Related article: Secondary hyperparathyroidism
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.
Thumbs Down on Calcium and Vitamin D to Prevent Hip Fracture January 2018
Supplementation and Fracture Incidence in Community-Dwelling Older Adults: A Systematic Review and Meta-analysis December 2017
Vitamin D Supplements Don't Help Bone Health, Meta-Study Finds October 2018
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.. It seems the only way to achieve long-term reversal of bone loss is to kill the Th1 pathogensThe community of bacterial pathogens which cause chronic inflammatory disease - one which almost certainly includes multiple species and bacterial forms. 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 diseaseAny of the chronic inflammatory diseases caused by bacterial pathogens. can cause bone pain and quite a few of our members have reported bone pain as a Herx symptom.
MP patients with pre-MP levels of 1,25-D higher than 45pg/ml, those who have osteoporosis or may be at risk for osteoporosis, and those who did not assess their 1,25-D pre-MP should consider that light exposure may increase 1,25-D to levels that promote bone resorption. They should weigh the risk/benefit ratio of light exposure vs. their need or desire to expose themselves to light.
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:
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.
Main article: Bone density conservation agents
Related article: Osteoporosis and osteopenia
A variety of medications including the bisphosphonates have been touted to conserve or increase bone mass. These drugs have a number of side effects and are known or suspected to interfere with proper immune function.
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:
Bone loss is complicated and multi-factorial.
<html><!– In addition, if the VDR is blocked, the enzyme CYP24 is not transcribed. Since CYP24 is needed to keep levels of 1,25-D 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-D into 1,25-D. As more conversion occurs, the level of 1,25-D in the body rises.5) 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.6) 7) –> </html>
Calcitonin 8)
Salmon calcitonin (after this referred to as “calcitonin”) is an analog of human calcitonin used in the treatment of postmenopausal osteoporosis, Paget disease of bone, and hypercalcemia. Its clinical importance derives from its ability to inhibit osteoclasts and increase renal excretion of calcium.
Through these processes, bone matrix resorption and serum calcium are both decreased.
boron deficiency is common in western diets
Boron deficiency causes greatly increased amounts of calcium and magnesium to be lost with the urine. A borax supplement will reduce the daily loss of calcium by nearly 50%. As this calcium comes mainly from resorbed bone and teeth, boron deficiency may be the most important factor in causing osteoporosis and tooth decay.
An optimal correlation of cannabinoid dose, duration, moment of action, and affinity can lead to an increased bone regeneration capacity 9)
Heavy cannabis use is associated with low bone mineral density, low BMI, high bone turnover, and an increased risk of fracture. 10) Response by H W Daniell, M.D.
interpretation of those results; suggestion by S M Hanis, M. Sc. and K Mansori, Ph. D.
Cannabinoids induce incomplete maturation of cultured human leukemia cells. 11)
The psychoactive component of marijuana, delta9-tetrahydrocannabinol (THC) suppresses different functions of immunocytes, including the antimicrobicidal activity of macrophages. 12)
the first observations of GcMAF effects on the transcriptionomics of the endocannabinoid system and expression of CB2R protein. These data point to a potential nexus between endocannabinoids, vitamin D and its transporter proteins, and the immune dysregulations observed with autism. 13)
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-alphaA cytokine critical for effective immune surveillance and is required for proper proliferation and function of immune cells. lead to a short-term increase in patients’ spine and femoral bone mineral density. 14)
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. 15) 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.
Calcium supplements have been widely used by older men and women. However, in little more than a decade, authoritative recommendations have changed from encouraging the widespread use of calcium supplements to stating that they should not be used for primary prevention of fractures. This substantial shift in recommendations has occurred as a result of accumulated evidence of marginal antifracture efficacy, and important adverse effects from large randomized controlled trials of calcium or coadministered calcium and vitamin D supplements. In this review, we discuss this evidence, with a particular focus on increased cardiovascular risk with calcium supplements, which we first described 5 years ago. Calcium supplements with or without vitamin D marginally reduce total fractures but do not prevent hip fractures in community-dwelling individuals. They also cause kidney stones, acute gastrointestinal events, and increase the risk of myocardial infarction and stroke. Bolland MJ, Grey A, and Reid IR 2013 16)
Web of industry, advocacy, and academia in the management of osteoporosis BMJ 2015;351:h3170
“Calcium and vitamin D supplementation continue to be recommended to prevent and treat osteoporosis despite evidence of lack of benefit, say Andrew Grey and Mark Bolland. They examine why change is difficult and call for advocacy organisations, academics, and specialist societies to abandon industry ties”
| Author/Year | Study Design | Findings |
