANKL). RANK is produced by osteoblasts (yes, osteoblasts — these bone building cells work in concert with osteoclasts to continuously replace old or damaged bone with new bone). When RANKL activates the RANK receptor on the precursor cells for osteoclasts, this signals these osteoclast- wannabes to develop into mature osteoclasts ready to remove worn out bone. By preventing RANKL from doing its job, denosumab (Prolia, Xgeva) prevents osteoclasts from ever maturing and doing theirs.

What problems might arise?

Since denosumab, like the bisphosphonates, prevents normal bone remodeling, one would expect the denosumab twins, Prolia and Xgeva, to produce similar adverse effects, and they do. Far fewer studies tracking outcomes are available in comparison to the bisphosphonates because denosumab just got FDA approval as Prolia in June 2010, and as Xgeva in November 2010. But, already denosumab has been found to cause osteonecrosis of the jaw. Given the hundreds of studies which have now confirmed that, by preventing normal bone remodeling, the bisphosphonates cause not only ONJ, but “atypical” femur fractures, one wonders why the pharmaceutical companies are now attempting to sell us yet another drug that prevents osteoclast function.

Denosumab’s most common side effects, noted to date, include infections of the urinary and respiratory tract, cataract, constipation, rashes and joint pain. A small study has also already found slightly increased risk of cancer and severe infections.  Another trial showed significantly increased rates of eczema and skin infections so severe they required hospitalization.

Why might denosumab increase risk of severe infection or cancer? Well, guess what else must bind to RANKL in order to develop – T and B cells, key cells of our immune system! Obviously, the potential adverse ramifications of this fact of human physiology were somehow overlooked when FDA gave denosumab its stamp of approval.

Osteoclasts and Our Immune System – Tight Buddies

Recent papers have begun to discuss “The tight relationship between osteoclasts and the immune system.” A new interdisciplinary research field called “osteoimmunology” is just beginning to look at the interplay between our bones and the immune system. Already, however, a substantial body of evidence is showing that our bones and immune system are connected by two-way regulatory mechanisms that bring them into much closer association to each other “than one could ever predict,” —  to quote a review paper published January 2012.(2)  Well, I’m predicting that by causing osteoclast genocide, denosumab is going to produce some extremely unhappy, “unexpected” (but should have been!) results.

Osteoclasts are strongly linked to our immune system because they belong to the monocyte/macrophage family (these are the white blood cells of our innate immune system), have tight relationships with B and T cells (the adaptive immune system’s fighter squadrons), and differentiate (develop into mature osteoclasts) in response to RANKL, which is also produced by lymphocytes and—here’s the real stinger — RANKL regulates lymphopoiesis!

What’s lymphopoiesis, and why should I care?

Lymphopoiesis is the generation of a broad class of immune cells called lymphocytes, which include natural killer cells, T cells and B cells. And we (all of us, including the pharmaceutical companies) should care because lymphopoiesis is absolutely necessary for life.

Mature lymphocytes are cells that are a critical part of our immune system, and (except for memory B and T cells which are slightly longer-lived), our immune defender cells have very short lives (just days or weeks) and must be continuously generated. Were this generation to stop, the body would be largely undefended from infection. And how are these immune cells generated? By RANKL’s binding to cell receptors on their precursor cells. And what does denosumab do? It binds to and uses up all available RANKL.

Both pre-osteoclasts and immune cell precursors share the requirement of activation by RANKL, which allows them to develop into mature, active cells. Because osteoclasts share this need for RANKL activation with our immune cells, it has recently been hypothesized that osteoclasts are actually immune cells themselves.

Back in 2009, before its FDA approval, a red flag was raised about denosumab’s across the board shut down of RANKL in an editorial in the New England Journal of Medicine: “Perhaps the major concern about long-term use of denosumab relates to its possible effects on the immune system, since RANKL is expressed not just on bone cells but also on immune cells.”(3)

Denosumab’s already seen adverse effects

It seems we don’t have to wait “long-term.” After just a few years since denosumab’s FDA approval, side effects already being seen that certainly suggest its effects on immunity are an issue! Compared to placebo, denosumab has produced significant increases in rates of eczema and hospitalizations for cellulitis, which is inflammation of connective tissue either localized or spread throughout the body along with severe inflammation of the dermis (the layer of the skin immediately below the skin’s surface or epidermis) and its subcutaneous layers (which consist of connective tissue). In a study involving 314 postmenopausal women with low bone mineral density who were treated with denosumab, neoplasms (cancers) developed in 6 patients and serious infections in 3, whereas none of the 46 patients in the placebo group had such complications.(4)

As Amgen, the drug company that developed and holds the patent on denosumab, has noted, the drug produces the same adverse effects as the bisphosphonates:(5)  “Overall rates of adverse events and serious adverse events were generally similar between the two drugs.” Here Amgen is referring to denosumab (Prolia / Xgeva) and zoledronic acid (this is the bisphosphonate marketed under the trade names Zometa, Reclast, and Aclasta). Common side effects for zoledronic acid (and denosumab) include osteonecrosis of the jaw, back pain, pain in the extremities, musculoskeletal pain, high cholesterol levels, and urinary bladder infections.

Of major concern is that far fewer studies have been done using denosumab than the bisphosphonates. As mentioned above, denosumab was only approved by the FDA for use in postmenopausal women with risk of osteoporosis under the trade name Prolia in June 2010, and for prevention of “skeletal-related events” in patients with bone metastases from solid tumors under the trade name Xgeva in November 2010. The point being that we only have short term results as of yet. Denosumab, however, may have much nastier outcomes in store for us than the bisphosphonates because, by binding to RANKL, this drug interferes with our production of immune cells.

A recent review (Bridgeman et al.) of what research has been done on Prolia for reduction of bone loss in postmenopausal osteoporosis (from 1995 – 2011) summarizes a long list of adverse effects associated with the drug:(6)

  • After 24 months, compared with placebo, denosumab was associated with significantly greater prevalences of urinary tract infection and hypertension.
  • After 12, 24, and 48 months, the most commonly reported adverse effects with denosumab use included upper respiratory tract infection, arthralgias, back pain, and nasopharyngitis.
  • Infections requiring hospitalization were reported in denosumab-treated patients (10/314 [3.2%]) but not in patients given alendronate (Fosamax) or placebo.
  • Prevalence of malignant neoplasms (cancer) were higher in the denosumab than in the Fosamax (alendronate) or placebo groups (4.8%, 4.3%, and 4.3%, respectively), as was the overall prevalence of serious adverse events after 48 months of treatment (17.8% for denosumab, 17.4% for Fosamax, and 10.9% for placebo).
  • A greater number of patients developed infections that required hospitalization in the denosumab group compared with placebo (8 vs 1). For some reason, for which no justification or explanation is given, “Infections were not considered to be related to denosumab.”The types of infections included pneumonia, urinary tract infection, pyelonephritis, diverticulitis, appendicitis, sepsis, and cellulitis.
  • Four patients in the denosumab group were reported to have neoplasms compared with 1 patient in the placebo group, but again for some reason for which, again, no explanation is given, the higher incidence of cancer in those given denosumab is said to not be related to the drug.
  • Other adverse events reported at significantly greater rates with denosumab compared with placebo included constipation (11.0% vs 4.8%), sore throat (9.1% vs 3.0%), and rash (8.5% vs 3.0%)

If all this weren’t sufficient cause for concern, Bridgeman et al. go on to also warn that drug-drug interactions may be a serious problem with denosumab:

“Studies of the potential for denosumab to affect the metabolism of other pharmacologic agents were not identified in the literature search. [Translation– no studies looking into this have been conducted]. However, based on reports of serious infections associated with the use of denosumab, the concurrent use of immunosuppressants, including corticosteroids, chemotherapeutic agents, and immune modulators, may increase the risk for infection.” (Many drugs fall under these classifications including drugs prescribed for allergies, asthma, depression, epilepsy, and insomnia. For more on those, check out the following blog post: Prescription Drugs that Cause Osteoporosis.

Elsewhere we are simply told that data regarding interactions between denosumab and other drugs are “missing.” (Translation – they haven’t looked into this.) But we are assured such interactions are “rare,” so “it is unlikely that denosumab exhibits any clinically relevant interactions.” (Translation – we haven’t seen this yet, so are not going to worry about it until enough people have been harmed that a class action suit is brought.) (7)

The following quote from the concluding section of Bridgeman et al’s review of the research on denosumab use in postmenopausal women at risk of osteoporosis summarizes the adverse events already seen:

“Adverse events reported with the use of denosumab have included back pain (34.7%); pain in the extremities (11.7%); general musculoskeletal pain (7.6%); elevated cholesterol (7.2%); inflammation of the bladder (5.9%); and dermatologic conditions including dermatitis, eczema, and rashes (combined prevalence, 10.8%). Serious adverse events have included hypocalcemia (1.7%), pancreatitis (0.2%), and severe infection (0.2%). Several cases of osteonecrosis of the jaw have also been reported.”

Shockingly, the next sentence, the concluding statement of this review, is: “Based on the data from the available literature, denosumab is an efficacious and well-tolerated treatment for postmenopausal osteoporosis.” This was such a non-sequitur to me, I read the paragraph several times trying to make sense of it – I couldn’t.

Denosumab has little benefit, nasty side effects in men with prostate cancer

Most recently, Amgen has attempted to have denosumab as Xgeva also approved to increase bone mass in men with non-metastatic prostate cancer who are at high risk for fracture because they are being given “androgen deprivation therapy” (drugs that shut off men’s production of testosterone). Remember, in men, a little testosterone is converted into estrogen that plays a very important role in building men’s bones. Drugs that prevent a man from producing testosterone therefore also cause him to lose bone.

Amgen approached FDA for approval using data from its study of 1,432 men with non-metastatic, castration-resistant prostate cancer. These men were randomly assigned to receive calcium and vitamin D supplements plus either 120 mg subcutaneous denosumab every four weeks or placebo. (Dosing for denosumab is a 60 mg subcutaneous injection every six months for postmenopausal osteoporosis and 120 mg every 4 weeks for patients with solid tumors.)

Men in this study who were given denosumab did have, on average, about four months longer before developing bone metastases compared to those in the placebo group (29.5 months versus 25.2 months), but the men’s overall survival and cancer progression-free survival were not any better in the denosumab group versus placebo. Nor did denosumab lessen the men’s pain or improve their health-related quality of life compared to placebo.

As expected from prior studies, denosumab did, however, cause a number of adverse effects in these men, including more hypocalcemia (1.7% versus 0.3% with placebo) as well as a 5% rate of osteonecrosis of the jaw, which didn’t occur at all in the control group. Just think about this – it’s bad enough having prostate cancer and suffering the effects of having your testosterone wiped out, but to also have to endure a rotting jaw is completely unacceptable!

FDA reviewers concerned about “unresolved safety issue”: might denosumab cause cancer?

FDA reviewers were also concerned about an “unresolved safety issue”: whether denosumab might cause cancer to spread to non-bony sites. Why is the FDA concerned? Remember denosumab works by shutting down RANKL, which is required for the activation of our T and B immune cells. In just living our lives, normal bodily metabolism and environmental exposures result in each of us experiencing insults to our cells’ DNA that produce hundreds of potentially cancerous cells every day; our immune system, if not overloaded and not prevented from functioning properly, destroys them.

Amgen argued that denosumab should be approved for the added indication anyway “because no other therapy has been shown to prevent the development of bone metastases in patients with non-metastatic castrate-resistant prostate cancer.” Am I missing something in the logic chain here? Denosumab should be approved–not because it has been shown to help prevent bone cancer in men with non-metastatic prostate cancer or extend their lives or even improve the quality of whatever time they have—but because no other drug has been shown to do so? (8)

Denosumab – another pharmaceutical company experiment — on us!

