Osteoporosis Myth: The Dangers of High Bone Mineral Density.


Bone Scans or Scams? How Dense Bones Can Harm Your Health

The present-day definitions of Osteopenia and Osteoporosis were arbitrarily conceived by the World Health Organization (WHO) in the early 90’s and then projected upon millions of women’s bodies seemingly in order to convince them they had a drug-treatable, though symptomless, disease.

Osteopenia (1992)[i] and Osteoporosis (1994)[ii] were formally identified as skeletal diseases by the WHO as bone mineral densities (BMD) 1 and 2.5 standard deviations, respectively, below the peak bone mass of an average young adult Caucasian female, as measured by an x-ray device known as Dual energy X-ray absorptiometry (DXA, or DEXA). This technical definition, now used widely around the world as the gold standard, is disturbingly inept, and as we shall see, likely conceals an agenda that has nothing to do with the promotion of health.

Deviant Standards: Aging Transformed Into a Disease

A ‘standard deviation’ is simply a quantity calculated to indicate the extent of deviation for a group as a whole, i.e. within any natural population there will be folks with higher and lower biological values, e.g. height, weight, bone mineral density, cholesterol levels. The choice of an average young adult female (approximately 30-year old) at peak bone mass in the human lifecycle as the new standard of normality for all women 30 or older, was, of course, not only completely arbitrary but also highly illogical. After all, why should a 80-year old’s bones be defined as “abnormal” if they are less dense than a 30-year old’s?

Within the WHO’s new BMD definitions the aging process is redefined as a disease, and these definitions targeted women, much in the same way that menopause was once redefined as a “disease” that needed to be treated with synthetic hormone replacement (HRT) therapies; that is, before the whole house of cards collapsed with the realization that by “treating” menopause as a disease the medical establishment was causing far more harm than good, e.g. heart disease, stroke and cancer.

As if to fill the void left by the HRT debacle and the disillusionment of millions of women, the WHO’s new definitions resulted in the diagnosis, and subsequent labeling, of millions of healthy middle-aged and older women with what they were now being made to believe was another “health condition,” serious enough to justify the use of expensive and extremely dangerous bone drugs (and equallydangerous mega-doses of elemental calcium) in the pursuit of increasing bone density by any means necessary.

One thing that cannot be debated, as it is now a matter of history, is that this sudden transformation of healthy women, who suffered no symptoms of “low bone mineral density,” into an at-risk, treatment-appropriate group, served to generate billions of dollars of revenue for DXA device manufacturers, doctor visits, and drug prescriptions around the world.
The Manufacture of a Disease

WHO Are They Kidding?

Osteopenia is, in fact, a medical and diagnostic non-entity.  The term itself describes nothing more than a statistical deviation from an arbitrarily determined numerical value or norm.   According to the osteoporosis epidemiologist Dr. L. Joseph Melton at the Mayo Clinic who participated in setting the original WHO criteria in 1992, “[osteopenia] was just meant to indicate the emergence of a problem,” and noted that “It didn’t have any particular diagnostic or therapeutic significance. It was just meant to show a huge group who looked like they might be at risk.”[iii] Another expert, Michael McClung, director of the Oregon Osteoporosis Center, criticized the newly adopted disease category osteopenia by saying ”We have medicalized a nonproblem.”[iv]

In reality, the WHO definitions violate both commonsense and fundamental facts of biological science (sadly, an increasingly prevalent phenomenon within drug company-funded science).  After all, anyone over 30 years of age should have lower bone density than a 30 year old, as this is consistent with the normal and natural healthy aging process.  And yet, according to the WHO definition of osteopenia, the eons-old programming of our bodies to gradually shed bone density as we age, is to be considered a faulty design and/or pathology in need of medical intervention.

How the WHO, or any other organization which purports to be a science-based “medical authority,” can make an ostensibly educated public believe that the natural thinning of the bones is not normal, or more absurdly: a disease, is astounding. In defense of the public, the cryptic manner in which these definitions and diagnoses have been cloaked in obscure mathematical and clinical language makes it rather difficult for the layperson to discern just how outright insane the logic they are employing really is.

