Creation of abnormally large osteoclast cells
Osteoporosis drugs, or bisphosphonates, like virtually all pharmaceutical drugs being irresponsibly prescribed today for chronic conditions, are designed to affect a specific biological mechanism within a complicated series of interconnected and interdependent such mechanisms. In doing so, they disrupt the body's normal-- and critically important-- regulatory functions at the cellular and organ system levels, causing far worse health problems than those that they were designed to incompetently treat.
The extensive fraud behind the marketing and prescribing of bisphosphonate drugs, such as Fosamax and Boniva, to treat a so-called epidemic of osteoporosis in the society is placing the health of millions of unaware users at risk of serious adverse effects, ranging from osteonecrosis (bone death, and its associated complications) to cancer.
Despite the accumulating knowledge that this class of drugs destroys normal bone function, bisphosphonates have been increasingly prescribed since the mid-1990s to allegedly build healthy bone and to reverse the loss of bone density. Decreased bone density is characteristic of osteoporosis, a condition that begins to affect mainly women as they near the start of menopause ( at around age 50, and also men, to a lesser extent).
While Fosomax and Boniva are the two most popular brand names of bisphosphonates, others include: Aredia (removed from the market after a series of class action lawsuits for causing osteonecrosis of the jaw), Reclast, Actonel, and Zometa.
These drugs were designed to alter two normal and essential processes in human bone at the cellular level, by (1) disabling or killing osteoclast bone cells, whose function is to dissolve old bone, and (2) replacing the body's normal phosphate-derived molecules (pyrophosphates) with bisphosphonates in the bone's calcium-phosphate-collagen bone matrix— to keep the bone from becoming less dense.
The newest round of osteoporosis drugs, such as Prolia (renamed Xgeva by the biotech manufacturer Amgen), have similar adverse effects on the bone, and osteoporosis hormone altering drugs, such as Forteo, which alters parathyroid hormone levels, have the capacity to cause cancer (see part 2 of this series).
While inactivating normal bone regulation -- to artificially create dense bone-- may sound like a logical way to stop bone loss, it instead creates a highly abnormal environment within the bone at the cellular level. This leads to compromised bone construction, which in turn causes the bone's progressive destruction in the form of abnormal fractures or disease.
Bone is designed around two basic components at the cellular level that provide the bone with its unique strength and flexibility, while at the same time sustaining its ability to continually replace old bone and repair itself.
About 70% to 80% of bone is composed of the bone matrix— a very organized, interlaced, crystalline structure throughout the main body of the bone (outside the inner bone marrow). The bone matrix is composed mainly of a combination of calcium and phosphate minerals for strength, and collagen filaments for flexibility.
The other roughly 20% of bone is comprised of two types of bone cells: osteoblasts, which lay down the foundation of the bone matrix and afterwards become embedded into this very organized crystalline lattice structure, and osteoclasts, which are bone cells that dissolve the old bone matrix, to allow for new bone matrix to be laid down by the osteoblasts.
The activity of these two types of bone cells perpetuate a continuing, and essential, evolutionarily-designed, regulatory/biological cycle to sustain the health of the bone— whether the bone is young or old— known as bone remodeling.
And it doesn’t matter whether the person’s bone is dense or thin (lacking a less dense bone matrix of calcium-phosphate minerals). The constant bone remodeling process is the only way that bone can sustain both its health and strength, and its elastic structure to withstand everyday stress on the bone.
This critical bone remodeling sequence-- of osteoclast cells continually eroding away old bone and osteoblast cells following up by laying down new bone-- is also how bone repairs and “heals” itself. If a defective area of the bone develops, that area of old or impaired bone must first be dissolved away before it can be replaced with new bone. Old, compromised, or diseased bone cannot be "healed" in any other way.
If you interfere with the ability of the bone to dissolve old or defective areas of bone, you stop the bone from being able to continue to remodel in its normal manner, and you disrupt any ability for normal bone construction or healing to occur, regardless if a person has thin or dense bones. (In thinner bones, the bone regulation process, of degrading before building up new bone, still occurs, only it occurs more slowly.)
If old bone is not first properly re-absorbed by the circulating osteoclast cells, the osteoblast cells, which follow them in the next stage of the bone remodeling process, lack the proper foundation upon which to lay down the down the critically important bone matrix, which must be highly organized and structured in order to allow the clear access of blood vessels and nerves to pass through it, in order to supply essential nutrients to the bone.