Even for its use only to prevent excessive bone loss in individuals with osteoporosis, denosumab has only received approval by the FDA as of 2010. As two recent papers in leading medical journals focusing on osteoporosis clearly warn, bone remodeling continues throughout the human lifetime, so any treatment used to prevent excessive bone loss must be safe over many years – for which reason, “the collection of long-term efficacy and safety data [on denosumab] is warranted.”(9) “Denosumab has been introduced recently, and its extra-skeletal effects still have to be assessed.”(10)

Despite these concerns voiced in leading medical journals and by the FDA, the fact that denosumab has already been found to produce adverse effects, and its far less than stellar results in men with non-metastatic castrate-resistant prostate cancer, a Wall Street Journal post entitled, “Analysts React to FDA Panel: ‘It Wasn’t a Perfect Day for Amgen,” noted that annual worldwide sales of denosumab are still projected to reach $5 billion by the year 2015. (11) Well, at least Amgen should have plenty of money available for the lawsuits sure to come when denosumab’s impact on bone and immune health has resulted in serious harm to sufficient people. Don’t be one of them!

Haven’t the atypical fractures and osteonecrosis of the jaw caused by the bisphosphonates provided a clear enough warning? Why would we want to expose ourselves to yet another drug that shuts off osteoclasts and prevents the normal levels of bone remodeling essential for healthy bones? And denosumab’s undesirable long term effects could be much, much worse because this drug not only prevents osteoclasts from developing, but does so by locking up RankL, which key cells of our immune system, our T and B cells, also require in order to develop.

Latest research proves you can restore the health of your bones—safely and effectively — naturally

Why participate in yet another pharmaceutical company experiment and expose yourself to these risks when the latest research proves you can maintain and restore the health of your bones – safely and effectively — naturally?

Just last month (February 2012), right after the annual meeting of the American Academy of Orthopaedic Surgeons officially warned doctors that the bisphosphonates increase risk for “atypical femur fractures,”(12) the results of the one-year long Combination of Micronutrients for Bone (COMB) Study were published in the prestigious Journal of Environmental and Public Health. The COMB study unequivocally demonstrated that providing our bones with the nutrients they need along with regular weight-bearing exercise is as or more effective than any of the bisphosphonates or strontium ranelate (the unnatural drug version of strontium). And a lot less expensive!

What was the protocol utilized in the COMB Study?  Daily vitamin D3 (2,000 IU), DHA (250 mg), K2 (in the form of MK-7,100 mcg), strontium citrate (680 mg), magnesium (25 mg), and dietary calcium. In addition, daily impact exercise was encouraged.(13)

As one of the lead researchers, aptly named Dr. Stephen Genius, noted, not only was this combination of nutrients that bones require “at least as effective as bisphosphonates or strontium ranelate in raising BMD levels in hip, spine, and femoral neck sites,” but the nutrient supplement regimen was also effective “in individuals where bisphosphonate therapy was previously unsuccessful in maintaining or raising BMD.”

What a concept – by providing our bodies with the nutrients our bones require and enjoying a little weight-bearing exercise, we can build strong bones for life, safely, effectively – naturally!  If you are taking AlgaeCal Plus and Strontium Boost, you’ll more than match the nutrient levels provided in the COMB study. All you need to add to your bone building program to mimic the COMB recommendations is some daily, weight-bearing exercise.

The COMB study’s recommendation for daily weight-bearing exercise is based on earlier studies in which regular exercise improved women’s bone density.(14), (15)The most recent of these studies, Niu K et al. 2010,  is especially encouraging since it showed that even 3 short exercise sessions each week can have a beneficial effect on bone density. This study used a video-guided exercise program, which premenopausal women in Japan were asked to participate in during short breaks at work at least three times a week.

Each exercise session included a 3-minute warm-up (stretching), followed by 10 additional minutes of stretching and balance exercises or some “high intensity” exercises (this routine also began with stretching, then added some jumping, and after 6 months, stair-stepping, followed by a 3 minute cool down of more stretching). The women in the high intensity program started out with as few as 5 jumps. Programs were modified monthly by increasing the number of jumps up to 50 jumps during the first 3 months. After 6 months, stepping up and down using a 10-centimeter step bench was also added. Both the stretching and “high intensity” exercise sessions were done with the accompaniment of music and supervised at least 4 times a month by an experienced health fitness instructor. Both exercise programs – stretching and “high intensity” — were beneficial, but women in the stretching program maintained their BMD, while those in the “high impact” program increased theirs, both in the spine and neck of the femur.

The “take home” message here: just a few daily minutes of energetic exercise – exercise that puts enough load on your bones to send them a clear “get buff” message — can really help your bones! Combine exercise with a healthy dose of the nutrients your bones require to build, and you’ll have strong, healthy bones for life – naturally.


  1. ^Prolia is the trade name given to denosumab marketed to women at risk of osteoporosis; Xgeva is the trade name given to the drug when used for the prevention of skeletal-related events in patients with bone metastases from solid tumors.
  2. ^Fattore AD, Teti A. The tight relationship between osteoclasts and the immune system. Inflamm Allergy Drug Targets. 2012 Jan 20. [Epub ahead of print] PMID: 22280239
  3. ^Khosla S. Increasing options for the treatment of osteoporosis. N Engl J Med. 2009 Aug 20;361(8):818-20.PMID: 19671654
  4. ^McClung MR, Lewiecki EM, Cohen SB, et al. Denosumab in postmenopausal women with low bone mineral density. N Engl J Med 2006;354:821-831. PMID: 16495394
  5. ^
  6. ^Bridgeman MB, Pathak R. Denosumab for the reduction of bone loss in postmenopausal osteoporosis: a review. Clin Ther. 2011 Nov;33(11):1547-59. PMID: 22108301
  7. ^Haberfeld, H, ed. (2009) (in German). Austria-Codex (2009/2010 ed.). Vienna: Österreichischer Apothekerverlag. ISBN 3-85200-196-X.
  8. ^Walker, Emily P. (February 7, 2012). “Benefit of Bone Drug in Prostate Cancer in Doubt“. MedPage Today.
  9. ^Dore RK. Data from extension trials: denosumab and zoledronic Acid. Curr Osteoporos Rep. 2012 Mar;10(1):16-21. PMID: 22086442
  10. ^Body JJ, Bergmann P, Boonen S, et al. Extraskeletal benefits and risks of calcium, vitamin D and anti-osteoporosis medications. Osteoporos Int. 2012 Feb;23 Suppl 1:S1-23. Epub 2012 Feb 4. PMID: 22311111
  11. ^
  12. ^Am Acad Orthopaedic Surgeons 2012 Mtg: Abstract 190, presented 2-8-12):
  13. ^Genuis SJ, Bouchard TP. Combination of Micronutrients for Bone (COMB) Study: bone density after micronutrient intervention. J Environ Public Health. 2012;2012:354151 PMID: 22291722
  14. ^Korpelainen R, Keinänen-Kiukaanniemi S, Heikkinen J, et al. Effect of impact exercise on bone mineral density in elderly women with low BMD: a population-based randomized controlled 30-month intervention. Osteoporos Int. 2006 Jan;17(1):109-18. Epub 2005 May 12. PMID: 15889312
  15. ^Niu K, Ahola R, Guo H, et al. Effect of office-based brief high-impact exercise on bone mineral density in healthy premenopausal women: the Sendai Bone Health Concept Study. J Bone Miner Metab. 2010 Sep;28(5):568-77. Epub 2010 Mar 30. PMID: 20349354


Is there a way to reverse what 8 years of biphosphonate use and 18 months of Forteo injections have done, or am I doomed to another horrible adverse effect?

Lara Pizzorno

Of course! Your body will always attempt to heal — if given the nutritional support it needs. In the studies, women on bisphosphonates recovered their bone remodeling capacity eventually, although it can take up to a year or longer. Just get started on a sound, safe and effective natural bone building regimen. If you have not read my book, Your Bones, PLEASE do so! Cost is around $9 or less as the publisher is a non-profit. Kindle edition is even less –around $7.00 If you do not wish to purchase the book, your library should carry it. Become well informed and you can take control of your health and rebuild your bones, safely and naturally.

Bonnie Mercer

I would like to know if Lara Pizzorno has studied the drug Fosomax and written about it.

Lara Pizzorno

Hi Bonnie,
Yes, I have studied and written about Fosamax (an oral bisphosphonate) at length — Your Bones includes more than 30 pages (pages 11-45 in the book) discussing the bisphosphonates and explaining in detail why they should be your last choice for healthy bones, although now I think denosumab is at least as bad for us, probably worse. I also wrote a blog that was posted on AlgaeCal several months ago now summarizing additional research that has come out showing that the bisphosphonates are harmful since Your Bones was published in May 2011 — here is a link to this blog:
Hope this information will be helpful for you, Lara


Hello Ms. Lara,

Have you read, The Bone Building Solution by Sam Graci? If you have, is your book similar? Do you agree with most of Graci’s beliefs?

I am trying to see if my local library has your book. I have osteoporosis and was just told by my doctor to get on Prolia and I need to make a decision soon.

Thanks for any suggestions that you might have.

Nora Rodriguez

Lara Pizzorno

Hi Nora,
Sorry, but I am not familiar with Sam Graci’s book, so do not know if his recommendations are similar to what I present in Your Bones. PLEASE do get hold of a copy and become well informed. As the COMB study clearly demonstrates, provding your bones with the nutrients they require along with daily weight bearing exercise will improve your bone density and restore healthy bones for you safely, naturally and inexpensively. I very much hope you will consider a 6 month trial of a natural bone building regimen before exposing yourself to well documented risks already associated with Prolia.

Jill Orton

I have tried to get a copy of the Bone Healthy recipe book on you website but all I get is a reply to say I am already subscribed. I have not had a recipe book although I have been receiving your newsletters for quite a few months now, ever since I found I had osteoporosis and have found it to be a great help. Thanks


I take Xgeva to slow bone metastases from stage 4 breast cancer. Do you think this is a reasonable use of it? I have been taking it monthly, so far for 16 months. I have been getting chemo (paclitaxel) for 12 months. So far, my white blood cell count is fine (for a person on chemo). Do you recommend an alternative to Xgeva?

Lara Pizzorno

Hi Janice,
Slowing bone metastases in stage 4 breast cancer is a use for which Xgeva has been approved. Since its use will be short term, and given the severity of your condition, it is certainly a treatment that would be considered reasonable. And I expect your oncologist looked at the risk/benefit ratios in relation to your specific situation before recommending you take Xgeva. Fortunately, it sounds like you are tolerating Xgeva well as you did not mention experiencing any of the common side effects and are maintaining your white blood cell count.
I do have one suggestion for a complimentary therapy that you might discuss with your oncologist. Vitamin K, as both vitamin K1 and vitamin K2(as MK-7), has been found to improve the RANKL/OPG ratio. I’ve written a blog on this new research that should be posted on AlgaeCal in the next week to 10 days – meantime, here is the reference for the study:
Kanellakis S, Moschonis G, Tenta R, et al. Changes in Parameters of Bone Metabolism in Postmenopausal Women Following a 12-Month Intervention Period Using Dairy Products Enriched with Calcium, Vitamin D, and Phylloquinone (Vitamin K(1)) or Menaquinone-7 (Vitamin K (2)): The Postmenopausal Health Study II. Calcif Tissue Int. 2012 Apr;90(4):251-62. Epub 2012 Mar 4. PMID: 22392526
This research showed that both vitamin K1 (100 micrograms/day, K1 is the form found in leafy greens) and vitamin K2 (specifically as MK-7, also in a dose of 100 micrograms/day) improved the RANKL/OPG ratio. (This is what Xgeva is supposed to do — it binds to RANKL, thus serving as a decoy receptor for RANKL kind of like OPG. The difference is that Xgeva does this at a much greater level than would be normally accomplished by OPG, thus the drug’s potential for distorting physiology.) Vitamin K1 lowers RANKL more than K2/MK-7, while K2/MK-7 increases OPG more than K1.
Soy foods — specifically a bioactive compound in soy called genistein, also improve the RANKL/OPG ratio — I discussed this research in detail on another blog posted on AlgaeCal — here is a link to it:
To sum up, both vitamin K (K1 and K2/MK-7) and soy foods may also be helpful for you in conjunction with your current Xgeva and paclitaxel therapy.

