Osteoporosis

Osteoporosis, literally “porous bone,” is defined as a deterioration of the structure matrix of the bone, associated with continuous migration of calcium out of the bone, along with an increased risk of fractures that worsen as the disease progresses. Adding dietary and/or supplementary calcium does not diminish fracture risk, and while the root cause of this disease remains unaddressed, and less and less calcium is left in the bone, bone strength decreases and fracture risk increases.

Since the body’s ability to excrete excess calcium is limited, all remaining amounts accumulate in other parts of the body. Such deposits are directly linked to a significantly increased risk of heart disease, cancer, high blood pressure, stroke, and many other chronic degenerative diseases as well.

Truly, calcium migration from bone is quite serious. Nevertheless, it is not the cause of osteoporosis but rather a symptom of it.

Bone performs four vitals roles. Three of these: Structural support, organ protection, and the production of blood cells. They are commonly acknowledged. The fourth is as important but less known function is the storage of minerals for on demand use by other parts of the body. These minerals include magnesium and phosphorus but by far the most plentiful of these warehouse minerals is calcium.

The process of withdrawing calcium from bone is called resorption, whereas the reincorporation of calcium back into the bone matrix is called absorption. These two processes, absorption and resorption are constantly changing the shape and structure of the bone in a cycle that is called bone remodeling.

The normal stresses of life cause micro and mini fractures in bone tissue that normally go unnoticed but ultimately weaken the structural strength. Bone remodeling is the process the body uses to shape and heal these fractures. Under certain conditions, withdrawal of calcium from the bone is abnormally high and deposition of calcium in the bone is abnormally low. When calcium withdrawal in the bone continually exceeds deposit, the calcium deficit is called osteoporosis.

Several factors contribute to an osteoporotic condition, but there is one that is responsible for the lion’s share of calcium loss. It initiates and severely worsens an imbalance in the bone remodeling. In clinical terms, the major cause of osteoporosis is a focal scurvy of the bone, quite simply scurvy (is severe vitamin C deficiency), whether general or localized (focal) can be prevented, cured, and reversed with appropriate dosing and administration of vitamin C, an utterly important nutrient.

The bone has two cells that work together in balance. One is the so-called osteoblast, the key players in the production of new bone. Another type of special cell is the osteoclast. This is the bone destroyer. It literally dissolves crystal in bone tissue in the resorption process. Repeat, osteoblast creates new bone. Osteoclast destroys existing old bone. As we age, the balance between the two progressively shift towards increasing the osteoclastic activity. In the absence of vitamin C, bone-making osteoblasts fail to form and at the same time since vitamin C impedes the creation of bone dissolving osteoclasts, a focal scurvy inside the bone will allow them to multiply in an uncontrolled manner, thus initiating the imbalance that results in a detrimental breakdown in the bone integrity, along with calcium loss.

A deficiency of vitamin C in the bone also directly increasing the oxidative stress. Oxidative stress is a destructive process that greatly impairs the production of healthy bone matrix, and it even prevents that production when the bony vitamin C deficiency exists. Studies in cell culture, animals, and humans have confirmed the rules of oxidative stress in the cause and development of osteoporosis. In short, vitamin C prevents bone loss and fracture. The higher the dose of vitamin C, the lower the risk of fractures. Oxidative stress has already been linked to virtually every disease known to man. Vitamin C is the foundation and the cornerstone of strong bone.

In summary:

• Osteoporosis is primarily a scurvy, or severe deficiency of vitamin C and other supportive antioxidants in the bone.
• Vitamin C is essential in every aspect of bone physiology.
• Vitamin C is a frontline defender against oxidative stress.
• Supplemental vitamin C results in greater bone density.
• Supplemental vitamin C lowers fracture risk.
• Supplemental vitamin C accelerates and improves quality of bone healing.
• Supplemental vitamin C protects against dangerous calcification.
• Supplemental vitamin C protects against calcium laden kidney stones.
• Supplemental vitamin C lowers all causes of mortality.
• Supplemental vitamin C is nontoxic and safe.

Stay alert for the rest of the story – The brutal truth about osteoporosis and why you are probably doing it wrong.

As a result of this unhealthy union, the danger of excess calcium is greatly amplified while the benefit of vitamin D supplementation is severely diminished. Therefore, calcium and vitamin D should not be consumed together. Excessive calcium ingestion from food and/or supplementation is greatly hazardous to health and life in general.

Like iron and copper, calcium is absolutely essential for good health. However, excessive levels of these three nutrient elements are very toxic. Deficiencies of these nutrients are certainly not desirable, but they are only rarely encountered in the United States.