(And every single physician and nurse is aware of elemental bone regulation at the cellular level, because it is covered in elementary physiology, which every physician and nurse studies before graduating. And this basic bone physiological knowledge is also known to every pharmaceutical researcher who has or is developing “bone drugs,” for the very same reason.)
Once you abnormally alter the extremely important organization of the bone at the cellular level— which exists regardless if the bone is thin or dense (thinner bones only have a thinner bone matrix, while their bone remodeling process is normal, but only slowed down) — you begin to destroy the integrity of the bone. Then you open up the process by which abnormal fractures, infection, and disease of the bone can develop.
And bisphosphonate drugs accomplish this exact abnormal process.
Bisphosphonates disable or kill off osteoclast cells that dissolve old bone, and replace naturally-derived phosphate minerals— normally incorporated by the osteoblasts into the bone matrix— with abnormal, synthetic-derived, bisphosphonate compounds.
These abnormal bisphosphonate compounds bind almost permanently to the bone matrix and stop those available osteoclast cells (which are not disable or killed off by the bisphosphonate) to dissolve the old bone matrix. A critically first step needed to set up a clean foundation, upon which only a new bone matrix and new bone cells can be organized to create healthy bone.
This is accomplished by the bisphosphonate compounds being highly resistant to the acids secreted by osteoclasts that were designed by evolution to specifically dissolve the old bone matrix.
In addition, because these synthetic drugs obviously do not exist in chemical forms and structures found in nature, they are not identifiable to human cells and molecules. And because of this, these laboratory created drugs also elicit an abnormal immune system reaction-- of inflammation in any area of the body they gain access to.
This is opposed to a normal, local, inflammation response, which was designed by evolution to occur so that the body’s immune system cells (white blood cells and their components) could better diffuse through widened blood vessels into an area impacted be a foreign entity, such as a bacteria or a virus (or now a manmade drug) in order to be able to better attack and disable the foreign entity causing the immune system response.
Bisphosponates create an abnormal immune reaction in the bone
As early as 2000, Japanese researchers publishing in the Archives of Oral Biology showed that bisphosphonates were eliciting just such a classic, general immune system reactions in the bone. (for sources see end of article)
The researchers found that bisphosphonates created the same general immune system reaction of inflammation as produced by the presence of both periodontal and endodontal bacterial infections of the gums and the jawbone. The Japanese research clearly revealed that the immune system cells equated bisphosphonates to bacteria, and were eliciting a general immune response in an effort to remove them from the bone.
Over a decade earlier, beginning in the mid-1980s, while bisphosphonates were being developed in pharmaceutical labs, research studies were already being published in multiple scientific journals showing that bisphosphonates actively depressed a variety of immune system cells, such as: macrophages, monocytes, T-Iymphocyte cells, and natural killer T -cells, along with the disruption of important complimentary functions of these cells— all involved in various aspects of the immune system response needed to keep the body free of disease.
Additionally, the body's pivotal immune system organ, the thymus gland— critically involved in the development, maturity, and function of immune system cells— was also shown in early research studies to be depressed by the presence of bisphosphonates.
Not only were these early, and highly significant, research findings ignored then, as they remain ignored today by the FDA and by the U.S. medical community heavily prescribing this class of drugs, but the abnormal process of inflammation would be exploited by the pharmaceutical industry as a fraudulent “proof”’ (via bone scans, see below) that bisphosphonates were allegedly creating increased, healthy, bone density in their users.
In fact, the “increased volume” registering on the bone scans are due to inflammation at the cellular level, and by abnormally created, and unstable, “dense” bone.
Bone Density Scams
Bone density X-ray scans, used to approximate the bone's density, measure bone volume only, and cannot distinguish the quality of the bone at the cellular level.
Bone that has absorbed bisphosphonate molecules is not only inflamed bone-- due to the ongoing immune system response that is trying to remove it as a foreign substance within the bone-- but is also older bone which has stopped remodeling. And as a result, this bone has lost the normal water content present in healthy new bone. Subsequently, while this bisphosphonate infused bone may appear dense on bone X-ray scans, it does not tell the viewer of the scan anything about the true integrity and health of the bone.
The "higher" bone density revealed in these bone density scans after bisphosphonate use does not translate into bone having become thicker and stronger, or more flexible or healthier as claimed, but in fact translates into them having become more compact, inflexible and brittle bones, and susceptible to more severe and abnormal breaks.