Juliette Stenning

I filled in my details to be on your mailing list for osteoporosis info and recipes for same, but cannot find any “submit” box. Sooooo…I’m leaving you a comment hoping you will forward this to the right place. I’ve been on your “algaecal” site for about an hour reading much interesting info. I’ve been taking strontium ranelate for 18 months, with another bone density in 6 months. I’m very anxious about my bones as I’ve been sitting on the osteo time bomb for about 30 years – it’s in my genes, back to my great -grandmother. Very scary. Thanks for the information.


It´s hard to find someone who has a thorough knowledge of and is interested in osteoporosis, and I have so many questions that no one seems to be able to answer (or wants to). Also, most information is about prevention or for postmenopausal women with much better bones than I have.

I am 36 years old and have osteoporosis (about -5 in the spine and -3,5 in the hips) partly caused by genetic factors but probably primarily as a consequence of gastroparesis which resulted in chronic malnourishment and low bodyweight for many years. I was diagnosed 2006 following a compression fracture in the spine and was given Fosamax. The doctor who prescribed it said I had to take it, or else I would soon become severely disabled. Unfortunately I followed his advice, which I deeply regret and never would have done if I had known then what I know now. To make it even worse I really had to force myself taking it since it made me terribly nauseous, and after a year I had to stop because I simply couldn´t eat or drink any more. I don´t know if it was caused by the Fosamax or would have happened anyway as a consequence of my GI-problems, but I believe it at least contributed. After that I was on TPN for three years but eventually was fortunate enough to meet a doctor who understood what was wrong with my digestive tract and took me off TPN and on tube feedings (G/J-tube, bypassing my stomach and duodenum) which made it possible to gain weight and I have now reached a normal BMI. But my bones haven´t improved and since last May I´ve had four fractures in the spine (that I know of) and find it hard to stand the pain and to stay active. The doctors wanted me on bisphosphonates once again, but when I refused they offered Forteo instead, which I have been taking since August, without any, other than very short-lived, reduction in pain or improvement in my ability to exercise (I also take HRT (estrogen and progestine), AlgaeCal and Strontium Boost). But since I can´t eat I am still on tube feedings and the formula is really not good for anyone´s health since it basically contains vitamin enhanced sugar with small amounts of fat and some proteins added, which – although much better than TPN – obviously is a diet no one would choose if they had a chance not to. The last few weeks I’ve tried to add some powder of fruits and vegetables to the prepacked formula, and I´m hoping I will be able to completely switch over to a home-made blenderized diet, but it´s difficult for a lot of reasons including that the tube is so narrow it easily get clogged (and my doctors say I shouldn´t even try, and that I get all the nutrition I need). They also tell me that I won´t get any more fractures because I´m on Forteo (which I don´t understand how they can be so sure of) and that I should take painkillers and live like I did before the fractures. And I really do want to be more active, but every time I try to take even short walks the pain eventually gets so bad I fear I’ve had another fracture and have to stop. When I´m able to try again, often weeks later, the same thing happens, so maybe I´ve reached a point where I´m fracturing no matter what I do, just a little bit faster if I´m active? At the same time I am very much aware of the fact that bones need weight-bearing exercise, so I feel like being trapped in a catch 22-like situation.

Anyway, sorry about the long background story, but I felt I had to explain why I have osteoporosis at an unusually young age, and why it is so hard for me to follow diet recommendations or do exercise.

Having all that information, do you think I have a chance to get better bones? Should I take more AlgaeCal than recommended because my osteoporosis is so severe? Or has my year on Fosamax made it impossible to build new bone (so the extra calcium I take maybe ends up in my arteries instead)? And regarding supplements, why isn´t phosphorus recommended, since bones contain of almost as much phosphorus as calcium? After reading your article about soy foods I´ve also considered taking genistein, but maybe that would compete with the estrogen I take? And should I try to get bioidentical HRT instead (if that’s possible) and if so why? I also read your comment about Forteo which makes perfect sense, but it seems to me that I´m not in a position where I can take the risk of not using it? However, after the 18 months on Forteo they want me to switch to Prolia because all the gain in bone density Forteo is supposed to give will disappear when you stop taking it, which doesn´t make it any easier to hold on to some kind of hope.

I absolutely understand if you don´t want to comment or give any advice – or have the time to answer my way too many questions. I wouldn´t have written here if I had been able to find a doctor – or someone else – with whom I could discuss what I should do.
Thanks anyway for dedicating so much of your time to inform about how to fight osteoporosis. I´m sure it makes a huge difference in many people’s lives.

Beverly McClain

Greetings. I have to say that I’m a bit horrified at your take on the MBC bone mets person (Janice) who posted earlier. Granted, she’s on an intense chemo and has been for a while, which implies things have been tough. But your answer basically said “well you’re not going to be around for long so it’s probably a non-issue”. How do you know that? And even if you did, your answer was incredibly insensitive. There are a good number of us (I have early bone mets, fairly superficial so far) who live with bone mets for many years and I intend to be one of them. I’ve been on Faslodex/Xgeva for a year (disease is stable), and my onc decided she was only going to give it to me once every 3 months now, because of brittle bone concern. I’m also very concerned with ONJ. Anyway, given that at least some of us live with mets for years, do you know of research that has included Strontium supplements for bone repair instead of Xgeva for people like us? I don’t want to die sooner than I have to but this stuff is evil!

Carmen Gonzalez

Hello, I just read your post and was I glad I did. I also have bone mets (sternum and rib) and Zometa and Xgeva have caused me a great deal of pain because I have developed ONJ. I don’t wish this upon anyone. And I completely agree with you, “this stuff is evil!” You have every right to be concerned about ONJ, it’s horrible. I wish you good health! Thank you.

Lara Pizzorno

Hi Beverly,
When I wrote Janice that her use of Xgeva would be short-term, this response was simply because this drug is only approved to be used short-term, so I assumed her doctor would only be giving it to her short-term. I absolutely did NOT mean to imply in any way that she was not going to be around longer! I am so distressed that what I wrote was so unclear that it could be read as you have. Please accept my apologies! I am going to have to become much better in being more explicit in what I write. I have great faith in our bodies’ ability to heal and recover — regardless of how ill or challenged we have been. We are extremely resilient and our inborn drive to heal is amazingly strong.
Regarding strontium for mets — I ran a number of searches on PubMed and finally found one very hopeful — although older, 1981 — study. I’ve copied in the abstract for this paper below — perhaps you could share this with your oncologist? Dr. Skoryna used strontium gluconate, but strontium citrate should be just as helpful — it’s the strontium doing the work. In fact, as I mentioned in the blog I wrote on strontium for AlgaeCal, citrate provides the benefit of making the body’s pH more alkaline, so might be even more helpful. Here’s a link to the article on strontium:

Here’s the abstract for the study showing strontium may be very helpful — the key text in this abstract is:
“An increase in density that corresponded to the deposition of stable strontium was observed in areas of bone lesions due to metastatic cancer in patients receiving stable strontium supplementation. This suggests the possibility of using strontium to mineralize osteophenic areas and to relieve bone pain.”
And this paper is free access — you can read and download the pdf for the entire paper by going to PubMed and clicking on the link on the upper right side of the page where it says “Free full text article in PubMed Central” – here is a link to the abstract on PubMed:

OK–here’s the reference and the abstract:
Skoryna SC. Effects of oral supplementation with stable strontium.Can Med Assoc J. 1981 Oct 1;125(7):703-12.PMID: 6120036

The biologic effects of stable strontium, a naturally occurring trace element in the diet and the body, have been little investigated. This paper discusses the effects of oral supplementation with stable strontium in laboratory studies and clinical investigations. The extent of intestinal absorption of various doses of orally administered strontium was estimated by determining serum and tissue levels with atomic absorption spectrophotometry. The central observation is that increased oral intake produces a direct increase in serum levels and intracellular uptake of strontium. The results of these studies, as well as those of other investigators, demonstrate that a moderate dosage of stable strontium does not adversely affect the level of calcium either in the serum or in soft tissues. In studies of patients receiving 1 to 1.5 g/d of strontium gluconate, a sustained increase in the serum level of strontium produced a 100-fold increase in the strontium:calcium ratio. In rats, studies indicate that an increase in intracellular strontium content following supplementation may exert a protective effect on mitochondrial structure, probably by means of a stabilizing effect of strontium on membranes. The strontium:calcium ratio in animals receiving a standard diet is higher in the cell than in the extracellular fluid; this may be of physiologic significance. An increase in density that corresponded to the deposition of stable strontium was observed in areas of bone lesions due to metastatic cancer in patients receiving stable strontium supplementation. This suggests the possibility of using strontium to mineralize osteophenic areas and to relieve bone pain. Also, because of reports of an inverse relation between the incidence of dental caries and a high strontium content in drinking water, the use of natural water containing relatively high levels of stable strontium should be considered. In each of these instances it is important to maintain a normal dietary intake of calcium.

I so hope this will be helpful to you, Lara

Lara Pizzorno

Hi Truls,
YES — you can regain your health overall and the health of your bones! You just need really good support to help your body heal. I am in the very fortunate position of knowing many outstanding clinicians all over the U.S. — if you can let me know where you are, I can provide some suggestions / referrals to doctors who will be willing and able to help you restore your health naturally, and who will definitely not think you are asking too many questions! Keep asking! You can write to me directly, so you won’t have to post where you are publicly.
It would be very helpful if you could share what the genetic issues are that you have which contributed to your bone loss — if it’s a VDR SNP (vitamin D receptor single nucleotide polymorphism) that results in your needing lots more vitamin D than the average person, I know all about that — I have one of the VDR SNPs that causes me to need at least 10,000 IU per day of D3 to get my blood levels into decent range. You can get vitamin D3 in the form of sublingual drops that would be absorbed in the mouth, so would not need to go through your stomach. And a number of other nutrients are also available in this form or via nebulizer.

If you’ve read Your Bones, you know that with vitamin D, you must have vitamin K, specifically K2, since it is required to activate the proteins that put the calcium whose absorption will be increased by vitamin D into your bones and keep this calcium out of your arteries. If you have sufficient vit K2 on board, you will not calcify your arteries.

Phosphorus is not recommended because it is so abundant in virtually all foods that we do not need to supplement.

Re HRT — PLEASE consider bio-identical hormone replacement! Here are links to some of the articles I have written on the differences between HRT and BHRT — they are very significant, and switching to BHRT could make a huge difference for you. Please do some reading and talk to your doctor about this. If your doctor won’t help you switch to BHRT, find another doctor! I can help with referrals:

Re genistein — this soy isoflavone is so much less potent (more than a thousandfold less potent) than human estrogen that it could not possibly interfere– and if you are taking conventional HRT, you are taking estrogens from pregnant mares, which are WAY more potent than human estrogens. We’re definitely talking dwarf Bambi verus Super Sized Godzilla here.

RE Prolia — as you’ve read in the above article, this drug will produce all the side-effects caused by the bisphosphonates and may also greatly disturb immune function. In my opinion, you would be much better served by getting optimal amounts of all the nutrients your bones need to rebuild and going on BHRT.

Re exercise — Pilates may be wonderful for you. It’s gentle, you can do it lying on a mat or on the Pilates equipment called the “Reformer”. STOTT Pilates has a special certification program for instructors to work with people with osteoporosis — if you use “STOTT Pilates” as your Google search term, a listing will come up of STOTT Pilates instructors in your area. You could call some and see if they have taken this certification — it is very important to work with someone who knows how to use Pilates specifically for osteoporosis. I recently did some videos demonstrating a few basic STOTT Pilates exercises adapted to specifically meet the needs of people with osteoporosis — I believe AlgaeCal will be posting these soon. I need to send in some written descriptions of the exercises to go with the video clips and haven’t had a moment free to do so, but I promise to get this done shortly. I haven’t seen the clips, but I hope I was able to demonstrate the exercises well enough to give you a good idea of what to do.
Truls — fight for yourself! You can beat this — you just need good support, Lara

Carmen Gonzalez

Hello, after being in remission 10 years for breast cancer, now I’m Stage IV with bone metastasis. Received 4 treatments of Zometa and 4 of Xgeva and have developed Osteonecrosis of the Jaw. What this pharmaceutical companies have to do is tell you how difficult this is to heal, that there is nothing no one can do about it, that is a chronic disease.. Yes, they tell you about oral hygiene, etc., etc.,and that you might develop ONJ……but they don’t tell you that you are stuck with this forever. I’ve been suffering with ONJ since September 2011 and it’s getting worse.
Thank you!