|---|---|---|
| Steven R. Cummings, MD; Douglas P. Kiel, MD, MPH; Dennis M. Black, PhD, 2016 17) | Two “high” doses (60 000 IU of vitamin D3 per month or 24 000 IU vitamin D3 plus 300 mg of calcifediol per month) achieved a serum 25-hydroxyvitamin D (25[OH]D) level of 30 ng/mL in 80% of participants, a level that has been recommended as best for reducing the risk of fractures | compared with a dose of 24 000 IU of vitamin D3 per month (equivalent to 800 IU per day), the higher doses had no effect on lower extremity physical performance and increased the risk of falls. |
| Karen E. Hansen, MD, MS; R. Erin Johnson, BS; Kaitlin R. Chambers, BS et al., 2015 18) | randomized, double-blind, placebo-controlled clinical trial from May 1, 2010, through July 31, 2013, and final visit on August 8, 2014. A total of 230 postmenopausal women 75 years or younger with baseline 25(OH)D levels of 14 through 27 ng/mL and no osteoporosis were studied. | “We found that compared with placebo, high-dose cholecalciferol had a very small effect on calcium absorption (1%) that did not translate into meaningful changes in lumbar spine, mean total-hip, femoral neck, or total-body BMD, trabecular bone score, TUG score, STS test score, muscle mass, number of falls, or number of fallers. ” |
| J Christopher Gallagher,Prachi S Jindal, Lynette M Smith, 2014 19) | A total of 198 white and African American women, aged 25 to 45 years, with serum 25OHD <20 ng/mL, were randomized in a double-blind study to vitamin D3 400, 800, 1600, 2400 IU, or placebo. A calcium supplement was given to increase mean calcium intake at baseline from 706 mg/d to 1031 mg/d. Calcium absorption was measured at baseline and after 12 months using a single isotope method with radiocalcium45 and 100 mg of calcium. Mean baseline serum 25OHD was 13.4 ng/mL (33.5 nmol/L) and increased to 40 ng/mL (100 nmol/L) on the highest dose of 2400 IU. | “ There is no need to recommend vitamin D for increasing calcium absorption in normal subjects. Very efficient calcium absorption at very low levels of serum 25OHD explains why people do not develop osteomalacia provided that dietary intakes of calcium and phosphorus are adequate.” |
| Gallagher JC1, Yalamanchili V, Smith LM., 201220) | a randomized double-blind placebo-controlled trial at Creighton University Medical Center, Omaha, NE. included 163 postmenopausal Caucasian women with insufficiency, defined as a serum 25OHD below 20 ng/ml (50 nmol/liter). | There was no evidence of a threshold for reduced calcium absorption in the serum 25OHD range of 10-66 ng/ml. The results challenge assumptions about the value of adding vitamin D to increase calcium absorption except when serum 25OHD is less than 10 ng/ml. |
| Brunner et al., 200821) | The largest randomized double-blind placebo-controlled study (the most valid study design possible) on vitamin D and calcium to date. More than 33,000 50-79 year old women at 40 centers participated. | “Calcium and vitamin D do not protect against decline of physical functioning in older women.” |
| Tang et al., 2007 22) | The largest meta-analysis of calcium and vitamin D trials in people over 50. combined the results of 29 randomized trials in which researchers had given participants supplements of calcium and vitamin D. | Although the team did find a small reduction in fracture risk (12%) correlated with calcium supplementation, they state, “Addition of vitamin D supplementation was not shown to offer additional risk reduction over and above the use of calcium alone.” |
| Porthouse et al., 200523) | Randomized controlled trial of 3,314 women, 70+ years old who were at risk for hip fractures because of decreased bone mass. The women supplemented with 1000 mg of calcium and 800 IU of vitamin D over a period of 24-62 months. | There was no measurable change in the bone quality of any of the women. Researchers found “no evidence that calcium and vitamin D supplementation reduce the risk of clinical fractures in women with one or more risk factors for hip fracture.”24) (Other well-designed studies on elderly women at risk for fractures have come to identical conclusions.25) 26) 27)) |
| Sanders KM1, Stuart AL, Williamson EJ, Simpson JA, Kotowicz MA, Young D, Nicholson GC. 201028) | A double-blind, placebo-controlled trial of 2256 community-dwelling women, aged 70 years or older, considered to be at high risk of fracture were recruited from June 2003 to June 2005 and were randomly assigned to receive cholecalciferol or placebo each autumn to winter for 3 to 5 years. The study concluded in 2008. | “CONCLUSION: Among older community-dwelling women, annual oral administration of high-dose cholecalciferol resulted in an increased risk of falls and fractures.” |
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.29)
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. 30)
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.31) 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.
Yet another example came in a 2010 double-blind, placebo-controlled trial of 2256 community-dwelling women, aged 70 years or older, considered to be at high risk of fracture. Over the course of three to five years, every year subjects were given 500,000 IU of cholecalciferol or placebo. Women in the vitamin D group were significantly more likely to experience falls or fractures.32)
Contrary to most received wisdom, vitamin D does not enhance the absorption of calcium. As Aloia showed there is no relationship whatsoever between 25-D levels and calcium absorption.33) 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,34) 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 leads to an increase in bone growth.