The method of measuring bone density is determined by taking an X-ray picture of the bones (in and of itself technically capable of destroying bone cells), and then visually interpreting that image to determine if the bone density is "normal."
If a certain standard of deviation is found below that considered to be "normal" peak bone density— the bone density of a 30 year-old—the patient is technically required to be told that she should be prescribed a bisphosphonate to, ostensibly, retain, or build, "healthier," denser bones. (The patient is “required” to be told this by the medical provider as a result of “laws” lobbied for by the pharmaceutical industry and the American Medical Association, so as to identify a “medical condition." And then, once “identified,” the "condition" can then be “treated” with a drug.)
This is not only fraud on the false assumption that older bones of 50 year-olds and older should be compared to those of 30 year-oIds, and if they do not match up in density should on that basis of comparison be determined to qualify for disease classification— as fraudulent as stating that older skin should be considered abnormal by comparison to skin 20 years younger, or that of any other body tissue or organ— but it was also based on fraudulent assessments of the bone scans themselves, which can in no way determine the actual quality of bone at the cellular level showing up in the X-ray scans.
Not only is the bisphosphonate infused bone disorganized and chaotically constructed at the cellular level—with overly dense bone matrix built-up on top of older bone, or hollowed out areas of bone where the normal remodeling process, essential for creating healthy bone, has been derailed, leading instead to unstable and more brittle bone— but this is further compounded by abnormal blood flow to the bone, and to the presence of inflamed areas of the bone.
Creation of abnormally large osteoclast cells
In addition, bisphosphonate presence in the bone creates an elevated numbers of abnormally large osteoclast cells (the bone cells designed to break down the bone matrix in the normal bone remodeling process targeted by bisphosphonates).
Abnormal-sized osteoclasts, which exist only in bones treated with bisphosphonates, have been shown to contain between 20 to 40 nuclei per cell, instead of a normal number of 8 to 12.
Multiple nuclei in osteoclasts are normally created as a result of osteoclasts having developed in the bone marrow from the fusion of multiple immune system cells, called macrophages.
But the abnormal increase of nuclei in osteoclast cells exposed to bisphosphonates may predispose these osteoclast cells to develop into more pronounced cell mutations, which may increase the risk of later tumor development in the bone— as orally taken bisphosphonates have been shown to pose a risk for creating cancer in the cells of the lining of the esophagus (see also Sally Field’s Boniva Advertising Campaign, in Part 2)
Bisphosphonates can abnormally remain in the bone up to 30 years, or longer
Compounding the immune system impact and abnormal bone construction is the added hazard that these drugs have an estimated half-life of at least ten years. This makes this class of drugs significantly more dangerous than most other conventional drugs that are metabolized (broken down) by the body almost immediately after they have been taken into the system— within hours, or at most, within days or weeks.
And, as a result, this makes drug statute of limitations clauses (of only being able to sue for damages a few years after taking a drug) irrelevant. Allowing the pharmaceutical industry and the doctors prescribing these drugs to escape accountability for placing the health of the public using these drugs at known risk, well after the patients may have stopped taking the drugs.
Having a half-life of ten years means that in ten years time only half of the bisphosphonate molecules taken into the body and incorporated into the bone matrix will have been broken down by the body's naturally-derived enzymes and acids— with the possibility of the half-life of bisphosphonates being even longer.
After ten years, or after fifty percent of the originally absorbed bisphosphonate molecules still remain in the bone, it will take another ten years for that remaining fifty percent remaining to be reduced by another half— to a twenty-five percent composition within the bone matrix. And for another ten years after that until that amount will finally be reduced to roughly ten percent.
Meaning that if a person took a dose of bisphosphonates for a year or less, it would take roughly thirty years for the bisphosphonate levels in that person's system to be reduced to roughly the ten percent level.
Compounding this hazard is the criminally irresponsible stance taken by the pharmaceutical industry, and backed by the American medical community, that aggressively promotes and encourages the use of these highly destructive drugs for, at minimum, years at a time. And preferably up to, and including, a lifetime of use, as incredibly, "preventative" measures to ostensibly sustain healthy bones.
(See the article cover photo of Sally Field standing next to a www.bonehealth.com placard that reads: “I promise to take my bone medication as recommended.”)
In fact bone damage produced by these synthetically-derived bisphosphonates often continues years after the drug has been incorporated into the bone, and then remains ongoing— with the extent of the bone damage depending upon the amount of bishposphonate that had been incorporated into the bone.