Actually, the amount of calcium needed for healthy cellular function is infinitely small, relative to the amount of calcium found in bone. Most of the adult population has no need for significant calcium intake and the amount needed rapidly decreases with age, as older individuals are already significantly accumulating calcium. Like iron and copper, calcium quickly becomes toxic as concentrations barely inch over required levels. Almost without exception, osteoporotic individuals have toxic excess of calcium outside the bounds of bone tissue. This fact alone highlights the fallacy of calcium supplementation for the treatment of osteoporosis. It is this excess of ingested calcium, along with calcium chronically released from osteoporotic bone that poses the most dangerous threat to health and life, as it moves in and around all of the cells in the body, promoting diseases whenever it accumulates. This notably includes heart disease, high blood pressure, stroke, and cancer. However, truth be known, it fuels and accelerates all chronic degenerative diseases.

The important role of vitamin D in decreasing the chances of osteoporotic fractures has been clearly established. When adequate vitamin D has been supplemented, a significant reduction in fracture risk has resulted.

Studies have long established the important relationship between vitamin D level, calcium, and bone. This includes the following:

• Vitamin D deficiency is a cause of osteoporosis.
• Vitamin D deficiency is associated with an increased risk of fracture in children, in adults, and in patients with osteoporosis.
• Vitamin D excess increases bone resorption, worsened osteoporosis, and causes ectopic calcification throughout the body.
• Bone loss secondary to vitamin D excess rebounds quickly when vitamin D levels return to normal.
• Correcting a vitamin D deficiency after menopause suppresses resorption of bone and loss of bony calcium, and in osteoporotic bone it results in a rapid recovery of bone mineral density.
• Vitamin D status is a key determinant of bone mineral density in children and adolescents.

Vitamin D plays a large role in regulating calcium metabolism and optimizing the correct assimilation of calcium into a renewed healthy bone mineral matrix. Proper supplementation with vitamin D increased bone density with a decrease in the incidence of fracture. Calcium, on the other hand, can only produce a cosmetic increase in bone density without affecting bone quality and structural integrity.

Vitamin D administered without calcium demonstrates the same degree of fracture protection seen in studies where vitamin D and calcium are used together. Calcium supplementation does not reduce the incidence of fracture, and calcium supplementation does not help vitamin D provide such protection. This vitamin D is such an important nutrient that vitamin D receptors have been identified in nearly all the organs and tissues of the body. We now know that vitamin D affects the expression of hundreds and perhaps as many as one thousand to two thousand genes.

Recent findings indicate that vitamin D plays a beneficial role in:

• Autoimmune disease
• Cell differentiation and proliferation
• Male reproduction
• Skeletal muscle
• Multiple sclerosis
• Immune function
• Cancer regulation
• Asthma
• Ankylosing spondylitis
• HIV infection
• Diabetes
• Hypertension
• Atherosclerosis
• Inflammation

Optimal dosing of vitamin D has also proven to be extremely effective in reducing the incidence of a wide array of diseases and medical conditions. These include cancer, coronary artery disease, as well as some bacterial and viral infections.

Vitamin D lowers all-cause mortality.

It is very important to maintain vitamin D level in the normal range. Abnormal elevation of vitamin D in the blood will always lead to excess calcium assimilation. As a consequence, the clinical manifestation of vitamin D excess mirrors the effects of calcium excess by increasing bone resorption, sufficiently elevated abnormal level of vitamin D pulls calcium out of the bone and dumps it into the blood.

An excess of vitamin D induces loss of calcium from the bone and makes such level of vitamin D an additional cause or aggravation of osteoporosis. Given these facts it is vital that vitamin D level be maintained in a normal range. Both vitamin D excess and vitamin D deficiency promote bone resorption with much of the calcium loss from the bone contributing to excess calcium elsewhere in the body, particularly the heart valve and the lining of the coronary artery.

In summary, assuming the maintenance of optimal blood level of D, the following benefits are:

• Help prevent osteoporosis.
• Lower risk of bone fracture.
• Suppresses resorption of bone and loss of bony calcium.
• Produces rapid recovery of bone mineral density.
• Decreases the incidence of many cancers.
• Boosts immune system.
• Beneficial in the treatment of multiple diseases, including hypertension, atherosclerosis, cancer, asthma, diabetes, and inflammation.
• Vitamin D decreases all-cause mortality.

Magnesium has long been regarded as a physiological or naturally occurring calcium channel blocker with many different established clinical applications. Supplemental magnesium has been shown to be beneficial in:

• Asthma
• Tetanus
• Inflammation
• Atherosclerosis
• Acute myocardial infarction
• Myocardial protection during heart surgery
• Prevention and treatment of heart rhythm abnormalities
• Eclampsia and preeclampsia
• Migraines
• Hypertension
• Stroke
• Prevention and treatment of convulsions
• Osteoporosis

Magnesium and calcium can largely be characterized as a biological antagonist.

A state of calcium excess actually assures that a state of magnesium deficiency is present as well.