So, let’s look closer at the definitions now, which are brilliantly elucidated by Washington.edu’s  published online course on Bone Densitometry, which can viewed in its entiretyhere.

The Manufacture of a Disease through Categorical Sleight-of-Hand

bone mineral density loss

The image above shows the natural decrease in hip bone density occurring with age, with variations in race and gender depicted.  Observe that loss of bone mineral density with age is a normal process.

Bell Curve Bones

Next, is the classical bell-shaped curve, from which T- and Z-scores are based.  T-sores are based on the young adult standard (30-year old) bone density as being normal for everyone, irregardless of age, whereas the much more logical Z-score compares your bone mineral density to that of your age group, as well as sex and ethnic background.  Now here’s where it gets disturbingly clear how ridiculous the T-score really system is….

WHO definitions osteoporosis

Above is an image showing how within the population of women used to determine “normal” bone mineral density, e.g. 30-year olds, 16% of them already “have” osteopenia” according to the WHO definitions, and 3% already “have” osteoporosis! According to Washington.edu’s online course “One standard deviation is at the 16th percentile, so by definition 16% of young women have osteopenia! As shown below, by the time women reach age 80, very few are considered normal.”

Osteopenia and Osteoporosis Rates with Age

Above you will see what happens when the WHO definitions of “normal bone density” are applied to aging populations. Whereas at age 25, 15% of the population will “have” osteopenia, by age 50 the number grows to 33%. And by age 65, 60% will be told they have either osteopenia (40%) or osteoporosis (20%).

On the other hand, if one uses the Z-score, which compares your bones to that of your age group, something remarkable happens: a huge burden of “disease” disappears!  In a review on the topic published in 2009 in the Journal of Clinical Densitometry, 30-39% of the subjects who had been diagnosed with osteoporosis with two different DXA machine models were reclassified as either normal or “osteopenic” when the Z- score was used instead of the T-score. The table therefore can be turned on the magician-like sleight-of-hand used to convert healthy people into diseased ones, as long as an age-appropriate standard of measurement is applied, which presently it is not.

Bone Mineral Density is NOT Equivalent to Bone Strength

As you can see there are a number of insurmountable problems with the WHO’s definitions, but perhaps the most fatal flaw is the fact that the Dual energy X-ray absorpitometry device (DXA) is only capable of revealing the mineral density of the bone, and this is not the same thing as bonequality/strength.

While there is a correlation between bone mineral density and bone quality/strength – that is to say, they overlap in places — they are not equivalent.  In other words, density, while an excellent indicator of compressive strength (resisting breaking when being crushed by a static weight), is not an accurate indicator of tensile strength (resisting breaking when being pulled or stretched).

Indeed, in some cases having higher bone density indicates that the bone is actually weaker. Glass, for instance, has high density and compressive strength, but it is extremely brittle and lacks the tensile strength required to withstand easily shattering in a fall. Wood, on the other hand, which is closer in nature to human bone than glass or stone is less dense relative to these materials, but also extremely strong relative to them, capable of bending and stretching to withstand the very same forces which the bone is faced with during a fall.  Or, take spider web. It is has infinitely greater strength and virtually no density. Given these facts, having “high” bone density (and thereby not having osteoporosis) may actually increase the risk of fracture in a real-life scenario like a fall.

Essentially, the WHO definitions distract from key issues surrounding bone quality and real world bone fracture risks, such as gait and vision disorders.[v] In other words, if you are able to see and move correctly in our body, you are less likely to fall, which means you are less prone to fracture. Keep in mind also that the quality of human bone depends entirely on dietary and lifestyle patterns and choices, and unlike x-ray-based measurements, bone quality is not decomposable to strictly numerical values, e.g. mineral density scores.  Vitamin K2 and soy isoflavones, for instance, significantly reduce bone fracture rates without increasing bone density.  Scoring high on bone density tests may save a woman from being intimidated into taking dangerous drugs or swallowing massive doses of elemetal calcium, but it may not translate into preventing “osteoporosis,” which to the layperson means the risk of breaking a bone.  But high bone mineral density may result in far worse problems….