Bone news: the bone in my injured leg healed quickly except for the region at the knee (it was not quite dense enough). But a new xray in December showed the knee region now is also very good (and I can have the metal out if I need to). Yay! And that's after avoiding “vitamin D” like the plague for seven years! So much for “vitamin D” and bone health….
Dogster, MarshallProtocol.com
I was prime candidate for osteoporosis. From age 10 to 17, I was either ill in bed or hiding behind the tennis wall with a library book so the sports teacher could not notice that I was neither running nor jumping. When I left school I simply lay on my bed to read at every spare moment.
My husband's father was a scout master, so hubbie (not on MP) was a more normal child, but his spine and hip bones show clear evidence of osteopenia in scan. (DHubbie is halfway into the black on both scans)
On the other hand, my own scan showed only slight osteopenia of hip bone (grey area) but no osteopenia at all in a spine that rarely had much work to do. I now avoid scans in confidence I do not need it.
Sallie Q
Summary - still in OSTEOPENIA category,
but increased density for both femurs and spine
Chris, MarshallProtocol.com
| year | where | bmd | t-score | z-score |
|---|---|---|---|---|
| 2007 | L1-L4 | 1.058 | 87% -1.3 | 87% -1.3 |
| 2009 | L1-L4 | 1.153 | 94% -0.5 | 96% -0.4 |
| 2014 | L1-L4 | 1.178 | 97% -0.4 | 99% -0.1 |
| 2016 | L1-L4 | 1.255 | 0.3 | 0.7 |
| 2007 | left femur neck | 0.870 | 81% -1.5 | 88% -0.9 |
| 2009 | left femur neck | 0.928 | 87% -1.1 | 98% -0.3 |
| 2014 | left femur neck | 0.976 | 97% -0.4 | 103% -0.2 |
| 2016 | left femur neck | 1.033 | 97% -0.3 | 103% 0.8 |
| 2007 | right femur neck | 0.777 | 73% -2.3 | 79% -1.6 |
| 2009 | right femur neck | 0.862 | 81% -1.6 | 98% -0.8 |
| 2014 | right femur neck | 0.794 | -2.1 | -1.2 |
| 2016 | right femur neck | 0.821 | -1.9 | -0.8 |
(BMD = bone mass density in gm/cm3)
t-score (young adult)
z-score (age-matched)
% increase by 2016
| Spine | 6.4% |
| Left femur neck | 5.8% |
| right femur neck | 3.4% |
Zhao JG, Zeng XT, Wang J, Liu L. in Association Between Calcium or Vitamin D Supplementation and Fracture Incidence in Community-Dwelling Older Adults: A Systematic Review and Meta-analysis. 38)
Results:
A total of 33 randomized trials involving 51 145 participants fulfilled the inclusion criteria. There was no significant association of calcium or vitamin D with risk of hip fracture compared with placebo or no treatment (calcium: RR, 1.53 [95% CI, 0.97 to 2.42]; ARD, 0.01 [95% CI, 0.00 to 0.01]; vitamin D: RR, 1.21 [95% CI, 0.99 to 1.47]; ARD, 0.00 [95% CI, -0.00 to 0.01]. There was no significant association of combined calcium and vitamin D with hip fracture compared with placebo or no treatment (RR, 1.09 [95% CI, 0.85 to 1.39]; ARD, 0.00 [95% CI, -0.00 to 0.00]). No significant associations were found between calcium, vitamin D, or combined calcium and vitamin D supplements and the incidence of nonvertebral, vertebral, or total fractures. Subgroup analyses showed that these results were generally consistent regardless of the calcium or vitamin D dose, sex, fracture history, dietary calcium intake, and baseline serum 25-hydroxyvitamin D concentration. Conclusions and Relevance:
In this meta-analysis of randomized clinical trials, the use of supplements that included calcium, vitamin D, or both compared with placebo or no treatment was not associated with a lower risk of fractures among community-dwelling older adults. These findings do not support the routine use of these supplements in community-dwelling older people.
Bolland MJ, Grey A and Avenell A. in Effects of vitamin D supplementation on musculoskeletal health: a systematic review, meta-analysis, and trial sequential analysis. 39)
INTERPRETATION:
Our findings suggest that vitamin D supplementation does not prevent fractures or falls, or have clinically meaningful effects on bone mineral density. There were no differences between the effects of higher and lower doses of vitamin D. There is little justification to use vitamin D supplements to maintain or improve musculoskeletal health. This conclusion should be reflected in clinical guidelines.
Rivadeneira F.
Assessment of the genetic and clinical determinants of fracture risk: genome wide association and mendelian randomisation study.
This large scale GWAS meta-analysis for fracture identified 15 genetic determinants of fracture, all of which also influenced bone mineral density. Among the clinical risk factors for fracture assessed, only bone mineral density showed a major causal effect on fracture. Genetic predisposition to lower levels of vitamin D and estimated calcium intake from dairy sources were not associated with fracture risk. 40)