The presence of calcium excess in nearly all older women further assures that there exists magnesium deficiency comparable in degree to that calcium excess.

Therefore, raising bodily concentration of magnesium to normal or even slightly supranormal, in an effort to alleviate and possibly eliminate calcium toxicity appears to be universally advisable.

Biological properties of magnesium (as related to calcium):

• Dissolve calcium deposits and keeps them in solution.
• Decreases intracellular oxidative stress by decreasing elevated intracellular calcium levels.
• Regulates active calcium transport.
• Increases bone density and decreases fracture incidents.

• Excess calcium deposition
• Increased intracellular calcium levels
• Promotion of prostate cancer cell proliferation
• Initiation of osteoporosis

Additional important biological effects of magnesium that may or may not directly involve its interaction with calcium include the following:

• Regulate insulin action and insulin-mediated glucose uptake; magnesium deficiency is an important aspect of insulin resistance.
• Help prevent metabolic syndrome; magnesium deficiency is associated with significantly increased risk of this syndrome, which increases risk of heart disease.
• Supplementation blocks the atherosclerosis induced by excessive vitamin D in pigs.
• Supplementation suppressed bone turnover; a major factor in age-related osteoporosis.
• Possibly improve brain function and hearing.
• Requires cofactor in more than three hundred enzymatic reactions.

• Induction of inflammation and increased oxidative stress; this magnesium deficiency – induced inflammation – can be lessened by the additional induced deficiency of calcium, further indicating that it is a relative excess of calcium to magnesium that determines the presence of inflammation and increased oxidative stress.
• Prevention of cellular release nitric oxide.
• Induction of endothelial dysfunction.
• Acceleration of the aging process when deficiency is chronic.

Vitamin K: Dissolves unwanted calcium deposits, reduces fracture risk.

Mainstream medicine in the United States makes little use of vitamin K in the treatment of osteoporosis. This is in spite of an enormous amount of scientific evidence documenting its important role in bone physiology, in the reduction of osteoporotic fractures, and in the mobilization/dissolution of abnormal calcification

A major way in which vitamin K contributes to bone health is through its rule as a cofactor in the carboxylation, or activation, of the bone formation marker osteocalcin. A low degree of osteocalcin carboxylation in the body has been related to osteoporosis. Any randomized, placebo/controlled, double blind study, postmenopausal women with osteopenia were given either 5 mg of vitamin K1 or a placebo daily, Even though the study was aimed at following the age-related decline in bone mineral density, additional significant observations were made.

The researchers noted that although the age-related decline in bone mineral density was not affected, an increased percentage of osteocalcin was carboxylated, indicating a lessening of osteoporotic activity. Furthermore, fewer women in the vitamin K1 group had fractures, and fewer had cancers.

In the treatment of osteoporosis, vitamin K supplementation will refer primarily to vitamin K2 (MK-7) and to a lesser degree, vitamin K1.

In a study on rats, it was shown that vitamin K2 (MK-7) improved the quality of bone to the point that the vertebral fractures were prevented, even though bone mass was not increased. In another study, vitamin K2 (MK-7) prevented the bone loss that would otherwise develop from the loss of hormone production in rats subjected to the removal of the ovaries.

In another study with rats without ovaries, vitamin K2 (MK-7) administration resulted in significant improved bone strength and less susceptibility to fractures.

In humans, low intake of vitamin K or low blood level of vitamin K, as well as of vitamin D, were found to be significant, an independent determinant of osteoporosis and bone fracture risk. Furthermore, the risk was found to be independent of any generalized malnutrition. A low dose (180 mcg daily) of vitamin K2 (MK-7) over a three-year period was found to decrease bone loss in postmenopausal women.

It would appear that vitamin K is not just an important part of an osteoporosis treatment regimen, but a mandatory one.

The lack of toxicity of vitamin K is nearly as impressive as its effectiveness in decreasing the incidence of osteoporotic fractures, preventing new ectopic calcification, and dissolving existing ectopic calcifications.

Vitamin K2 also has demonstrated no known toxicity or undesired side effects when administered to newborns or pregnant women.

Vitamin K reliability:

• Inhibits abnormal calcification outside of the bones.
• Helps dissolve preexisting abnormal calcification.
• Neutralizes the anticoagulant, warfarin, which promotes abnormal calcification.
• K2 (MK-7) lessens susceptibility to coronary artery disease.
• K1 may increase bone density but definitely decreases fracture risk.
• K2 as MK-4 prevents fractures, sustains bone density, and improves bone quality via increased collagen content and collagen cross-linking when administered in a pharmacologic dose.
• K2 can compensate for bone weakening induced by magnesium deficiency.
• Can prevent and/or effectively treat some forms of cancer.
• K2 as MK-4 can augment deposited bone effect of bisphosphonate.
• K2 (MK-7) decreases cardiac mortality, as well as all-cause mortality.

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