High Bone Mineral Density & Breast Cancer

High Bone Mineral Density & Breast Cancer

One of the most important facts about bone mineral density, conspicuously absent from discussion, is that having higher-than-normal bone density in middle-aged and older women actually INCREASES their risk of breast cancer by 200-300%, and this is according to research published in some of the world’s most well-respected and authoritative journals, e.g. Lancet, JAMA, NCI. (see citations below).

While it has been known for at least fifteen years that high bone density profoundly increases the risk of breast cancer  — and particularly malignant breast cancer — the issue has been given little to no attention, likely because it contradicts the propaganda expounded by mainstream woman’s health advocacy organizations. Breast cancer awareness programs focus on x-ray based breast screenings as a form of “early detection,” and the National Osteoporosis Foundation’s entire platform is based on expounding the belief that increasing bone mineral density for osteoporosis prevention translates into improved quality and length of life for women.

The research, however, is not going away, and eventually these organizations will have to acknowledge it, or risk losing credibility.

 

Treatment of low bone density in young people with cystic fibrosis: a multicentre, prospective, open-label observational study of calcium and calcifediol followed by a randomised placebo-controlled trial of alendronate.


Background
Long-term complications of cystic fibrosis include osteoporosis and fragility fractures, but few data are available about effective treatment strategies, especially in young patients. We investigated treatment of low bone mineral density in children, adolescents, and young adults with cystic fibrosis.
Methods
We did a multicentre trial in two phases. We enrolled patients aged 5—30 years with cystic fibrosis and low bone mineral density, from ten cystic fibrosis regional centres in Italy. The first phase was an open-label, 12-month observational study of the effect of adequate calcium intake plus calcifediol. The second phase was a 12-month, double-blind, randomised, placebo-controlled, parallel group study of the efficacy and safety of oral alendronate in patients whose bone mineral apparent density had not increased by 5% or more by the end of the observational phase. Patients were randomly assigned to either alendronate or placebo. Both patients and investigators were masked to treatment assignment. We used dual x-ray absorptiometry at baseline and every 6 months thereafter, corrected for body size, to assess lumbar spine bone mineral apparent density. We assessed bone turnover markers and other laboratory parameters every 3—6 months. The primary endpoint was mean increase of lumbar spine bone mineral apparent density, assessed in the intention-to-treat population. This study is registered with ClinicalTrials.gov, number NCT01812551.
Findings
We screened 540 patients and enrolled 171 (mean age 13•8 years, SD 5•9, range 5—30). In the observational phase, treatment with calcium and calcifediol increased bone mineral apparent density by 5% or more in 43 patients (25%). 128 patients entered the randomised phase. Bone mineral apparent density increased by 16•3% in the alendronate group (n=65) versus 3•1% in the placebo group (n=63; p=0•0010). 19 of 57 young people (33•3%) receiving alendronate attained a normal-for-age bone mineral apparent density Z score. In the observational phase, five patients had moderate episodes of hypercalciuria, which resolved after short interruption of calcifediol treatment. During the randomised phase, one patient taking alendronate had mild fever versus none in the placebo group; treatment groups did not differ significantly for other adverse events.
Interpretation
Correct calcium intake plus calcifediol can improve bone mineral density in some young patients with cystic fibrosis. In those who do not respond to calcium and calcifediol alone, alendronate can safely and effectively increase bone mineral density.
Source: Lancet

Expansile, lytic and hypermetabolic bone lesions not always metastatic cancer .


A 44-year-old man was referred for evaluation of hypercalcemia. He had atraumatic rib and clavicle fractures in the setting of marked hypercalcemia and symptomatic nephrolithiasis.

His medical history included chronic kidney disease due to obstructive bilateral hydronephrosis and coronary artery disease requiring multiple percutaneous coronary interventions. His symptoms, consistent with hypercalcemia, included polyuria, nocturia, malaise, muscle weakness, depression and early morning nausea. He had no family history of endocrine disease. Physical examination was remarkable for widespread nonspecific bony tenderness on deep palpation. Proximal muscle weakness was prominent, including an inability to rise from a crouched position or walking up a step without aid. Thyroid and neck examination were unremarkable.