Lara Pizzorno

Hi Carmen,-
I’m at a major international functional medicine symoposium this week — the Institute for Functional Medicine conference and have been in sessions since 7am, so am heading off to get some sleep before it all starts up again tomorrow morning — so just a few minutes to respond, but just wanted to say I’m so glad you wrote. Will check into what are the best treatment options for ONJ — do NOT accept that you cannot heal this! Our bodies come naturally pre-programmed to heal absolutely everything. We just need to stop doing the things that prevent healing and really boost those that do. I will look into ONJ treatments that have had the best responses and get back to you with what I can learn. Do you still need to be taking Xgeva (denosumab) and Zometa (IV bisphosphonate) or are you finished with your course of these drugs ? Hang in there!

Carmen Gonzalez

Hi Lara,
I was very glad to receive your message. It means a lot, thank you very much. I hope everything is going well at the symposium. I agree, I can’t accep t that I cannot heal ONJ. I am my own advocate and believe me, I have been doing a lot of research about this. I am no longer on Zometa or Xgeva, my oncologist is not recommending I re-start treatment, so I’m only taking Arimidex.
I look forward to hearing from you again.
Thank you!
Carmen Gonzalez

Lara Pizzorno

Hi Carmen,

Looking at the current research on treating BRONJ (bisphosphonate-related – as in caused by bisphosphonates – ONJ), the most recently published paper I saw was the best, particularly since it was a study of patients with cancer who had developed BRONJ. I’ve copied in the abstract for this study below along with some key text from the full paper, so you can share it with your doctor. They got much better results when combining platelet-rich plasma (PRP) with laser phytotherapy. Their results are very encouraging! I so hope this will be helpful to you.

Do let me know how you are doing – you will be in my thoughts and prayers,

Oral Oncol. 2012 Jan;48(1):79-84. Epub 2011 Sep 21.

Association of laser phototherapy with PRP improves healing of bisphosphonate-related osteonecrosis of the jaws in cancer patients: a preliminary study.

Martins MA, Martins MD, Lascala CA, Curi MM, Migliorati CA, Tenis CA, Marques MM.
School of Dentistry, Universidade de São Paulo, São Paulo, SP, Brazil.

The aim of this study was to compare retrospectively the effect of three different treatments on the healing outcome of bisphosphonate-related osteonecrosis of the jaws (BRONJ) in cancer patients. Twenty-two cancer patients were treated for BRONJ with one of the following protocols: clinical (pharmacological therapy), surgical (pharmacological plus surgical therapy), or PRP plus LPT (pharmacological plus surgical plus platelet rich plasma (PRP) plus laser phototherapy (LPT). The laser treatment was applied with a continuous diode laser (InGaAlP, 660 nm) using punctual and contact mode, 40 mW, spot size 0.042 cm(2), 6 J/cm(2) (6 s) and total energy of 0.24 J per point. The irradiations were performed on the exposed bone and surrounding soft tissue. The analysis of demographic data and risk factors was performed by gathering the following information: age, gender, primary tumor, bisphosphonate (BP) used, duration of BP intake, history of chemotherapy, use of steroids, and medical history of diabetes. The association between the current state of BRONJ (with or without bone exposure) and other qualitative variables was determined using the chi-square or Fisher’s exact test. In all tests, the significance level adopted was 5%. Most BRONJ lesions occurred in the mandible (77%) after tooth extraction (55%) and in women (72%). A significantly higher percentage of patients reached the current state of BRONJ without bone exposure (86%) in the PPR plus LPT group than in the pharmacological (0%) and surgical (40%) groups after 1-month follow-up assessment. These results suggest that the association of pharmacological therapy and surgical therapy with PRP plus LPT significantly improves BRONJ healing in oncologic patients. Although prospective studies with larger sample sizes are still needed, this preliminary study may be used to inform a better-designed future study.

Copyright © 2011 Elsevier Ltd. All rights reserved.

PMID: 21940198

Here is some of the key text from the full research paper:

“Platelet-rich plasma (PRP) is an autologous concentration of human platelets obtained by centrifuged blood. This process produces a very high concentration of human platelets and contains several protein growth factors that are secreted actively by platelets and that initiate wound healing.51 They could stimulate the production of collagen, produce anti-inflammatory agents, initiate vascular ingrowth,
induce cell differentiation, control the local inflammatory response, and improve soft and hard tissue wound healing.33 PRP has been used by some authors27,28 on BRONJ as an adjunctive therapy to enhance bone healing.
Phototherapy with a low intensity laser is used in various areas of the biological sciences to promote tissue regeneration of injured tissues. This therapy produces analgesic, anti-inflammatory and biomodulatory effects.35,52 The laser light within the red visible and near infrared wavelengths corresponds to the energy absorption
spectrum of respiratory chain components, increasing the cellular metabolism of organisms under stress conditions.33,52–55 The photon energy is converted into chemical energy within the cell, forming ATP57, which may lead to increased intracellular Ca+2.55 This will ultimately stimulate the duplication of DNA,56 increase protein synthesis,56 induce the action of enzymes that control the oxidative stress,52 modulate the production of fibroblast growth factors37 and other cytokines.57 These events will stimulate proliferation of different types of cells involved with tissue regeneration. 54,58–61 Moreover, LPT using visible red light has demonstrated expressive results in angiogenesis,39 which is essential to
wound healing.62–64 Some authors have reported an increase in the expression of growth factors by smooth muscle cells, fibroblasts, cardiomyocytes and cardiac myocytes in response to LPT using different wavelengths.40,41,43 This therapy promotes bone and soft tissue wound healing, and has also been used as adjunctive
therapy for treating several diseases, such as oral mucositis48,49 and herpes simplex.65 In our study, most of the patients that presented a complete response,
showing non-exposed bone, were treated with pharmacological therapy plus surgical therapy and PRP plus LPT. The association of microbial growth control, by using systemic antibiotics and local irrigation, the biomechanical effect of necrotic bone
resection, the biologic effect of osteoinductive factors like PRP, and the biophysical properties of LPT proved successful in the management of BRONJ. In fact, the positive effect of LPT associated to PRP in 16 out of 22 cases, represented by the closing of the exposed bone, could be the result of an improvement in angiogenesis, cell proliferation and extracellular matrix synthesis induced by LPT and PRP. These results suggest that the association of pharmacological therapy and surgical therapy with LPT plus PRP significantly improves BRONJ healing in oncologic patients.

Mary DiSalvo

Ten years ago I had beast cancer (after many years of HRT). In February I was diagnosed with metastatic breast cancer on my thoracic spine and on two lymph nodes in my neck. The treatment since diagnosis is one mg of Anastrozole (Arimedx) daily to block estrogen and a subcutaneous shot of Xgeva monthly to rebuild bones starved of estrogen. Your article is of great concern to me. I feel like I have already served my time as a test case with HRT. My question is, what else can I do? Can I take the Anastrozole and approach bone building another way than Xgeva? I do take D3, 250 mg of Strontium and get Calcium from food and take a good Probiotic. I am 73 and otherwise very healthy and experiencing no symptoms of the cancer.

Your advice would be so appreciated. Thanks.


Lara Pizzorno

Hi Mary,
First, it’s wonderful that you are feeling good and having no symptoms. This is extremely encouraging! It is my expectation that your oncologist looked into the options and chose what she or he believes will be best for you at this time. As I mentioned in the blog, Xgeva is only approved for short term use, so you won’t be taking it for that long, which means a lesser chance of adverse side effects developing. Once your cancer is in remission, which hopefully will be very soon, you will no longer need Arimidex or Xgeva.
If, however, you are not comfortable with your oncologist’s advice, you might look into working with a physician associated with Cancer Treatment Centers of America. Their approach is integrative / holistic.
In addition to vitamin D3, strontium and calcium, a number of other nutrients are absolutely essential for bone health, and you should definitely ensure that you are receiving optimal amounts of all of them. I discuss all of the nutrients our bones require in my book, Your Bones, how to determine how much your diet is providing and how much YOU need in supplemental form. Your Bones should be available at your library if you do not wish to purchase a copy. It is being sold on Amazon for as little as $5.64 used. While I cannot summarize an entire book here, of particular concern to me is that you did not mention vitamin K2. Vitamin D3 increases your body’s ability to absorb calcium — it does nothing to help regulate where that calcium goes. You want the calcium to deposit in your bones, and NOT in your arteries, breasts, kidneys. Vitamin K2 activates the proteins responsible for putting calcium in bone (osteocalcin) and keeping it out of arteries, etc., (matrix Gla protein). The most effective form of K2 is MK-7; daily recommended dose that has been shown in the research to build bone and reduce risk of calcification elsewhere (so protects against cardiovascular disease as well) and to be extremely safe (unless you are on Coumadin, in which case, you can still take it but need to work with your doctor to ensure your INR remains stable) is just 100 micrograms.
If you are taking AlgaeCal Plus as your calcium supplement, you will be getting K2 (as MK-7) in the correct dose, along with other bone building nutrients including a wide range of trace minerals, many of which research is now showing play important roles in bone, boron and vitamin C. You will also be getting some D3 (do have your levels of 25(OH)D checked –this is the best indicator of body stores of vitamin D and checking is easy — just a blood test. Optimal blood levels of 25(OH)D are 60-80 ng/mL. If you are not within this range, you will want to discuss increasing your daily vitamin D3 intake with your doctor. Many people need 5,000 IU /day or even more — 7,500 IU or even as much as 10,000 IU per day is not uncommonly needed to get vit D levels into optimal range. If you have not already done so, please have your blood levels of 25(OH)D checked and, if not in optimal range, discuss increasing your intake of D3 with your doctor.
I very much hope this helps. There is much you can do to support your bones while utilizing short term drug treatments to promote cancer remission. Be well!

Keith Auzenne

Hi Lara;

My wife has stage 4 breast cancer and has been on Xgeva now for about 4 months. You’ve indicated in a few of your articles that Xgeva is a short term drug. What is your meaning of short term, 6 months, 12 months a couple of years? She has been taking New Chapter Bone Strength Take Care since starting the Xgeva. It has all of the essential ingredients you mention that a person should be sure they are getting to maintain bone health. Is this enough to offset some of the damage caused by the Xgeva? Is there a natural alternative to Xgeva? Thank you, Keith

Lara Pizzorno

Hi Keith
Sorry not to have responded sooner. I have been out of town (national park with no internet) for the last week and a half then up in Canada for a medical meeting, so just home now. I checked on AlgaeCal and do not see your question there so responding to you directly.

I’m sending you separately the Novartis write up regarding Xgeva for physicians. Re time limit on Xgeva, it states: “The median duration of exposure for safety analysis for Zometa 4 mg (core plus extension phases) was 12.8 months for breast cancer and multiple myeloma, 10.8 months for prostate cancer, and 4.0 months for other solid tumors.”
I would expect your wife will not be kept on this drug for more than 12 months.

Given her health issues, using Xgeva now may be her best option, but along with it, providing her body with the best nutritional support is clearly critical, and not just for her bones, but overall. I cannot condense into an e-mail what I covered in several hundred pages in Your Bones. I am attaching for you a summary overview of the nutrients required for bone health that will be in the next edition of Your Bones, which will be out in January 2013 – so what I am sending you is the draft material – some changes may be made to it and it refers to the full book for a complete explanation of what is presented in many places. PLEASE, I request of you that this is for your personal use only – my publisher, Praktikos, (a non-profit) would be most unhappy with me for sending out this material ahead of publication.
I urge you to just get a copy of Your Bones (your library should have it if you don’t want to spend the less than $10 to get it on Amazon – I think used copies are now selling for a little more than $5.00) and read it. I promise it will provide the answers you seek in detail with plenty of back up in the peer-reviewed medical literature on PubMed if you want to use it to talk with your wife’s doctors in developing the best nutritional support plan for her.