Typically, the damage to the bone continues slowly, remaining outwardly unnoticed, until the underlying damage reaches a level where it finally begins to manifest itself into recognizable conditions— such as abnormal bone fractures, or bone infections, or tooth loss from an underlying diseased jawbone. Problems which have developed directly from abnormal bone remodeling, and which will eventually lead to various levels of bisphosphonate-induced bone death.
Bisphosphonate damage in bone remodeling
The major damage produced by the presence of bisphosphonate molecules is the disruption of normal bone remodeling required for normal bone health (whether the bone is thin or dense).
In the presence of bisphosphonates, “bone remodeling” still occurs, but now since the bone cells cannot dissolve the synthetic bisphosphonate molecules impregnated in the bone, the remodeling develops around this older, less healthy, bone, with new bone being laid on top of an uneven and unstable bone foundation.
This would be like building up a house using part of an older, ragged foundation, with the higher the house is built, the more vulnerable it becomes to collapse.
As a result of disorganized and unstructured bone, the normal abundance of blood vessels and nerves that pass through bone tissue are adversely affected.
Blood vessels and nerves can only optimally travel through bone that is constructed in a highly organized and structured crystalline matrix, which provides aligned openings for the blood vessels and nerve fibers to pass through-- a proper bone construction at the cellular level that bisphosphonate use destroys.
And the adverse impact on compromised blood flow through the bone tissue is extremely relevant, because blood vessels supply key nutrients and energy sources to the bone cells, such as oxygen and glucose, which are needed to keep them alive and healthy.
In addition, the blood vessels are also responsible for delivering immune system cells (white blood cells) to any area in the bone, in order to keep in check the development of bacterial colonies that can easily gain a foothold when the blood supply to bone becomes compromised.
In 2002, French researchers publishing in the scientific journal, Cancer Research, also showed that bisphosphonates inhibited the formation of blood vessels at the cellular level.
Bisphosphonates accomplish this by inhibiting the formation and activity of endothelial cells— a type of cell in the body that creates the lining of blood vessel walls. These stop the formation of normal blood vessel growth (angiogenesis) towards areas of new cell or tissue development in the bone.
The French researchers were publishing in a journal dealing with cancer issues because bisphosphonates have been used as a final stage therapy in very serious degenerative bone conditions, such as cancer of the bone, in order to try and permanently fuse together bones to keep them from breaking from the pressure of continually growing tumors that result from this disease. As well as for the drug being used in certain other cancers to reduce blood vessel growth, which helps to suppress the supply of nutrients to fast growing tumor cells.
And while inhibiting the formation of blood vessels to supply nutrients to fast growing tumors in the bone might be advantageous as a last ditch effort to try and slow the ravages of bone cancer, it is highly destructive as an alleged "treatment" of osteoporosis.
Destroying the ability of normal blood vessel formation through the bone destroys healthy bone. Every tissue in the body requires good blood flow, and without it, the tissue eventually dies, including the bone.
Because of their extensive and multiple adverse effects in disrupting normal bone remodeling, bisphosphonates— and in particular intravenous delivered bisphosphonates, such as Aredia, Zometa or Reclast, which are absorbed completely into the circulation, delivering the highest concentrations of bisphosphonates to the bones— should never have been allowed to be prescribed to anyone but those suffering from crippling and rare cases of extremely serious bone abnormalities, such as Piaget's Disease, or bone cancer originating in the bone, or for cancers that have metastasized to the bone.
And the pharmaceutical companies were well aware of the hazards of bisphosphonates for years. Well before being mildly confronted on these hazards by the FDA. And all the while putting an unawares public taking these drugs at criminally irresponsible risk of serious, debilitating, and ongoing damage to their health. If anyone is paying attention, this is called reckless endangerment, and that is a felony.
Osteonecrosis of the jawbone
The most significant danger to the bone from the use of bisphosphonates has been known since at least 2003, and has been marginalized as insignificant ever since— by not only the pharmaceutical companies like Novartis (makers of IV bisphosphonates, Aredia and Reclast) and Merck and Roche (makers of the oral bisphosphonates, Fosomax and Boniva), but also by the FDA, and by U.S physicians prescribing these drugs.
