The Food and Drug Administration (FDA) does a good job of policing the drug companies and protecting the public health in the United States. It assures the safety, effectiveness, and security of human and veterinary drugs, vaccines and other biological products, medical devices, our nation’s food supply, cosmetics, dietary supplements, and products that give off radiation. It is responsible for product approvals, over-the-counter and prescription drug labeling and drug manufacturing standards.

In Europe, however, this job is performed by the European Medicines Agency (EMA). The EMA’s responsibility spans a decentralized, European Union, spanning over a European medicines network of 40 plus national regulatory authorities. It has to be an onerous task to police over 40 national regulatory authorities. However, the EMA is not as effective as the FDA. Drug companies in that European Union commit bad acts because they know they can get away with it.

Case in point is the October 23, 2012 news that the EMA is investigating allegations that Roche failed to comply with its EMA imposed obligations to monitor the science and adverse event reporting activities to detect, assess, understand and prevent patient injuries from adverse effects of its European manufactured and distributed drugs. These allegations came from the 2012 inspection of the UK Medicines and Healthcare products Regulatory Agency (MHRA), which showed several deficiencies in the safety reporting systems at Roche Registration LTD. It showed that Roche had not evaluated information it had received to determine whether or not the same constituted adverse reactions which would need to be reported to the competent authorities in the EU. Roche callously put patient care and safety in the back seat of the profit mobile.

We are not talking about a few reports that Roche did not have time to follow up on. At the time of the inspection, Roche identified some 80,000 reports that had not been evaluated to determine whether or not they should be reported as suspected adverse reactions. More astounding is that these reports included 15,161 reports of patient deaths.

For the worldwide pharmaceutical companies, Europe is the old west’s Hole-in-the Wall where they hide out from the law.


Understanding the Fosamax problem

FOSAMAX works by inhibiting bone resorption and suppressing bone turnover. Bone mineralization occurs in two phases. Primary mineralization occurs while new bone is forming. Because FOSAMAX severely suppresses bone turnover, bone remodeling and primary mineralization are inhibited. Secondary mineralization of existing bone however, continues to occur. This results in an increase in the tissue mineral content of the bone which translates to an increase in bone mineral density (BMD). Increased BMD does not necessarily correspond with reduction of fracture risk. Additionally, through the bisphosphonate mechanism of action, bone becomes highly mineralized, homogenous, brittle, and more susceptible to fracture.

MERCK knew or should have known that by inhibiting bone turnover while at the same time allowing the secondary mineralization of old bone to continue, long term FOSAMAX therapy would result in bones becoming highly mineralized, brittle and more susceptible to fracture. This is especially true given the fact that the effects of FOSAMAX on the bone accumulate and continue for years after treatment is discontinued.

MERCK’s 1997 Fracture Intervention Trial (FIT) reported a 47% reduction in the risk of new vertebral fractures and a 28% reduction in the risk of clinical fractures in postmenopausal women taking alendronate compared to those taking a placebo. Ensrud et al., Treatment with Alendronate Prevents Fractures in Women with Highest Risk, 157 Arch. of Int. Med. 2617 (Dec. 8/22, 1997).

Medical researchers in the January 19, 2008, issue of British Medical Journal revealed the manner in which bisphosphonates such as FOSAMAX are presented to reduce fracture risk for those women who actually do have osteoporosis tends to exaggerate the actual fracture reduction benefit conferred. According to the authors, published critical trials exaggerated the fracture-reduction benefits through the use of relative risk rather than in terms of absolute risk. As the authors state: Impressive sounding reductions in relative risk can mask much smaller reductions in absolute risk. By using the math of relative risk rather than absolute risk, the purported benefits of the drugs appear larger than they actually are in the general population. As a result, billions of dollars are being spent on a drug that has questionable utility for the ultimate goal of fracture reduction.

Correspondingly, when examined in a clinical setting, later observational studies revealed that the FIT study exaggerated the benefit derived from alendronate therapy in reducing the risk of fracture. The 2006 ICARO study concluded that the incidence of fractures during treatment with antiresorptive agents, including FOSAMAX, in a clinical setting is considerably higher than that observed in randomized clinical trials, especially when therapy was not supplemented with calcium and vitamin D. Silvano et al., Fracture Incidence and Characterization in patients on Osteoporosis Treatment: The ICARO Study, 21 J. Bone and Mineral Research 1565 (2006).

It is really not a question of whether a woman who has taken Fosamax for over 5 years will suffer a femur break. It will happen, and the really question is simply, “When?” Thanks, Merck for targeting and putting millions of women at huge risk for a broken femur so you could make your billions.