If I can be of further help, don’t hesitate to contact me – you now have my personal email. I wish you and your wife every blessing. Be well,

vicky velasquez

Dear Lara,
I am 50, diagnosed with stage 3 breast cancer 2 years ago. I am replacing now Tamoxifen for Anastrazol. My oncologist put me on oral BF and due to GI complications I could not tolarated it. She has me now schedule of IV Danasumab but I am afraid of all the side effects of this drug.
Do you think your approach is sufficient to prevent bone loss with the use of AIs? or I can complement your TX with a less harmful drug.
Thank you so much for your opinion.

Lara Pizzorno

Hi VW,
Regardless of what drugs you are taking, ensuring you are providing your bones with the nutrients they require to remodel healthfully via both your diet and supplements will be your best option. I wish I could give you more input, but I am not an oncologist. What I can suggest is a resource where you will find oncologists who are well informed regarding good nutrition and the use of supplements, which become even more important when one has cancer: Cancer Treatment Centers of America. This group has a number of hospital centers across the US, so there may be one reasonably close to you.
Here is a link to their website: They also have an 800# you can call — anytime — to discuss your treatment options 800-392-7355. I very much hope this will be of help to you, Lara

John Mulligan

Lara- Have you followed the other new Amgen drug for osteoporosis, AMG 785? It has a completely different mechanism of action (it blocks a negative regulator of osteoblast function) and should thus have a completely different spectrum of side effects. In human genetic studies, patients that are missing one copy of the target gene (sclerostin) had high bone density but no other detectable changes.


I have been diagnosed with stage 4 breast cancer with bone mets. I’m on xgeva shots and have had two so far. After reading the book “The China Study” I am now on a vegan diet which means no animal products, including cheese, yogurt, milk etc. I am also on arimedex to block estrogen in my body, since my cancer is estrogen and progesterone receptor positive. In the five weeks since diagnosis of my returning cancer, my lymph nodes have shrunk, I have less water around my lungs, and according to the ca 27-29 tumor marker test my markers have dropped from 2000 to 1000. I don’t know if it’s the drugs or the diet but I feel that I have to keep doing both. My bone mets are primarily in my vertebrae and pelvis. The vertebrae have been compromised to the extent that I am not allowed to lift more than 5 pounds. Do you have any suggestions for recipes that would be helpful for me that are vegan friendly?

Lara Pizzorno

Hi Chris, I have a great resource for you — The World’s Healthiest Foods’ website — Lots of great recipes — you can select the foods you want to include and/or exclude, nd run a search for just those you are interested in. And WHFoods also offers reliable information on virtually all aspects of healthy eating — all free, not even any ads, completely supported by the George Mateljan Foundation. Hope you find this website helpful, Lara

jacki gutman

my recent bone density is reported as high risk for fractures. i have taken actonel, forteo & other biphosphanates & as a result have developed barretts esophogus. my endocronologist now suggests prolia. i was taking infusion of reclast for 3 yrs from johns hopkins endocrine center & stopped for one yr. they too want to put me on prolia. do you have a doctor in the ny area who can help me. i have not had any spontaneous fractures but some from trauma. i dont know what to do now. i am 76yr with a family history of osteoporosis. i remember my mother having multiple small fractures & always being in pain. this was before the new meds came out. please help me to make a decision.

Lara Pizzorno

Hi Jacki,
I am so distressed by your story! You are completely correct — Prolia is NOT what you need! The good news is that there are excellent physicians in the NY area. I suggest you contact Dr. Peter Bongiorno, Inner Source Health. You may have seen Peter’s amazing wife, Dr. Pina LoGiudice, recently on Dr. Oz. Here is a link to the clinic website:
I am absolutely certain they will be able to provide you with the help you need to turn things around in 2013 — Be WELL! Lara

Ann Ohlmacher

Lara, thank you so much for all this generous information — it is so enlightening and helpful for me at this point in time. I have been diagnosed with Breast Cancer with bone mets. For the most part, I have been treating myself with natural supplements and diet and feel great. However, I do have an oncologist, and am taking femara. And he also recommended aredia — I took two doses and then balked as it seemed to be worsening Thoracic Outlet Syndrome (which I have had for years). Now he wants me to take xgeva, but after reading your info, I don’t feel that I can do that. I live in Canada near Ottawa. Are there any resources here?? Thanks Again for your wisdom and courage, Ann

Lara Pizzorno

Hi Anne,
SO sorry — I just saw your question — AlgaeCal has been fixing some technical problems, so I am now receiving a number of questions that did not get through to me before.
Yes, there are some excellent resources in Canada — if you go to the Institute for Functional Medicine’s website (the link below) you will find a listing of physicians in Ottawa who are functional medicine certified and can help you:


I took Fosamax for 7 years and my bone density got worse instead of better. I have been off it for two years and my doctor wants me to get a Prolia injection. I have read about it and am not comfortable with what I have learned. Are there any doctors that you would recommend in the greater Detroit, MI area that might be able to help me using more natural remedies? Also, do you have any exercise videos that you could recommend for building bone density?
Thank you.

Lara Pizzorno

Hi Ann
Well, the good news is that research has proven that providing your bones with the nutrients they require to rebuild is effective — even in women who did not respond to a bisphosphonate (e.g., Fosamax). I wrote about this research in detail in the 2nd edition of Your Bones — which will be out this March 2013. If you would like to look at the study in full, it is accessible for free on PubMed — here is the abstract for the study followed by a link to it on PubMed:

Combination of Micronutrients for Bone (COMB) Study: bone density after micronutrient intervention.

J Environ Public Health. 2012;2012:356798. doi: 10.1155/2012/356798. Epub 2012 Jan 19.
Environmental determinants of chronic disease and medical approaches: recognition, avoidance, supportive therapy, and detoxification.

Sears ME, Genuis SJ.

Source: Children’s Hospital of Eastern Ontario Research Institute, Ottawa Hospital Research Institute, Ottawa, ON, Canada K1H 8L1.

The World Health Organization warns that chronic, noncommunicable diseases are rapidly becoming epidemic worldwide. Escalating rates of neurocognitive, metabolic, autoimmune and cardiovascular diseases cannot be ascribed only to genetics, lifestyle, and nutrition; early life and ongoing exposures, and bioaccumulated toxicants may also cause chronic disease. Contributors to ill health are summarized from multiple perspectives–biological effects of classes of toxicants, mechanisms of toxicity, and a synthesis of toxic contributors to major diseases. Healthcare practitioners have wide-ranging roles in addressing environmental factors in policy and public health and clinical practice. Public health initiatives include risk recognition and chemical assessment then exposure reduction, remediation, monitoring, and avoidance. The complex web of disease and environmental contributors is amenable to some straightforward clinical approaches addressing multiple toxicants. Widely applicable strategies include nutrition and supplements to counter toxic effects and to support metabolism; as well as exercise and sweating, and possibly medication to enhance excretion. Addressing environmental health and contributors to chronic disease has broad implications for society, with large potential benefits from improved health and productivity.

PMID: 22315626 [PubMed – indexed for MEDLINE] PMCID: PMC3270432 Free PMC Article
Here’s a link to the abstract — from there you will be able to acess the full paper:

Regarding a referral to a competent physician in the Detroit area — your best move is to go to the website for the Institute for Functional Medicine ( and utilize their practitioner referral link, which is listed under Functional Medicine Resources – the “Find a Functional Medicine Practitioner” tab. Any physician who has undergone the advanced training provided by the IFM (called the AFMCP) will be able to help you.

Re exercise videos — You could take a look at Sharon Betz, PT’s video, Pilates Exercises for Osteoporosis. Optimal would be to work with a STOTT Pilates certified instructor who has taken the Pilates for Osteoporosis STOTT training. You should have a postural analysis to determine precisely what YOUR issues are and then have a mat (and possibly reformer work) program designed for YOUR needs. Once this has been done, you can do your workout anywhere you can put down a mat on the floor, and you would just need to meet with your instructor every few months to refine (and increase the challenge) of your program as you improve, which you definitely will if you are good about doing the mat work daily for a half hour. In the 2nd edition of Your Bones, I have added a large section on Pilates for Osteoporosis with some sample exercises, so you can have an introduction / oerview of Pilates’ special benefits for osteoporosis.

Hope this helps, Lara


Does anyone know how long denosumab lasts in the bone once you stop taking it?

Lara Pizzorno

Hi Dikla,
The short answer to your question is “No.”
Denosumab is a potent antiresorptive agent with a long duration of activity because of its long half-life as well as effects in inhibiting osteoclast recruitment and activity. Preclinical studies suggested that the delay in osteoclast recovery observed after withdrawal of RANKL inhibition caused by denosumab is due to the time necessary for osteoclasts to regenerate from precursor cells (Lacey et al 2000; Capparelli et al 2003). On the potentially hopeful side here, denosumab is not incorporated into the bone matrix (unlike the bisphosphonates, which are incorporated into the bone) so once denosumab has been eliminated from the body and osteoclast’s are again being produced, reversibility of denosumab’s antiresorptive effect should be rapid. (Lewiecki EM, Denosumab: an investigational drug for the management of postmenopausal osteoporosis. Biologics. 2008 December; 2(4): 645–653. Here’s a link to this medical journal article on PubMed discussing this:
The problem is that no one knows how long it takes the body to again start producing osteoclasts — and, as we are not carbon copies of one another, the length of time for this function to return to normal may vary — significantly — from individual to individual.
In studies evaluting your question in regards to bisphosphonates — in some women, normal bone remodeling had not begun a year after “treatment” with these drugs was stopped. In other women, normal bone remodeling had restarted after a year.


Hi Lara –

This is an unbelievably informative thread. Thank you so much.

I also have breast cancer that spread to bones and organs, and was on Zometa for two years. I was told that that was the recommended duration of time to be on that drug, and no benefit would be gained from taking it longer.

Two years later, a different oncologist suggested Xgeva. I can’t find any studies done (maybe because none have been done) on the effects of taking these drugs sequentially. Do you know if anyone has looked at the effects of taking these drugs one after the other, for more than two years total time? Do you have an opinion on whether it seems like a good or bad idea?

In your article, you say that while Xgeva reduced time to bone events in men with prostate cancer, it didn’t reduce pain or extend life. Do you know if the studies show that the drug works differently for women with breast cancer? My oncologist claims the studies show it extends life, but I haven’t found specific studies that show this.


Lara Pizzorno

Hi Barbara,
Thanks, so glad you found the information helpful.
In response to your questions, I ran a PubMed search to locate peer-reviewed research on sequential use of IV bisphosphonates (Zometa, also marketed as Reclast and Aclasta) and denosumab (marketed as Prolia and Xgeva), and was unable to find anything on PubMed discussing this. The focus in sequential drug therapy is currently on the use of teriparatide (marketed under the name Forteo) following use of a bisphosphonate or denosumab, but since teriparatide use includes concerns of increasing risk for bone cancer, this is not likely to be your best option. What I was able to find regarding the two anti-resportive drug options (bisphosphonates and denosumab) specifically to women with metatastic breast cancer is a mixed bag in relation – potential for very nasty adverse effects from both types of antiresporptive agents coupled with potential for some benefit.
I’ve copied in below for you some of the key text from the most recent, most relevant medical journal articles. Obviously, this is a VERY personal choice that you need to make, being as well informed as possible and after discussion of all your options with your oncologist. I very much hope that the option of providing your bones with all the nutrients required for healthful bone remodeling while eliminating as many factors contributing to excessive bone loss as possible (all of which I cannot possibly lay out here but have discussed at length in 2nd edition of Your Bones) is one your oncologist is willing to include along with drug recommmendations in your healing program. If not, I urge you to look into working with an oncologist at one of the hospitals associated with Cancer Treatment Centers of America, which offers cutting edge integrative cancer treatment.

The two most recent papers I found that are relevant for you are:

(1) Mazziotti G, Bilezikian J, Canalis E, Cocchi D, Giustina A. New understanding and treatments for osteoporosis.
Endocrine. 2012 Feb;41(1):58-69. doi: 10.1007/s12020-011-9570-2. PMID: 22180055

(2) Lippuner K. The future of osteoporosis treatment – a research update. Swiss Med Wkly. 2012 Jul 19;142:w13624. doi: 10.4414/smw.2012.13624.