This is the highly progressive and destructive disease condition of the jawbone called osteonecrosis, where areas of the jawbone begin to die as bacterial colonies grow unchecked as a result of bone remodeling having become disorganized and chaotic. (also known as BRONJ (Bisphosphonate Related Osteonecrosis of the Jaw)
Multiple scientific studies— spearheaded by researchers and physicians in the area of maxillofacial surgery, such as Dr. Robert E. Marx, head of the Division of Oral and Maxillofacial Surgery at the University of Miami Miller School of Medicine, who have been dealing with increasingly abnormal numbers of osteonecrosis of the jaw in their patients since the early 2000s— have shown that the blood supply to the affected areas in the jawbone has been severely weakened as a result of bisphosphonate use.
The weakened blood flow— as a direct result of chaotic and abnormally constructed bone produced by the presence of bisphosphonates— allows bacterial colonies to develop unchecked within the affected bone tissue. The affected bone then begins to deteriorate, adversely affecting any structures dependent upon it, such as the teeth anchored into the bone of the jaw.
Osteonecrosis shows up in the jawbone for several reasons
Unlike all other bone tissue in the body, the bones of the jaw are only narrowly separated from high colonies of bacteria found in the mouth, which can easily gain access to the bone through the thin boundary of the gums.
In addition, a very high proportion of bisphosphonates are absorbed into the jawbones from the circulation, either after being ingested in pill form, or after being administered by IV solution (intravenously), due to the large amount of blood circulation directed to the jaw and head area.
The jawbones require a high degree of blood flow because of their continual high use in chewing, and in movement used in speaking and in the swallowing reflex— all of which require high levels of nutrients to be delivered by the blood to these high functioning bones.
Not only is basic bone remodeling in the jawbone disrupted, but basic bone "healing" of microfractures are disrupted.
Microfractures are constantly, and normally, produced as a result of heavy bone use— such as when the bones of the jaw are used in normal chewing, etc.— and these microfractures are normally fixed by normal bone remodeling. But they remain un-fixed by the suppression of bone remodeling in the presence of bisphosphonates.
And while osteonecrosis (bone death) can develop spontaneously in compromised bone created by the presence of bisphosphonates, the danger of initiating the development of osteonecrosis will steeply rise if there is any additional damage to the jawbone, or to the teeth anchored into the jawbone, which require bone "healing".
This means that if a person taking bisphosphonates trips and falls, or otherwise inadvertently hits their chin or jaw, and develops a bruise on the bone, the bone in this area, which has incorporated any bisphosphonates, will not be able to properly "heal."
The incorrect bone remodeling in the presence of bisphosphonates will create ill-constructed bone and adversely impact blood supply to the area, reducing the availability and access of immune system cells to get to any bacterial colonies that may begin to build up at the site of the bruise within the bone.
Extensive tooth damage and loss in “mild” Stage O of osteonecrosis
The likelihood of osteonecrosis damage to the jawbone will significantly increase with any damage to the gums, or as result of any dental work done to the teeth that requires removing a tooth, or extensive cavity work, or root canal, or treating of an abscess, etc.— all of which allow resulting bruising to the underlying bone, and/or exposure of the bone, even temporarily, to the multiple bacterial colonies that reside in the mouth.
This means that extensive tooth damage is almost invariably going to follow bisphosphonate use from variety of commonplace dental procedures— leading to unhealed normal cavity fillings or root canals, to unhealed infections developing in the tooth or gum, or to teeth loosening from their anchor in the jawbone and falling out.
The pharmaceutical industry, the Food and Drug Administration, and U.S. physicians have universally ignored this huge risk, while patronizing the public with the completely disingenuous and cavalier suggestion that to avoid such potentially catastrophic and permanent injury to the jawbone, patients should simply plan any dental work before they begin taking any course of bisphosphonate treatment. While omitting to mention the fact that this is an utterly impossible requirement to fulfill.
And without also mentioning that teeth will still be compromised, whether there is dental work done or not, since the underlying integrity of the jaw bone that anchors them is compromised in any bisphosphonate use.
The FDA, the medical community and the pharmaceutical industry try to downplay the tooth damage risk by stating that the risk will allegedly only increase after extensive years of bisphosphonate use. The implication of this is very clear.
Since the public is becoming increasing aware of the tooth loss risk, and since the FDA and the medical and pharmaceutical industries want to keep on prescribing and selling bisphosphonates for the $billions they are reaping in profits per year, they are willing to concede the long-term use of bisphosphonates may be harmful, but still want the public to use the drug in the short-term. But the argument is completely fraudulent because of the long half-life of the drug, and because any bisphosphonate that displaces the body's own generated phosphorous compounds in the bone is going to produce abnormal bone construction at the cellular level. And in the case of the jaw, this will place any teeth anchored above the compromised bone at risk of disease or loss.
