Osteoporosis News: Merck Ignored Warnings About Fosamax Side Effects, Merck’s VP Of Clinical Research Makes Shocking Admission, And Study On Toxic Osteopenia Drug Fails

Vivian Goldschmidt, MA Drugs News

Evidence-Based
8 min Read
osteoporosis news

Today, there’s a lot to cover on the latest osteoporosis news. From lawsuits against Merck to mad science and more. Plus you’ll read about the astonishing declaration by a major drug company’s VP of Clinical Research stating that a popular osteoporosis and osteopenia drug is useless for fracture prevention.

Intrigued? I know I was when I read the information I’m bringing you today. So let’s get started.

Fosamax Lawsuit: No Surprise to Merck

Fosamax has the distinction of being the first drug approved for osteoporosis in 1995. It has generated multibillion dollar sales for Merck, as (not coincidentally), the guidelines for what constituted an osteoporosis diagnosis were stretched and modified just one year before its release into the marketplace.

As side effects became more numerous and dire, lawsuits arose. One prominent class-action suit includes 3,300 cases of atypical femur fracture. That’s right – this drug that is supposed to β€œcure” osteoporosis has been implicated in thousands of cases of femur fracture. It’s quite ironic when you consider that doctors often scare their patients into taking osteoporosis drugs by telling them they’ll succumb to fractures if they don’t take the medications.

One particular ongoing lawsuit is going before a jury, the case of Bernadette Glynn. And her lawyer, Paul Pennock, has had some pretty bold and drastic accusations against pharmaceutical giant Merck.

An elementary school worker, Bernadette claims she bent over to pick something up in her garden when her thigh bone snapped in two places. Predictably, Merck claims that Glynn’s fracture was not β€œatypical” (the sort of unusual fracture associated with bisphosphonates like Fosamax), and further claims that Glynn actually had a fall that caused the femoral break.

News Excerpt

β€œPennock said femurs, as the strongest bones in the body, usually only break in high-force incidents, such as car accidents, and not from falling down. Because Fosamax is designed to repair daily bone damage by stopping the natural clearing of old bone, the process results in micro-fractures building up instead of being naturally replaced, he said.1

Note that it’s apparently common knowledge that Fosamax stops β€œthe natural clearing of old bone”. Additionally, Pennock accuses Merck of blatantly ignoring warnings by consultants that atypical fractures would inevitably happen:

β€œStarting in 1990, five years before Fosamax won approval by U.S. regulators, consultants began warning Merck that the drug could lead to spontaneous fractures in some users by preventing bones’ natural daily repair of so-called micro-fractures, Paul Pennock, the lawyer for plaintiff Bernadette Glynn, said today in federal court in Trenton, New Jersey. … β€˜The evidence is going to show you that it wasn’t a surprise — it wasn’t coming out of the blue,’ [Pennock] said of Merck’s discovery of Fosamax’s possible fracture risks. β€˜They looked for it and studied it — when all the information starting [sic] coming in, they did nothing about it.’” 1

Fosamax Useless for Osteopenia, Merck’s VP for Clinical Research Confesses

Believe it or not, Bernadette Glenn was never diagnosed with osteoporosis. According to her lawyer, she was given Fosamax for β€œlow bone-mass density” or osteopenia (an invented precursor to osteoporosis). As mentioned above, the reasons for prescribing these drugs get broader and broader so that the drug companies can profit more and more.

So β€œpatients” without osteoporosis – like Bernadette Glynn – are walking out of doctors' offices with a prescription for drugs like Fosamax, unknowingly becoming potential victims of the drugs’ dangerous and sometimes life-changing side effects.

But this might hopefully change soon. During a recent courtroom trial, Merck’s Associate VP for Clinical Research finally acknowledged that no study ever showed evidence of fracture reduction benefits for non-osteoporotic patients taking Fosamax.

News Excerpt

β€œIn the recent bellwether trial of Scheinberg v. Merck & Co., Merck’s Associate Vice President for Clinical Research Dr. Arthur Santora revealed that Merck’s drug Fosamax does not have any evidence of fracture reduction benefit for patients without osteoporosis.Β  In the label for Fosamax, Merck affirmatively indicates that Fosamax prevents fractures for patients [sic] for both osteoporosis patients and pre-osteoporosis patients (often called β€˜osteopenia patients’).

Dr. Santora’s trial testimony reveals that Fosamax does not, however, prevent fractures the [sic] patients without osteoporosis.Β  Under examination by Levin, Papantonio shareholder Timothy O’Brien, Dr. Santora admitted that there was no evidence of fracture reduction benefit for those patients without osteoporosis:

Q: Β Β Β Β  It’s my understanding, Dr. Santora, based on the clinical trial evidence that Merck had and presented to the FDA, Merck cannot say that for those patients without osteoporosis that the use of Fosamax prevents fractures, right?

A:Β Β Β Β Β  That’s correct, it doesn’t – – what you said is correct.

Q:Β Β Β Β Β  Because there’s no evidence that it does, right?

