Osteoporosis and osteopenia

Both osteoporosis and osteopenia are diseases marked by a decrease in bone mineral density. Osteopenia is a less severe form of and sometimes precursor to osteoporosis. The loss of bone mass leads to a porous bone structure, frequent fractures, and delayed healing.

Among doctors, and even many researchers, it is conventional wisdom that vitamin D supplementation reverses osteopenia and osteoporosis. However, a growing body of interventional trials and molecular evidence shows this is not the case. Instead, current research has demonstrated that osteoporosis and osteopenia are often the direct result of infection with the Th1 pathogens, a metagenomic microbiotaThe community of bacterial pathogens including those in an intracellular and biofilm state which cause chronic disease., which produce inflammatory cytokinesAny of various protein molecules secreted by cells of the immune system that serve to regulate the immune system. and inactivate the Vitamin D ReceptorA nuclear receptor located throughout the body that plays a key role in the innate immune response.. The only way to achieve long-term reversal of bone loss is to kill the Th1 pathogens driving the disease process.

Loss of bone density is usually painless, which is why many people do not know they have the problem until they suffer a fall or fracture (which can be painful). Patients with back pain or bone pain can ask their healthcare provider to see if they have a fracture. Th1 disease can cause bone pain and quite a few of our members have reported bone pain as a Herx symptom.

The Marshall ProtocolA curative medical treatment for chronic inflammatory disease. Based on the Marshall Pathogenesis. (MP) can kill the Th1 pathogens, which cause bone loss. While on the MP, you can minimize further bone loss by doing the following:

• consuming an adequate intake of calories and protein
• minimizing intake of caffeine
• refraining from excess alcohol or sodium consumption
• limiting smoking ¹
• weaning from drugs, which lead to bone loss including:
  • corticosteroids
  • high-dose thyroid replacement therapy
  • certain anti-seizure medications
• to the extent possible, increase physical activity or any kind of weight-bearing activity, which causes muscles to pull against bones

If you are not able to exercise now, you can look forward to recovering your stamina using the MP and then working up to exercises that will focus on building strong bones. Studies have shown that even postmenopausal women can improve bone density by adding weight bearing and muscle strengthening exercises to their routine.

Osteoporotic fractures can occur without any trauma, but people who are at risk should take care to prevent falls. To reduce the risk of injury and broken bones:

• increase your activity level gradually (but avoid unusually high impact sports)
• wear supportive shoes with low heels and non-slippery soles
• use support for walking, such as a cane, if you need it
• maintain a safe and uncluttered home to help prevent falls
• avoid throw rugs on your floors at home
• avoid icy, wet, or slippery surfaces, especially in the bathroom
• use nonskid mats in the shower and bathtub

According to the Marshall PathogenesisA description for how chronic inflammatory diseases originate and develop., osteopenia and osteoporosis are caused by a microbiotaThe bacterial community which causes chronic diseases - one which almost certainly includes multiple species and bacterial forms. of pathogenic bacteria known as the Th1 pathogens. The Th1 pathogens create proteins that bind and block the Vitamin D Receptor, preventing it from expressing many essential components required for health, including estrogen receptors, upon which the bone matrix is depedenent. The bone matrix is dependent on estrogen homeostasis (estrogen is important to stimulate osteoblast activity).²

In addition, if the VDRThe Vitamin D Receptor. A nuclear receptor located throughout the body that plays a key role in the innate immune response. is blocked, the enzyme CYP24 is not transcribed. Since CYP24 is needed to keep levels of 1,25-DPrimary biologically active vitamin D hormone. Activates the vitamin D nuclear receptor. Produced by hydroxylation of 25-D. Also known as 1,25-dihydroxycholecalciferol, 1,25-hydroxyvitamin D and calcitirol. in check, the level of 1,25-D becomes greatly elevated in individuals without the active enzyme. The cytokineAny of various protein molecules secreted by cells of the immune system that serve to regulate the immune system. release stimulated by Th1 pathogens activates the pathway which causes increased production of CYP27B1, the enzyme that converts 25-DThe vitamin D metabolite widely (and erroneously) considered best indicator of vitamin D "deficiency." Inactivates the Vitamin D Nuclear Receptor. Produced by hydroxylation of vitamin D3 in the liver. into 1,25-D. As more conversion occurs, the level of 1,25-D in the body rises.³ As 1,25-D rises above a certain range - approximately 43 pg/ml - elevated levels of 1,25-D stimulate bone osteoclasts, cells that remove minerals from the bone. ⁴⁵

This model of disease is partially validated by the fact that drugs such as TNF-alpha inhibitors, which prevent inflammationThe complex biological response of vascular tissues to harmful stimuli such as pathogens or damaged cells. It is a protective attempt by the organism to remove the injurious stimuli as well as initiate the healing process for the tissue., often lead to temporary increases in bone mass in patients with osteoporosis.

Stimulated osteoclasts dissolve bone material, causing it to be reabsorbed into the bloodstream. This leads to osteoporosis as well as calcium being deposited in the soft tissues of the body, including those in the lungs, breasts and the kidneys (where it forms kidney stones).