While another important point to note is that while osteoporosis has always occurred naturally, in degrees, in the population, it has never affected tooth loss. Tooth loss and tooth damage has only occurred with the introduction of bisphosphonates to "treat" osteoporosis.
In addition to destroying the integrity of the underlying jaw bone that anchors the teeth, bisphosphonates destroy the function of the extremely sensitive saliva glands, whose production of saliva is essential for protecting the gums from microorganism invasion, helping to mineralize the teeth and prevent their decay, among other critical functions. (In addition to bisphosphonates, there is a long list of dozens of classes of other drugs that also destroy the integrity of the saliva glands, and subsequently give rise to the condition of xerostomia, or "dry mouth.")
Not only is it absurd to assume that one can apparently predict when one will have to have a cavity filled, or require a root canal, or when someone might chip or crack a tooth, or require a tooth to be pulled, or be treated for any trauma to the gums— any of which can momentarily allow bacteria in the mouth entry into the underlying compromised bone of the jaw from bisphosphonate use— but for the entire duration of time bisphosphonates are being prescribed (and for thirty years afterwards, while the remnants of the drug still reside in the bone, due to its extremely long half-life) patients should be expected to avoid any dental work that could expose the underlying jawbone to, either, bone trauma or exposure to bacterial colonies within the mouth.
These are completely absurd precautionary measures that are apparently expected to be the responsibility of the patient, and not that of the drug’s hazards, and the reckless endangerment created by the pharmaceutical companies and the doctors irresponsibly prescribing them.
While making these absurd "precautionary measures"— which suggest completing all dental work before beginning several years, to a lifetime commitment, of treatment of bisphosphonate "therapy"— completely absurd to meet, is the fact that the population being marketed these drugs— roughly 35 to 55 million U.S. citizens in the middle-age and over — are at the very age when general dental and tooth problems are significantly increasing. At a time in their life when their teeth and gums become normally compromised with age, as does every other biological component of an aging human body.
Osteonecrosis cannot be treated
Compounding the extensive pain and suffering of various levels of osteonecrosis damage is that the diseased bone cannot be treated by antibiotics, because antibiotics cannot reach the bacterial colonies within the bone, as a result of bisphosphonate-created-compromised blood vessel access to the area.
Neither can the diseased bone be surgically removed, because the bone left in place after surgery cannot correctly remodel and heal due to the continued presence of bisphosphonates in the surrounding bone matrix. And the compromised blood flow, which created the initial bacterial problem in the first place, will continue to allow the bacterial problem to redevelop after surgery, to continue to create only more damage in the remaining bone.
The only way to manage the slow destruction of the jawbone is by continual treatments of antibacterial washes to any exposed bone in the mouth— which can in no way cure the problem, but only help to slow its progress.
And in cases where no exposed bone is present, and osteonecrosis is still occurring within the bone (with abnormal tooth problem or tooth loss occurring), no treatment is available, because a lack of blood flow to the area stops the capability of administering antibiotics through the blood supply to reach the infection— as would be the standard method of treatment in any other internal bacterial infection. The only inevitability is waiting for the teeth to progressively fall out.
Adding to the debilitating aspect of this continually worsening condition is the associated and continual pain, with its severity dependent upon the extent of the ongoing damage and infection to the jawbone.
Osteonecrosis causes ongoing low-level stress, leading to more bone loss and increased risk of stress-related disease development
Individuals who have contracted various forms of osteonecrosis are also under constant low-level stress at the cellular level, as the unresolved bacterial infection in the jawbone will continue to elicit a low-level immune system reaction that can never successfully stop or contain the bacterial growth in the bone.
And a condition of constant, unresolved, low-level stress in the body over time has long been shown in biological research studies going as far back as the 1930s to result in the undermining of the general immune system, leading to the depression of its capabilities. This in turn makes these individuals increasingly susceptible to secondary problems arising from the body's compromised immune system response, which can no longer adequately protect the rest of the body from infection, or from the development of secondary diseases such as cancers.
Additionally, continual low level stress at the cellular level from unresolved bacterial infections in the bone from bisphosphonate use will also result in increased bone loss.