Relevant text from (1) with some comments from me in […]:

Bone disease in neoplasia [the following suggests denosumab may be helpful for you]
Osteoclasts and RANKL/RANK/OPG pathway are the target of malignant tumors capable of forming skeletal metastases or causing hypercalcemia [61]. RANKL-mediated mechanisms have been described for a variety of osteotropic malignancies, such as breast, lung, and prostate cancer. Moreover, an enhanced and uncontrolled osteoclastic bone resorption was described in patients with multiple myeloma in close relationship with the osteolytic lesions [62]. Neoplastic cells may stimulate bone resorption by releasing cytokines capable of enhancing RANKL production by stromal cells [63]. Moreover, some neoplastic cells, such as myeloma cells, inhibit OPG production leading to an unbalanced activation of RANK pathway [64]. Activated osteoclasts produce cytokines that stimulate the growth of tumor cells creating a vicious cycle of bone destruction [65]. These experimental findings offer the rationale for targeting
RANK–RANKL–OPG in the prevention of skeletal-related events occurring in patients with bone lesions from several tumors. Denosumab at 120 mg every 4 weeks was shown to be more effective at delaying skeletal-related events, such as pathological fractures and spinal cord compression or the need for radiation or surgical treatment, than zoledronic acid in patients with bone metastasis from breast and prostate cancer [66, 67]. Moreover, denosumab was shown non-inferior to zoledronic acid in preventing or delaying skeletal-related events in patients with multiple myeloma or bone metastases from solid tumors [68]. Based on this evidence, denosumab at dosage of 120 mg every 4 weeks is approved for the treatment of patients with bone metastasis from solid tumors,
offering a therapeutic alternative to intravenous bisphosphonates for patients with bone metastases.

Selected clinical topics
Long-term safety of bisphosphonates
Bisphosphonates are the most commonly prescribed agents for the treatment of osteoporosis. Their efficacy in reducing fracture risk with a favorable safety profile is well-established. However, their long-term use has been associated with reports of undesirable events not previously recognized. These include ONJ and atypical femoral fractures. A systematic review published by Khan et al. [85] showed that high-dose intravenous bisphosphonates in oncologic patients is associated with an increased risk of ONJ that appears to be dependent on dose and duration of therapy.

Open issues [the following indicate denosumab is far from risk free—you should be very careful about undergoing any kind of dental procedures and should be extra vigilant about maintaining excellent dental hygiene, avoiding sugary highly processed foods, etc., and following the bone building Mediterranean-style whole foods, largely organic and GMO-free diet I discuss in Your Bones]

Several unresolved issues are the object of ongoing research: (1) A clinical trial is investigating the anti-fracture efficacy of denosumab in men with osteoporosis; (2) It is important to consider that because of the role of RANKL in T cell biology, denosumab could have adverse effects in the immune system [73]; (3) The safety of the long-term use of denosumab, possibly leading to prolonged suppression of bone turnover and to osteonecrosis of the jaw (ONJ) (2 cases crossed-over from the 3-year placebo arm in the
5 year denosumab extension trial for osteoporosis were reported to have ONJ), especially in predisposed patients, such as those with neoplasia. Although, the administration of recombinant OPG-Fc was shown to be effective in preventing bone metastasis in experimental animals with solid tumors [74], it is unknown whether denosumab may have similar efficacy in humans.

Relevant copy from article (2):

Due to the tight interrelationship with shared signaling pathways between the skeletal and immune systems, potentially associated risks deserve further scrutiny [19, 20]. Osteonecrosis of the jaw was not seen in the pivotal trial but was reported in the extension study [21, 22] and in studies with patients with metastatic bone disease or myeloma [23, 24].Compared to bisphosphonates, denosumab exhibits a much shorter terminal half-life of several months instead of several years [25].

While the safety profile of most bone active substances [i.e., the drugs currently being used] is at least partially [emphasis mine] known, there is considerable potential for improvement (ONJ, atypical fractures, interactions with the immune system). Treatment
alternatives are needed for patients exhibiting or at risk of side-effects. While a relative fracture risk reduction can be achieved for non-vertebral, hip, and spine fractures, respectively, still 30 to 80% of these fractures cannot be prevented. As osteoporosis is a systemic disease, there is an obvious need for improving the magnitude of the therapeutic effect at all fracture sites.[LUP—in other words, you are going to require more than a drug targeting one aspect of bone remodeling to deliver what not just your bones, but your entire body needs to become well!]

Based on postmarketing and clinical research experience available to date, denosumab exposes patients to a risk of hypocalcaemia, which is significant in patients with severe renal impairment or receiving dialysis, to a potential for adverse outcomes resulting from
the induced profound, even if reversible, suppression of bone remodelling such as osteonecrosis of the jaw, atypical fractures and delayed fracture healing, [emphasis mine – LUP]and to a potentially increased risk of severe infections consistent with its osteoimmunological effects. Epidermal and dermal adverse events not specific to the injection site (such as dermatitis,
eczema, and rashes) were significantly increased. Finally, cases of pancreatitis and new malignancies of the breast,
the reproductive system, and the gastrointestinal system were numerically more frequent with denosumab with no
established causal relationship to drug exposure [80]. Denosumab was also proven effective for increasing BMD
over 2 years in women receiving adjuvant aromatase inhibitor therapy for breast cancer [81] [LUP—you did not mention whether you are also taking an aromatase inhibitor—since these drugs block the enzyme aromatase, which synthesizes estrogen, they also block all the beneficial effects of estrogen on bone, thus causing increased bone loss. If your current drug protocol involves an aromatase inhibitor, then this factor favors – short term — use of denosumab despite its other risks.]

Barabara, I wish for you complete healing and vibrant health. I hope this information will help empower you to make the best choices for yourself. Be well! Lara


Dear Lara,
Please provide some suggestions for my situation.

I am a 72-year-old woman with osteoporosism which has gotten worse. My mother had it and suffered a spine fracture. I see my doctor next week—I’m afraid she will recommend taking a drug (like Reclast, Evista, Prolia). I would like to try more natural approaches. Here are some facts about me:

I have had several foot surgeries, which make it almost impossible to do weight-bearing exercises. Do you know of a website that would provide me some alternate exercises (or do you recommend an exercise program for me with feet problems)?

I consume at least four dairy servings a day (including three glasses of skim milk). Do I need a calcium supplement—I would think I would getting enough calcium the natural way.

I have been on coumadin for the past five months, but expect to stop taking it at the end of this month. I have been taking high doses of Vitamin D (5000 mg) for several months. How can I undo the damage (which I read about on this website) caused by this combination?

Besides osteoporosis, I have a thyroid condition (for which I take synthroid). I had a major life-saving surgery in November following a mistake made during a simple procedure (an ablation) to get rid of a-fib. I have been free of the a-fib for last several months, but I still am recovering from the “wounds” of the surgery.

Would your product—AlgaeCal—be appropriate for me (especially if I cut back on my consumption of dairy products)?

By the way, a neighbor drinks only unpasteurized milk in the belief that pasteurizing milk prevents calcium from being absorbed by the body. Your opinion?

I look forward to hearing from you with your thoughts. Thank you, Christine

Lara Pizzorno

Hi Christine,
Re exercises — if you can find a Pilates instructor trained to work with women with osteoporosis, this would be an ideal exercise for you. In the 2nd edition of Your Bones, I added a whole section on Pilates for Osteoporosis with exercises and photos included. It would be best for you to work out on the “Reformer” (special Pilates equipment), which would allow you to lie down and still target the muscles (and bones) you most need to build. Look for a STOTT Pilates certified instructor.
Re your consumption of cow’s milk — how is your digestion? Are you able to absorb your nutrients easily and well or do you get indigestion? If your digestion is fine, each cup of cow’s milk will be giving you approximately 297 mg of calcium. AlgaeCal Plus provides a LOT more than just calcium — it delivers calcium in the full matrix of all the trace minerals naturally present in the sea coral from which it is derived, and also provides magnesium, boron, vitamin D3 and K2 (for which reason, you should not be taking AlgaeCal without your doctor’s supervision since you are still on Coumadin.)
Re pasturized or unpasteurized milk — I know there continues to be some discussion around this, but there are no scientific studies, no peer-reviewed published research that shows calcium (and other nutrients) are not absorbed just as effectively from pasturized as unpasteurized milk.
Re Coumadin — VERY glad you are getting off this drug, which causes calcium to deposit in arteries and not in bones. It does this by interfering with our ability to recycle and use vitamin K. As you now know from reading my blogs on AlgaeCal’s website, vitamin D increases our body’s ability to absorb calcium but does nothing to impact where that calcium goes. You want it to deposit in your bones and not your arteries, breasts and kidneys. Putting calcium into your bones is the job of a vitamin K-dependent protein called osteocalcin. Keeping calcium out of your arteries, etc, is the job of another vitamin-K dependent protein called matrix Gla Protein. If you do not have sufficient vit K on board or are unable to utilize it (which happens when you take Coumadin), neither of these proteins can be activated. PLEASE work with your doctor to begin taking vitamin K2 in the form of MK-7 at a dosage of 100 micrograms per day as soon as possible. Even individuals taking Coumadin can take K2 as MK-7 (100 mcg) if working with their doctor, who can monitor their INR to ensure it remains stable and can adjust the Coumadin dose if needed.
RE your thyroid condition — if you are taking synthroid, I expect your thyroid function is low. A couple of questions for you — how much iodine are your getting daily? Thyroid hormones are made from iodine-if you are not getting enough iodine, you will be unable to produce thyroid hormones. Also selenium is required for proper thyroid hormone production and utilization. I would check my intake of both nutrients to be sure I was supplying my body with what is needed for normal healthy (drug-free) thyroid function. Also, you should have your doctor run the labs to monitor that your dose of synthroid is not too high for you — a higher dose than you need will cause bone loss.
Hope this helps, Lara


Can you tell me if you are qualified to tell people to not take drugs like Denosumab? I am a 72 year old female, still working full time, active, but in recent time have broken a shoulder and then a foot within 6 months of each other. I suffer chronic dizziness and nausea because of ear problem which cannot be fixed.I have narrowing of the spinal column in my neck which in turn is putting pressure on my spinal cord and causing me nausea, also a bone tumor in my wrist which I am having removed shortly. My specialist has recommended I go on the drug to decrease my chances of getting either a hip or back fracture. I eat well, am a vegetarian, and exercise on a regular basis. However my bone mass has decreased significantly over the last couple of years despite my attempts to keep it within normal range. I have weaned myself off all heart medication (A FIB (Lone) and have been taking hi D3, Taurine, Magnesium,Calcium,Fish Oil,and High C. If I dont take this drug I have been told I am more than likely going to break a major bone if I fall again.