His serum calcium levels ranged from 10.9 mg/dL to 13.3 mg/dL during the previous year, with corresponding intact parathyroid (PTH) between 3,111 pg/mL and 4,023 pg/mL. His 25-hydroxyvitamin D level was 23 ng/mL. Serum phosphorus level was suppressed to 2 mg/dL, and serum creatinine trended up from 1.5 mg/dL to 2.2 mg/dL.

His markers of bone turnover were very elevated, with an alkaline phosphatase of 1,344 units/L (reference: 25-100 units/L), spot urinary N-telopeptide of 311 nmol/mmol (reference: 9-60 nmol/mmol) and serum osteocalcin .300 ng/mL (reference: 9-38 ng/mL).

Extensive imaging studies were performed for the presumed diagnosis of pathological fractures. An 18F-fluorodeoxyglucose (FDG) PET/CT scan revealed hypermetabolic lesions corresponding to expansile and lytic regions in multiple ribs, vertebral bodies, iliac bones, pubic rami, acetabulum and right clavicle (Figures 1 and 2). Axial DXA bone mineral density scan showed osteopenia at both the lumbar spine (T-score –2.2) and femoral neck (T-score –2.2), and the distal radius showed marked bone loss (T-score –6.9) demonstrating preferential cortical bone loss from hyperparathyroidism (HPT). A bone biopsy of one of the larger lesions was performed with pathology consistent with osteitis fibrosa cystica (OFC).

A diagnosis of primary HPT was established with elevated PTH and calcium levels with nephrolithiasis, chronic kidney disease, osteoporosis and OFC with pathological multisite fractures.

Initial 99-technetium sestamibi PTH scan at an outside hospital was non-localizing, but when repeated with mediastinal views, abnormal uptake in the anterior mediastinum was seen, consistent with a 5-cm mediastinal PTH adenoma or carcinoma.

OFC was once the dominant clinical manifestation of primary HPT. With modern improvement in laboratory testing and early diagnosis, OFC has become exceedingly rare but is still seen in the developing world. Friedrich Daniel Von Recklinghausen is credited with describing the first case of OFC in 1891; however, the association with parathyroid disease was noted by Askanazy in 1904. OFC is also known as Recklinghausen’s disease of bone. The more severe cystic changes seen in OFC have been termed “brown tumors.” Histologically, these “tumors” are highly vascular and are composed of clusters of giant cells in a background of mononuclear or spindle cells with hemosiderin. OFC is characterized by PTH-mediated increase in osteoclast activity, peritrabecular fibrosis and “tunneling” resorption of trabeculae, which leads to the cystic changes and expansile, lytic features noted on imaging.

Cortical, rather than trabecular, bone loss is more prominent due to the anabolic effect of PTH on trabecular bone. However, in severe long-standing cases, trabecular bone is not spared and osteoporosis at axial skeletal sites is common. In severe forms of the disease, marked skeletal deformity, minimal trauma fractures and bony pain may result in severe disability. Primary HPT with osteoporosis or OFC would warrant surgical resection of the parathyroid adenoma, given the risk for progressive bone remodeling, fractures and potential skeletal deformity.

A case series of 51 patients in India with primary HPT and OFC were followed after parathyroidectomy with an intention to measure bone recovery postoperatively. BMD recovery was impressive and occurred early (within 1 week) and was more prominent in trabecular bone than cortical bone sites. Bone pain improved in 71% of patients. Despite improvements in BMD after surgery, re-mineralization was not universal at all bone sites and many patients never regained normal BMD after 4 years of follow-up. Brown tumors and skeletal deformity improved overall; however, radiological deformity persists and may require corrective surgery.

OFC is an increasingly uncommon presentation of primary hyperparathyroidism. The diagnosis should be suspected in patients with pathological fractures and hypercalcemia. Appropriate surgical removal of the causative parathyroid tumor has early and positive benefits on bone health, but the most severe form of HPT osteodystrophy, brown tumors or OFC, may not structurally return to normal and continue to be at an increased risk for fracture.

References:
  • Agarwal G. Surgery. 2002;132:1075-1083.
  • Kearns AE. Mayo Clin Proc. 2002;77:87-91.
  • Pai M. Clin Nucl Med.1997;22:691-694.

 

Source: the Oncologist.