This happens on three levels.
Chronic low-level stress results in the continual, abnormal release of cortisol from the adrenal glands— a regulatory hormone normally used by the body to help the immune system response during short periods of time to fight an infection.
But in prolonged release of cortisol from an unresolved immune system response— as created by the presence of bisphosphonate in the bone and unchecked bacterial colonies in the condition of osteonecrosis— collagen formation, and its normal presence in the bone matrix construction is reduced, decreasing normal flexibility of the bone and decreasing its protect from unnecessary breaks.
In addition, overproduction of cortisol, from chronic low-level stress, decreases the rate of osteoblast production in the bone marrow— the bone cells needed to build new bone in the bone remodeling regulation process. AND over production of cortisol also increases the production of osteoclast cells— the bone cells responsible for breaking down bone (see below).
Osteoclasts (bone breakdown cells) increase because abnormal, continual releases of cortisol from a sustained, low-stress response increases the production of immune system cells in the bone marrow— and among them, those of the monocyte-macrophage line, which go on to form the osteoclasts.
For the past decade, scientific research in the area of immunology has clearly shown the direct correlation between an increase in osteoclast cells resulting from an increase in their precursor immune system cells, stimulated by an increase of the immune system response.
So a chronic, unresolved, low-level immune system response in the body— created by bisphosphonate use— undermines not only the body's ability to build bone, but also increases the active break down of bone— by both reducing the number of available bone-building osteoblast cells and by increasing the numbers of bone-absorbing osteoclast cells.
Additionally, and also kept unmentioned from any government, healthcare or media source, is the fact that any product or environmental impact that elicits a chronic, low-level stress in the body is going to increase osteoporosis conditions.
And one of those major manmade influences which is eliciting a continual low-level chronic stress effect in the body is manmade electromagnetic radiation emitted from computers, cell phones, and other wireless and high-tech electronic devices, such as compact fluorescent lights.
These high-tech electronic sources all emit abnormal electromagnetic radiation (EMR) that can penetrate the human body and elicit abnormal immune system reactions, which include the abnormal the release of cortisol.
The only normal EMR recognized by the human body— and not eliciting an immune system effect— are the only two natural EMR sources the human body was designed by evolution to recognize—the earth’s magnetic field and sunlight (and also the rare static electricity of lightning).
The body was never designed to recognize all other manmade EMR sources. And because of this, the body’s immune system elicits an ongoing, chronic, and futile, unresolved immune response against these continual, and increasing, abnormal daily influences, which subsequently sets up an ongoing, low-level stress reaction in the body.
It is not coincidental that osteoporosis was not even considered a serious or prevalent disease condition before the 1980s, when coincidentally computers began to be mass released into the market and began to emit elevated and penetrating forms of manmade EMR at close range to increasing members of the public. A situation that has only exponentially increased with the ever increasing impact of cell phones, wireless products, and all other high-tech electronics, from appliances to light bulbs— which all emit various and hazardous forms of manmade EMR that the human body and its immune system were never designed to recognize, and subsequently is not capably of neutralizing.
Criminally suppressing the risk of osteonecrosis by a factor of at least 4,000
For years the pharmaceutical industry, the FDA and U.S. physicians— so as to “allegedly” not scare off patients and lose billions of dollars in yearly profits— have grossly and fraudulently downplayed the occurrence of osteonecrosis of the jaw.
And there has been much to lose from a purely economic standpoint. Bisphosphonate yearly sales are around $10 billion worldwide, with the far greater majority of those sales being attributed to the 35 million-plus users of these drugs in the United States.
Grossly downplayed estimates of the occurrence of osteonecrosis of the jaw have been claimed to be only on the order of 0.7 in 100,000, or less than 0.001%, with these statistics being provided by Merck Pharmaceuticals, which of course has produced one of the most widely prescribed bisphosphonates, Fosamax. And Merc has been one of the most widely sued pharmaceutical companies for osteonecrosis of the jaw, and for spontaneous fractures of the thigh bone— the largest and strongest bone of the body (see part 2 for abnormal spontaneous fractures from very low impact resulting from bisphosphonate use).
The highly-promoted, "supposed," extremely small risk of 0.001% for developing osteonecrosis from bisphosphonate use has been presented to the media as apparently “factual” and unbiased, and is parroted by the FDA, along with physicians prescribing the drugs, and by physicians and scientists who either work directly with the pharmaceutical companies producing the half dozen current bisphosphonate brands on the market, or who receive funding for their research work from these pharmaceutical firms.