Lara Pizzorno

Hello Joy,
I am not a physician. I am the editor of a medical journal, author of a number of medical books written both for doctors and for the public, and a medical writer with more than 30 years experience. Because osteoporosis runs in my family, and I was diagnosed with significant osteopenia when in my mid-40s (so well before menopause) — and I was “doing everything right” as well — my husband, Dr. Joe Pizzorno, and I became, of necessity, very motivated to figure out WHY osteoporosis develops and how to combat its development and restore health to our bones. I am now 64, and my bones are in excellent health. I will be the first woman in all the generations in my family I know of to NOT die early from osteoporosis. I wrote Your Bones to pass on the knowledge I was forced to accumulate, hoping to spare others from what I know to be a completely preventable and reversible disease– osteoporosis. Every statement made in the book is backed up by a reference from the peer-reviewed medical literature, and these are all cited in the book — well over 500 references’ worth. So, am I qualified? I surely am qualified to provide you with accurate information and my thoughts. Your decision, however, is one you must make for yourself — No one, not even your physician, knows your body and your ability to fight for your health better than YOU. Popping a pill or getting an IV drug is easy. Figuring out what YOU need to do to restore your bones’ health can be challenging.
The problem with denosumab and all the drugs currently available is that they are for short term use (so will only, at best, postpone your risk of a major fracture for a few years), and, these drugs come with risk for significant adverse side effects. Denosumab, like the bisphosphonates, works by preventing osteoclasts from doing their necessary job of removing old, brittle bone, so it can be replaced with new, healthy bone. Unlike the bisphosphonates, which poison osteoclasts after they have developed, denosumab prevents osteoclasts from ever developing by binding to, and thus blocking off, all available RANKL — RANKL is a ligand to which not only osteoclasts but our B and T cells, key cells of our immune system, must bind to develop. Thus, denosumab use (in addition to all the adverse effects of the bisphosphonate drugs, which denosumab has also be found to produce, and which include increased risk for hip fracture) carries with it risk of severely compromised immune function, which has shown up in some of the patients taking this drug in numerous studies now. I write about these studies in detail and provide references to the peer-reviewed medical literature for all statements made, both here in this blog and in Your Bones, 2nd edition.
From what you write about your current symptoms, it is clear that SOMETHING is causing significant excessive chronic inflammation in your body. THIS, not lack of denosumab, is your real problem, and identifying WHAT is causing the inflammation and eliminating it, is, in my educated opinion, your best option to restore your health, overall, not just that of your bones. There are many factors in our current modern lifestyle and diet that promote inflammation, and most of us, despite trying to eat well, are not getting optimal amounts of all the nutrients required for healthy bones, nor, in many cases if we are over age 50, are we able to produce sufficient stomach acid and digestive enzymes to properly digest our food and asborb its nutrients. I cannot go over all the factors I discuss in several hundred pages in Your Bones here; I urge you to get a copy of the 2nd edition of Your Bones and read all of it, especially the new 30+ page appendix at the end of the book in which I discuss all the lab tests one might have run to identify what is causing excessive bone loss — IF you have been following the recommendations fully laid out in Your Bones for 3-6 months and are still losing excessive bone. The book is published by a non-profit and is being sold for less than $9.00 on Amazon.
If you would prefer to take denosumab, PLEASE use the short amount of time it might give you to become well informed about all the things you can do to improve your bones’ health and all the many factors that, in modern society, mitigate against it, so you can avoid or eliminate as many of these as possible. And please be sure to thoroughly read about denosumab’s potential side effects, so if you begin to experience any of these, you can get help as quickly as possible.


Hi Lara, Came across this question and answer forum while browsing to find out if Prolia can cause muscle weakness and extreme fatigue and no appetite. I had a prolia shot on Monday and by Wed eve I was so exhausted I went to bed and have not until today been able to do anything. My Dr says it is highly unlikely that it is caused by the shot and that I probably have the flu. I take very good care of myself (hike 5 miles everyday ) eat right and it just seems like such a coincidence that this is happening so soon after the shot. I have researched a little and saw that denosumab (which prolia contains) can cause muscle weakness and fatigue in 45% of patients. Should I believe my dr?

Lara Pizzorno

Hi Laurie,
The side effects you are experiencing are known to be caused by both the bisphosphonate drugs and by denosumab (tradename, Prolia). Believe in your own body. Hopefully, you will soon feel better. Meantime, rest, and nourish yourself with light meals of healthful (organic, non-GMO, whole) foods (broth, steamed vegetables, salad–spring greens tossed with extra virgin olive oil and lemon juice). If dairy foods are OK for you, yogurt or kefir topped with some fresh blueberries would be a good idea as well. Be well! Lara

pam mccarthy

Dear Lara,
Just wondering if you have any data or info on long term ingestion of calcium channel blockers and osteopenia / osteoporosis? I am 65 with normal thyroid and parathyroid function and normal everything else blood test wise ,but severe bone loss with a T score at the wrist of-3.0 and -2.6 at the hip. I had a normal bone density at age 45 but it has gotten progressively worse over the years. All that I have read says there should be no connection between my bone loss and the 30 years I’ve been taking Diltiazem for coronary vasospasm, but I’ve got lingering doubts. Mt Doc recommends either an IV bisphosphonate or Denosumab but I’m obviously concerned about possible adverse side effects.
Your thoughts would be greatly appreciated!

Lara Pizzorno

Hi Pam,
My apologies for not responding sooner– AlgaeCal has been revamping the blog and some emails fell through — I just received your question today. As you know, I do not recommend the drugs – eg denosumab, bisphosphonates or teriparatide — currently available for treatment of osteoporosis, for MANY reasons, which I have detailed in over a hundred pages in 2nd edition of Your Bones. In regards to calcium channel blockers — fortunately, these are NOT among the drugs that promote bone loss. Here are two recent studies confirming this:

J Hypertens. 2006 Mar;24(3):581-9.
Treatment with beta-blockers, ACE inhibitors, and calcium-channel blockers is associated with a reduced fracture risk: a nationwide case-control study.
Rejnmark L, Vestergaard P, Mosekilde L.

Source:Department of Endocrinology and Metabolism, Aarhus University Hospital, Aarhus Sygehus, Aarhus, Denmark.

Cardiovascular diseases are associated with disturbances in calcium metabolism, including increased urinary calcium, vitamin D insufficiency, and decreased bone mineral density. Antihypertensive drugs may increase the risk of falling. However, risk of fracture in patients treated with non-diuretic cardiovascular drugs is largely unknown.

AIM: We investigated associations between fracture risk and treatment with commonly used cardiovascular drugs: beta-blockers, angiotensin-converting enzyme (ACE) inhibitors, and calcium-channel blockers.

DESIGN: A population-based pharmaco-epidemiological case-control study with fracture in year 2000 as outcome and drug use during the previous 5 years as exposure. We used nationwide computerized registers to assess individual use of drugs and related these data to individual fracture records and information on socio-economic and health-related confounders.

RESULTS: We included 124,655 cases that sustained a fracture and 373,962 age and gender-matched controls. After adjustment for potential confounders, risk of any fracture was reduced by 9% [odds ratio (OR) 0.91; 95% confidence interval (CI), 0.88-0.93] in users of beta-blockers, by 6% (OR, 0.94; 95%CI, 0.91-0.96) in users of calcium-channel blockers, and by 7% (OR, 0.93; 95%CI, 0.90-0.96) in users of ACE inhibitors. Moreover, risk of hip fractures was reduced significantly by 7-14% in users of the three groups of drugs. No major differences were found between men and women or in subjects younger or older than 70 years of age. Sub-analyses indicated differences between groups of calcium-channel blockers, as use of non-dihydropyridine drugs was associated with a larger risk reduction than use of dihydropyridine drugs.

CONCLUSION: Treatment with beta-blockers, ACE inhibitors, and calcium-channel blockers is associated with a small but significantly reduced risk of fracture.

PMID: 16467662

J Intern Med. 2006 Oct;260(4):350-62.
Effects of antihypertensive drug treatments on fracture outcomes: a meta-analysis of observational studies.
Wiens M, Etminan M, Gill SS, Takkouche B.

Source:Faculty of Pharmaceutical Sciences, University of British Columbia, Vancouver, BC, Canada.

OBJECTIVE: To quantitatively pool findings from observational studies on the risk of fracture outcomes associated with exposure to five antihypertensive drug classes: angiotensin-converting enzyme (ACE) inhibitors, diuretics (in particular thiazide diuretics), beta-blockers, calcium-channel blockers and alpha-blockers.

DESIGN: Systematic review and meta-analysis.

DATA SOURCES: Publications listed in the MEDLINE, EMBASE and LILACS databases, the ISI proceedings, and bibliographies of retrieved articles. Sources were searched from the earliest possible dates through December 2005.

REVIEW METHODS: We included case-control and cohort studies presenting relative risks and confidence intervals (CIs) for the association between exposure to antihypertensive agents and fracture outcomes. Data were extracted onto a standardized computer worksheet. Study quality was assessed using a 10-point questionnaire specific to case-control or cohort study design.

RESULTS: Fifty-four studies were identified. Pooled estimates were computed using the software HEpiMA. The pooled relative risk (RR) of any fracture with use of thiazide diuretics was 0.86 (95% CI 0.81-0.92) and 1.14 (95% CI 0.84-1.54) with use of nonthiazide diuretics. There was a statistically significant reduction of any fracture with use of beta-blockers, (RR 0.86, 95% CI 0.70-0.98). The one study with ACE inhibitor data showed protection (RR 0.81, 95% CI 0.73-0.89). No significant associations were found between fractures and exposure to alpha-blockers or calcium-channel blockers.

CONCLUSIONS: Thiazide diuretics and beta-blockers appear to lower the risk of fractures in older adults. However, these agents cannot be recommended as preventive therapies for fractures until data from randomized controlled trials have established their efficacy. Patients who use these inexpensive drugs as treatments for hypertension may also benefit from a reduction in fracture risk.

PMID: 16961672

My suggestion to you is to read a copy of the 2nd edition of Your Bones — should be available at your library and is on Amazon at a cost of less than $10 — and become aware of all the factors that contribute to bone loss — virtually all of which you can eliminate from your life, so your bones can rebuild. SOMETHING is causing you to lose excessive amounts of bone, and you are also likely to not be getting optimal amounts of all the nutrients your bones require to rebuild healthfully. A number of lab tests — discussed in a 30 page appendix to 2nd ed – can help you zero in on WHAT is causing your bone loss. I would definitely get well informed about what might be causing my bone loss and how to rectify this before I took denosumab or a bisphosphonate, both of which can actually promote fractures by keeping old brittle bone around and preventing healthy and necessary bone remodeling.



Just to counteract all the scaremongering that is going on here: although Denosumab lowers your immune system, it’s only in your body for 6 months, unlike Alendronate which remains in your body for years and years – and for a good number of patients the outcomes are extremely positive. I agree with you that is extremely important to be aware of the side effects of any drug that you take, but the reason you are advised to take this medication despite of possible side effects, is because you need it. If you didn’t need medication doctors would not prescribe them, it’s naive to believe otherwise. Denosumab works for many people, and it has been extremely important to me. It has brought my values down to ‘normal’ for the first time in my life, and I have had fibrous dysplasia (similar to osteoporosis) for all my life. I suggest you start reading up studies first-hand by browsing recently published medical articles. Novel results are published every year, shedding more and more light on possible side effects as well. If you really have osteoporosis or a related disease your bones are not going to get better by eating more healthy and exercising if you were (which you should have been doing already anyway!). Try checking side effects for some other studies too, the possibility, the chance of you getting side effects is inevitable, but this does not mean you will actually get them. So I agree with Lara, make sure you’re informed, but do so by reading the newest medical journals yourself. This book was already outdated when it was first published.

Lara Pizzorno

Hello Elisabeth,
I am delighted you are experiencing good results from denosumab – but do you have any idea what you are going to do to deal with your fibrous dysplasia (which is NOT osteoporosis, but a rare bone disease) after the 3-5 year period during which denosumab has been approved for use? Denosumab is not correcting the CAUSE of your fibrous dysplasia. Has anyone tried to help you figure out WHY you have this condition? Does it run in your family? Have you had this since you were a young child (which is typical) or did it develop suddenly? If so, can you remember anything that happened that might have triggered this disease?
The vast majority of us do not have fibrous dysplasia and do not “need” a drug like denosumab. What we need is to determine WHAT is causing our personal excessive bone loss, to eliminate the CAUSE(S), and to provide our bodies with all the nutrients required by our bones to remodel healthfully along with regular bone building exercise. This is what I have written about in depth in Your Bones — and it will never be out of date as long as human physiology remains the same, which I expect it to do for as long as humans are on the planet. It is naïve to believe otherwise.
I have read the studies — and if you look at Your Bones, you will find that every single statement made in the book is backed up with peer-reviewed research published on PubMed — the citations are provided in the EndNotes section of the book, which runs from pages 367 – 459 and contains more than 500 references (many of the 476 endnotes contain several references, not just one.)
I will be the first woman in all the generations of my family I know about to NOT die early from osteoporosis. My key issue — vitamin D receptors that don’t work well, so I require much more vitamin D than “normal” folks. Once we figured this out, my bones began to rebuild. As I learned more and more (from reading the research — I’ve been a medical writer and editor for 30+ years now) and added more support to my bone building program, my bones responded by doing what normal bones are preprogrammed to do — they rebuilt, strong and beautiful. I am now 64 and have GREAT bones. I am living proof that determining the real causes of our bone loss and dealing with them — not taking a drug that can have serious adverse effects, does not correct the real problem but actually prevents healthy bone remodeling while also suppressing immune function — is the best option for those of us with osteoporosis.
You have a rare disease, not osteoporosis. Why are you trying to prevent those of us who do have osteoporosis or are at risk for it from regaining and maintaining our bones’ health?