Low calcium in the bloodstream can lead to a condition called secondary hyperparathyroidism. The condition alters the level of parathyroid hormone in the body, which can result in bone loss. In the long run, the best way to reverse bone loss is to bring the level of 1,25D in the body back into a range where minerals will no longer be leached from the bones and the level of inflammatory cytokines can return to normal. In the meantime, getting the RDA of calcium from foods and supplements without vitamin D can be helpful.

Multiple research teams have found that drugs which inhibit production of TNF-alpha lead to a short-term increase in patients’ spine and femoral bone mineral density. ⁶

It should be noted that TNF-alpha blocking drugs do not provide a permanent solution to osteoporosis, since Th1 pathogens will continue to spread as the drug is administered. Also, TNF-alpha blocking medications are known to have serious side effects. However, the research is of interest since it confirms the importance of Th1 inflammationThe complex biological response of vascular tissues to harmful stimuli such as pathogens or damaged cells. It is a protective attempt by the organism to remove the injurious stimuli as well as initiate the healing process for the tissue. in osteoporosis.

Some clinicians encourage patients with inadequate bone density to supplement with vitamin D and calcium. While calcium has been shown to be somewhat helpful in certain patient cohorts, both controlled trials and molecular evidence do not support supplementation with vitamin D to reverse bone loss as, over the long term, it only exacerbates the disease process.

A number of recent studies examining calcium and vitamin D supplementation are compromised by a flaw in methodology: the authors mistakenly attribute positive increases in bone density to both calcium and vitamin D. Studies which separately measure the positive or sometimes equivocal effect of calcium from that of vitamin D tend to show that vitamin D has no positive effect on bone health.

For example, one study found that calcium supplementation (750 mg) improved bone density over a four-year period, whereas vitamin D supplementation (600 IU) had no effect. In fact, the effect of calcium on bone loss was blunted in subjects with the highest levels of vitamin D, causing the team to point out the danger of over-supplementation of the elderly with vitamin D if they have an adequate calcium intake.¹⁴

In the case of studies showing a neutral effect of vitamin D and calcium supplementation, it’s quite possible that calcium did have a positive effect on the bone mass of the study subjects. One likely explanation is that the positive effects of calcium were offset by the negative effects of VDR blockage and elevated 1,25-D caused by consumption of the vitamin D supplements.

Some research shows that vitamin D actually decreases bone mineral density. In 1999, researchers at Cedars-Sinai Medical Center in Los Angeles conducted a small study on patients with osteoporosis and hypercalciuria, a disease in which excessive calcium is excreted in the urine. The participants were taking supplements containing high levels of vitamin D. They were asked to stop taking the supplements for three years, and their bone mass was monitored during that period of time. After stopping the supplements, the level of 25-D in their blood returned to the normal range, the hypercalciuria resolved, and there were annual increases in bone density of all subjects involved.

Occult vitamin D intoxication was detected in patients who were using dietary supplements that contained an unadvertised high level of vitamin D. Resolution of vitamin D intoxication was associated with a rebound in bone mineral density.

J.S. Adams, et al. ¹⁵

Adams's study is particularly valuable because their three-year follow-up phase, which is significantly longer than some, showed that the increase in bone mineral density persisted after initial recovery.

Similarly, researchers at the University of Science and Technology in Norway published a study that measured the forearm bone mineral density of 3,042 Norwegian women, aged 50 to 70 years old. They found that those women who had not taken cod liver oil (a substance that contains high levels of vitamin D) during childhood had higher bone mineral density compared to those who had ingested cod liver oil.¹⁶ Since the study compared childhood intake of vitamin D to bone density at least 4-5 decades after ingestion, it is a good example of how only those studies which track vitamin D intake over long periods of time, namely decades, are likely to pick up on the harm the secosteroid causes in the long term.

Supplements are taken orally in the form of vitamin D which is converted to 25-D in the liver. 25-D blocks the ability of the VDR to transcribe the enzymes which keep 1,25-D in the correct range. This results in greater bone loss as even more 1,25D is produced.

Contrary to most received wisdom, vitamin D does not enhance the absorption of calcium. 25-D is a simple secosteroid which does not affect the genes responsible for calcium absorption. Further, there is no evidence to suggest that additional vitamin D leads to a more active Vitamin D Receptor.

By way of contrast, the Vitamin D Receptor is a receptor that transcribes thousands of genes,¹⁷ some of which do affect the metabolism of calcium.

In chronic disease, the two things - vitamin D itself and the VDR - are not synonymous.

Trevor Marshall, PhD

The latest molecular evidence simply does not support the conclusion that supplementing with vitamin D activates the Vitamin D Receptor.

• certain antibiotics help strengthen bones – NIH animal studies have shown that minocyclineBacteriostatic antibiotic used by Marshall Protocol patients., an MP antibiotic, increased bone density, “stimulated bone formation substantially” and slowed bone resorption. ¹⁸
• connection with disparate diseases – the NIH connects several Th1 diseases with higher risk of osteoporosis, including rheumatoid arthritis, celiac disease, anorexia nervosa, inflammatory bowel disease and lupus [cite needed]