A:Β Β Β Β Β  That’s another way of saying the same thing, that’s correct.

Q:Β Β Β Β Β  And in terms of Fosamax, the bottom line for efficacy of Fosamax is fracture reduction, right?

A:Β Β Β Β Β  That’s what is important to patients and physicians.”2

So if there’s no evidence that Fosamax works, how did the drug get approved? This just shows how Big Pharma operates: while the FDA looks the other way, they keep quiet about a problem that might hurt their profits. It seems as though the fox is guarding the chicken coop…

Alarming! Scientists Consider Using a Dangerous Toxin to β€œCure” Osteopenia

My regular readers already know that osteoporosis is not a disease. Rather, it’s the body’s response to a biochemical imbalance. So if osteoporosis is not a disease, then logically, its invented precursor osteopenia is even less so!

In fact, osteopenia is even more of a fabricated condition than osteoporosis. It’s basically a way to describe low bone density that isn’t low enough to qualify as osteoporosis. There’s no evidence that osteopenia leads to osteoporosis; nonetheless, as I mentioned earlier, doctors prescribe the same drugs for osteopenia as they do for osteoporosis, presumably to stop osteoporosis from developing.

Believe it or not, scientists are now trying to use fluoride to β€œtreat” osteopenia.

β€œSavers” know that fluoride causes brittle bones and a slew of other detriments to health. Yet led by the incorrect notion that fluoride reduces fracture risk, researchers set out to study the effect of fluoride tablets on bones.

News Excerpt

β€œIn this new trial, researchers led by Dr. Andrew Grey, MD, MB, ChB, Associate Professor of Medicine at the University of Auckland, and an Endocrinologist at Auckland Hospital, examined the skeletal effects of low doses of fluoride.

In this double-blind, placebo controlled, randomized trial over one year, 180 women postmenopausal women with osteopenia were recruited between June 2009 and March 2010, were at least five years past menopause.

The women were given daily doses of either of tablets containing placebo, 2.5mg fluoride, 5mg fluoride or 10mg fluoride.
The results revealed the primary endpoint was change in lumbar spine BMD at 1 year, secondary endpoints were hip and forearm BMD, and markers of bone turnover.

In comparison to the placebo, none of the doses of fluoride changed bone mineral density (BMD) at any site. On the other hand, the low doses of fluoride did appear to β€˜weakly activate bone remodeling,’ with significant changes in at least one marker of bone formation.

Levels of procollagen type-I N-terminal propeptide (P1NP), the preferred marker for bone formation did increase significantly with low doses of fluoride 5mg and 10mg compared to a placebo.

No difference were seen between the placebo group and any of the fluoride groups on Beta C-terminal telopeptide (Ξ²-CTX), a specific resorption marker for degradation of bone type I collagen by osteoclasts.

No fractures were reported in the placebo group, one metatarsal fracture in the 2.5-mg fluoride group (metatarsal is the long bones in the forefoot), two fractures in the 5-mg group (one in the ankle and one in the calcaneus, heel bone) and two fractures in the 10-mg group (one in the rib and one in the humerus, is a long bone in the arm or forelimb that runs from the shoulder to the elbow).

In their conclusion the researchers write β€˜Low dose fluoride does not induce substantial effects on surrogates of skeletal health, and is unlikely to be an effective therapy for osteoporosis.’”3,4

It’s bad enough that osteopenia is looked upon as a β€œdisease” that must be β€œcured”; but turning to a dangerous toxin to β€œtreat” it surely takes the cake!

Isn’t it good to know that thanks to the Osteoporosis Reversal Program you don’t need to play along with Big Pharma’s games? And if you don’t have the Program yet, you can try it risk-free with my one full year no-questions-asked double your money back guarantee.

Till next time,

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References

1 Larson, Erik. β€œMerck Knew of Fosamax Bone Risk in ’90, Lawyer Tells Jury.” Bloomberg. April 9, 2013. Web. https://www.bloomberg.com/news/2013-04-09/merck-trial-begins-on-claim-fosamax-causes-bone-breaks.html
2 Cousins, Farron. β€œMerck Vice President Reveals: Fosamax Has No Fracture Reduction Benefit For Many Patients.” Ring of Fire. February 19, 2013. Web. https://www.ringoffireradio.com/2013/02/19/merck-vice-president-reveals-fosamax-has-no-fracture-reduction-benefit-for-many-patients/
3 Nicholson, Debbie. β€œFluoride fails as osteopenia treatment.” All Voices. April 12, 2013. Web. https://www.allvoices.com/contributed-news/14402446-fluoride-fails-as-osteopenia-treatment
4 Grey, Andrew, et al. β€œLow dose fluoride in postmenopausal women: a randomized controlled trial.” The Journal of Clinical Endocrinology & Metabolism. April 3, 2013, doi: 10.1210/jc.2012-4062. Web. https://jcem.endojournals.org/content/early/2013/04/03/jc.2012-4062.abstract