Karen Wilson

Hello Lara,
I was incorrectly staged as Stage 4 breast cancer, with extensive bone metastases in axial skeleton, in 2010 (in UK). Turns out it is actually a benign condition called osteomesopyknosis, and that I was actually stage 3 (with 22/24 positive nodes, but no metastasis). This only came to light after I had been given palliative treatment. I am obviously extremely worried about not having had the appropriate treatment, especially given the 22 nodes. Initially, I was put on 4-weekly Zometa for the supposed bone mets. This has now been changed to 6-monthly Zometa, because of the recent studies showing that it may help to prevent recurrence, particularly in post-menopausal women (I am 49 and had an oopherectomy in 2010, shortly after diagnosis). What I am trying to figure out is whether it would benefit me to also take Xgeva, if it works in a different way from Zometa? Are you aware if anyone gets both at the same time? Any advice would be greatly appreciated.

Lara Pizzorno

Hi Karen,

First, it’s wonderful that you do not have Stage 4 breast cancer! Osteomesopyknosis is a benign dysplasia rather than cancerous condition, so your likelihood of being able to manage this and have a good life is quite good.

In answer to your questions about Zometa and Xgeva: yes, these two drugs have different mechanisms of action.

Zometa is a bisphosphonate. These drugs work by poisoning osteoclasts after they have formed and supposedly do not impact immune function; however, it is now becoming apparent that osteoclasts are a type of immune cell (below I’ve copied in the abstract of one of the most recent papers on this issue). By destroying osteoclasts, Zometa prevents bone remodeling, so you lose less bone, but the bone retained is old and brittle, not as healthy as bone your body would be forming in the process of normal bone remodeling. Zometa is thought to be helpful for patients with cancers, e.g., multiple myeloma, because one of the ways in which cancer cells derive nutrients for their unnaturally rapid growth is by activating osteoclasts, which in the process of removing old brittle bone also cause the release of nutrients the cancer cells can use. In your case, your body is forming bone in a somewhat dysfunctional fashion, so using a bisphosphonate to help lessen this process seems like a reasonable thing to do.

Xgeva is one of the trade names for denosumab, which works by binding to the RANK ligand (RANKL). RANKL is supposed to bind to and activate certain cells — including the precursor cells for osteoclasts and also our T and B cells, which are key cells of our immune system. By binding to RANKL, denosumab prevents it from binding to and activating the development of these other cells. Given that you are taking these drugs to help prevent the development of cancer, denosumab seems counter-intuitive to me since it disrupts maturation of immune cells, which are necessary to eliminate cells that are becoming or are already cancerous. You might ask your doctor to explain why denosumab is being recommended for you.

I do not know if both are being used concurrently. You could check with Cancer Treatment Centers of America for help answering this question.

I hope this information is helpful to you. If I can be of further help, please just let me know.

Here is the abstract I mentioned above discussing the development of the new field of osteoimmunology:

J Biochem. 2013 Jul;154(1):29-39. Epub 2013 Jun 7.

Immunology and bone.

Danks L, Takayanagi H.


Department of Immunology, Graduate School of Medicine and Faculty of Medicine, The University of Tokyo; and Japan Science and Technology Agency (JST), Explorative Research for Advanced Technology (ERATO) Program, Takayanagi Osteonetwork Project, Hongo 7-3-1, Bunkyo-ku, Tokyo 113-0033, Japan.


It is now well acknowledged that the immune and skeletal systems interact and affect one another during developmental physiology and pathology. With the aid of modern conditional gene targeting and transgenic technologies, this field of interdisciplinary research, known as osteoimmunology, is rapidly advancing. Numerous bone phenotypes have been described in immune-compromised gene-deficient mice and, albeit to a lesser extent, immune deficiencies exist in osteo-compromised gene-deficient mice, suggesting that bone cells themselves actually regulate the development of immune cells directly. In this review, I discuss the essential role of key cytokines, signalling transduction pathways and transcription factors during immune and bone development, and how pathology driven dysregulation of these shared mechanisms can lead to clinical manifestations. Diseases that are within the remit of osteoimmunology continue to cause significant morbidity, for example, rheumatoid arthritis, osteoporosis, multiple myeloma and breast/prostate cancer. The complexity and overlapping cellular and molecular interactions between the immune and bone tissues, mean that despite fervent research of these diseases, it remains a major challenge to discover therapeutics that can specifically target one system without detrimentally affecting the other.


RANKL, T cell, haematopoietic stem cell, osteoblast, osteoclast

PMID: 23750028

iherb at

Great article. I am dealing with many of these issues as well..


Does K2 thicken the blood the same as vitamin K


Hi Debbie,

Lara was asked a similar question on the blog post:

This was her response:

“Regarding vitamin K — vitamin K2, which is the form of this vitamin our bodies require to ensure that the calcium we consume goes into our bones and stays out of our arteries – has nothing to do with blood clotting and does not “thicken the blood.” Vitamin K1, which is found in leafy greens, is the version of vitamin K that activates clotting factors — and we really need this! Without enough vitamin K1, we would bleed to death from even a small scratch.”

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Keep on working, great job!

Donna Norton

Hi Lara

I am a 60 year old female diagnosed on May 13, 2013, with Stage 1 breast cancer, Estrogen Positive, Progesterone Negative and HER2 Positive cancer of the left breast.
I had my ovaries removed, 2 rounds of chemotherapy for 5 months & in February 2014, bi-lateral mastectomy with breast reconstruction. One month after finishing chemotherapy and bi-lateral mastectomy surgery, my oncologist said I am cancer-free and put me on Arimidex for 5 years. After reading all the side effects associated with Arimidex especially about bone loss 6.08% of the lumbar spine & 7.24% at the hip in a 5 year period, I was terrified to take the Arimidex but my oncologist said I had to take it to prevent recurrence of HER2 Positive cancer. I have been on Arimidex for 6 months and a bone density test was ordered by my doctor. The results are:

T-Scores 9/5/2014 2011 (Baseline)
Femoral Neck & Total Hip -2.2 -2.1
Lumbar Spine -2.8 -2.2
Diagnsis: osteoporosis of the spine Osteopenia

In 3 years, with all the chemotherapy drugs & Arimidex & being post menopausal, I went from osteopenia to ospteoporosis. My oncologist recommended I start taking Prolia . After doing all the research on Prolia & Fosamax and all the horrific side effects associated with both medications, I am terrified to take any of the osteoporosis medications that she suggested. I am having trouble sleeping scared to death about taking those drugs and what side effects I may get from them, and what natural alternatives I could take. In spite of all my efforts, walking, taking New Chapter Bone Strength, Vitamin D3, magnesium citrate, krill oil, flax seed, & multi vitamins; in addition to a calcium fortified & healthy diet; I am still having bone loss, most likely due to the all the drugs and treatment I have received this past year in addition to now taking Arimidex. As a second opinion while having my annual pap test, I asked my gynocologist and she told me I had no choice but to take Fosamax (she didn’t recommend Prolia b/c it was too new a drug). Because of the Arimidex bone loss; she said if I didn’t take it I could have a severe bone fracture within the next 5 years. She said it happened to one of her patients after two years of being on Arimidex. Like having breast cancer isn’t scary enough. Now I have the fear that my bones are growing bittle by the day if I don’t do what the doctor saids.

I am so happy that I came across the AlgaeCal website. I am starting to feel that there is some hope & maybe an answer to my prayers. I know you are not an oncologist but do you think that taking AlgaeCal & Strontium Citrate would be enough for me to take to prevent bone loss while I am on Arimidex & of course after the 5 year period is up?
Or do you think I have no choice but to take the Prolia or Fosamax in addition to taking a calcium & strontium supplement such as AlgaeCal? If I have to take it, which of the two drugs would you recommend.
Also, since I am on medication that causes bone loss, do I need to take more AlgaeCal than what is suggested on the bottle?
I read too much calcium is also bad, causing hardening of the arteries of the heart & possible kidney stones; so I don’t want to take too much calcium & develop other serious problems. I need to make a decision rather quickly as my oncologist wants to give me Prolia on my next visit because of my bone density results.

My insurance company told me I can’t do another Bone Density test until October 2016, so I won’t know if my T-Scores or bone density have improved while taking AlgaeCal Plus & Strontium. Are there any other tests that I can take that would show me before my next bone density test in 2016, if my bones have improved or gotten worst, or am I taking a big risk by not taking the Prolia or Fosamax?


I have been reading about nitroglycerin ointment as a treatment for osteoporosis that helps bones grow. I have been unable to find any recent publications on this use of nitroglycerin.

Lara Pizzorno

Hi Chris,

Me either – no support on PubMed for nitroglycerin ointment as Tx for osteoporosis. Here is the abstract for the most recently published peer-reviewed medical journal paper on this topic:

Ann Pharmacother. 2011 Dec;45(12):1566-70. doi: 10.1345/aph.1Q410. Epub 2011 Oct 18.

Nitroglycerin ointment for the prevention of postmenopausal osteoporosis.

Beckett RD, Sheehan AH.

Author information



To determine whether clinical trial data support the use of nitroglycerin for prevention of postmenopausal osteoporosis.


A literature search using MEDLINE (1966-September 2011) and EMBASE (1973-September 2011) was conducted using the search terms nitroglycerin, bone mineral density, fracture, and osteoporosis. References of identified articles were reviewed for additional citations.


All English-language articles related to the use of nitroglycerin ointment in postmenopausal women were reviewed.


Four observational studies reported significant improvements in bone mineral density of postmenopausal women with the use of nitrates. One pilot study and 2 prospective, randomized, placebo-controlled clinical trials reported conflicting results regarding the efficacy of nitroglycerin ointment.


Clinical data do not support use of nitroglycerin for this indication; its potential is limited at this time by inconclusive efficacy and a high incidence of headache. Further well-designed clinical trials demonstrating efficacy and safety of nitroglycerin ointment for prevention of postmenopausal osteoporosis are needed before this medication can be recommended for routine use.


Vickie Harris

I am so glad that I heard about and ordered and started taking AlgaeCal Plus and Strontium Boost just before my doctor called and wanted to start me on Prolia! I informed him that I had found a better source of calcium that would help me more than Prolia and so I wouldn’t be taking it. There was silence on the phone for a few seconds and then I relieved the tension by telling him that I would explain everything at my next appointment with him. But this was before I read the above article and I am so grateful that I saw the ad for AlgaeCal first and chose it instead. Besides, I have systemic lupus and rheumatoid arthritis so I really don’t need anything else that is going to damage my immune system, my own body does that on it’s own, and then there’s the occasional prednisone pills that I have to take for the lupus. If I were to take Prolia as my doctor suggested I would probably be in a lot of trouble, because my lupus is severe and I can get infections easily. I also have osteonecrosis in both tibiae and in both femurs. I’ve had both hips replaced because of it and I really don’t want any more. Thank you for your article!

Nicola Wood

I was diagnosed with a giant cell tumour of the sacrum and was given denosumab injections every 4 weeks for 18 months. I started getting pains in my left femur and then my right. The drug was stopped and I had a partial sacrectomy. Nearly 3 years on and the pain in both femurs is still very much there and probably worse. I have had a nail through my left femur as there is a hair line fracture and I am due to have a nail through my right femur. I have a build up of bone on both femurs and constant pain. All caused by denosumab.


Hi Nicola,

Wow – so sorry to hear about your experience with denosumab. Please let us know if you have any questions about AlgaeCal and other natural treatment options. Also, thank you so much for taking the time to comment and share with our readers.

– Monica from AlgaeCal

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