The truth is that Merck has fraudulently downplayed the osteonecrosis risk by at least a factor of four thousand. And that is a serious crime.
In 2007 researchers at the University of Southern California School of Dentistry, who had been seeing an increasing and alarming number of osteonecrosis patients over the years at its clinic, produced the only highly controlled institutional research study to date, which has been untainted by pharmaceutical influence or funding. And which clearly showed the incidence of osteonecrosis occurring in the population taking bisphosphonate drugs to be at least 4%. As opposed to Merck's estimate of less than 0.001%. That is a 4,000-fold increased risk over Merck’s assessment.
Meanwhile, dental health practitioners, who are being directly impacted by major increases in osteonecrosis cases from the tens of millions of individuals taking bisphosphonates— as a result of being unable to perform usual dental procedures on patients who are suffering from varying forms of the condition, because of fear of increasing the underlying damage to the jawbone— estimate the percentage of osteonecrosis from bisphosphonate use to be upwards of 10% of the population taking the drug.
And this risk of at least 10% has been corroborated in a significant 2004 internet survey conducted by the International Myeloma Foundation of Los Angeles and published in the New England Journal of Medicine in 2005, which found an over 12% risk of the development of osteonecrosis of the jaw in a survey of over 1200 patients who took bisphosphonates while being treated for either myeloma (a form of leukemia) or breast cancer, for the drug's impact on stopping blood vessel growth needed by tumor cells.
This 12% documented risk for the development of osteonecrosis of the jaw was due to bisphosphonate use only, and not produced by any other drug the patients were taking to treat their cancers. This documented risk amounted to over 10,000 times the supposed 0.001% risk that has been heavily promoted by Merck, and circulated as "factual" through the U.S. media.
Taking the lowest, currently assumed, amount of only 4% of bisphosphonate-prescribed patients affected by the development of osteonecrosis— out of a conservative population of 35 million bisphosphonate users in the United States (as many as 55 million prescriptions for these drugs were written in 2008)— would deliver a number in the range of nearly 1,500,000 sufferers of the this untreatable and progressive disease.
This staggering amount is equivalent to the populations of cities such as Philadelphia and Phoenix.
While if taking the likely higher percentage of the population that are likely being affected (10% currently) and basing that on the increasing numbers of users of up to 55 million taking the drug, that number jumps from over 3,000,000 to over 5,000,000 sufferers— equivalent to the populations in cities such as Houston, Chicago, or Los Angeles.
But whether this number is 1.5 or 3 or 5 million suffers, these epidemic numbers of individuals being affected in various degrees by this untreatable and debilitating condition is nothing short of criminally outrageous and condoned reckless endangerment.
A criminally irresponsible situation which has been allowed to develop by the FDA irresponsibly allowing these drugs on the market, by U.S. physicians who have acted with equal irresponsibly prescribing these drug, and by groups like the National Osteoporosis Foundation or Bone Health and their celebrity spokespersons, like the actress Sally Field.
All of these both groups or individuals are, in one form or another, abetting the criminal actions of the drug manufacturers and marketers in suppressing the highly damaging biological adverse effects of this class of drugs— or the next round of osteoporosis drugs, like genetically-modified monoclonal antibodies that also disrupt normal bone regulation at the cellular level, critical for healthy bone, whether the bone is dense or thin.
And all those involved are helping to place millions of bisphosphonate users at criminally irresponsible risk for permanent damage to their bones, while promoting these drugs as allegedly helping to improve and create healthy bones— a flat out impossibility.
Meanwhile, in 2006, the Association of Endodontists— dentists and oral surgeons that deal with diseases of the tooth and jawbone— declared a far more accurate and chilling assessment of those potentially at risk of developing some form of osteonecrosis of the jaw from taking bisphosphonates. Not to be 4% or 10%, but to be 100%.
End Part 1
Part 2 continues with:
spontaneous fractures of the largest bone in the body, the thigh bone, with bisphosphonate use,
the fraudulent bone building claims of Boniva and its spokesperson, actress Sally Field,
the downplayed risk of esophageal cancer with orally taken bisphosphonates,
how bisphosphonate therapy replaced estrogen replacement therapy when estrogen replacement therapy was connected with increased cancer risks,
and how the biological hazards of bisphosphonates have been known to the scientific and medical community for well over 150 years.
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