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 cytokines and inactivate the Vitamin D Receptor. 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 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 Protocol (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:
  • 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.

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.

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Fall prevention

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

Pathophysiology of bone loss

Bone loss is complicated and multi-factorial.

  • high levels of 1,25-D affect osteoclast activity – When functioning properly, the Vitamin D Receptor contributes to bone health in an underecognized way distinct from other classical calcium regulating hormones.2) However, proper functioning becomes disrupted when, according to the Marshall Pathogenesis, pathogenic microbes create proteins that bind and block the Vitamin D Receptor, preventing it from expressing many essential components required for health. These include the estrogen receptors, upon which the bone matrix is dependent. The bone matrix is dependent on estrogen homeostasis (estrogen is important to stimulate osteoblast activity).3) This model of disease is partially validated by the fact that drugs such as TNF-alpha inhibitors, which prevent inflammation, 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 bone loss 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).
  • osteoporotic bone has lower levels of expression of VDR – A recent study evaluating expression of (rather than by) the VDR in platelets in osteoporotic bone versus healthy subjects.4) The authors found:
    • lower levels of VDR in all patients,
    • number of VDRs was positively correlated with bone density, and
    • a decrease in the phosphorus levels in patients without differences in vitamin D levels and in the dietary calcium intake. The lower VDR expression in osteoporotic bone, the authors concluded, indicated a lower ability to respond to vitamin D, and could be the explanation of the increase in the PTH and decrease in the phosphorus levels in patients with respect to controls.

Other treatments

Calcium supplementation

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.

TNF-alpha drugs

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. 5)

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.

Vitamin D supplementation

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.

Interventional trials showing vitamin D is ineffective

Author/Year Study Design Findings
Steven R. Cummings, MD; Douglas P. Kiel, MD, MPH; Dennis M. Black, PhD, 2016 6)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 7)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 8) 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., 20129) 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., 200810) 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 11) 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., 200512) 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.”13) (Other well-designed studies on elderly women at risk for fractures have come to identical conclusions.14) 15) 16))
Sanders KM1, Stuart AL, Williamson EJ, Simpson JA, Kotowicz MA, Young D, Nicholson GC. 201017) 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.18)

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.

Interventional trials showing that vitamin D exacerbates bone loss

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. 19)

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.20) 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.21)

Molecular evidence against vitamin D supplementation

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.22) 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,23) 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.

Evidence of infectious cause

Patients experiences

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

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%
Chris commenced the MP in 2004

Notes and comments

Sallie Q 12.04.2016 thankfully removed the external link around the year, as pubmed now working

Sallie Q 11.26.2016 have been doing over latest PubMed refs but they still do not work & I can not think why :-( So I replaced the Year of study with an external link

Sallie Q 11.23.2016 adding Chris' experience — Sallie Q 11.20.2016 added 2 more recent studies — Sallie Q 07.08.2016 added 2010 study to Table


  • To do - create new article for secondary hyperparathyroidism.
  • To begin with, patients with chronic disease may obtain less of a benefit from calcium supplements since the calcium metabolism of patients suffering from chronic disease is different from that of healthy individuals.25)
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I removed this. I'm not too sure how this quote was helping. It is unprofessional, IMO. — Paul Albert 06.07.2010

Dr Paul Baldock, a neuroscientist from Sydney's Garvan Institute of Medical Research, has demonstrated in mice that the neurotransmitter Neuropeptide Y (NPY) directly controls osteoblasts, the cells that make bone. His findings are now published in the international online journal Public Library of Science ONE (PLoS ONE).

“It has always been thought that changes in bone mass are purely mechanical - you get heavier and your bones get denser to support the increased load,” said Baldock.

“While that's true to some extent, our findings show a sophisticated central surveillance system at work. It's as if the brain, as boss, sends out a global memo saying 'make more bone'.”

“Bone-making cells at local level appear to have the ability to fine-tune this directive, like office workers saying 'we're not going to waste time putting on bone here when it's needed more over there'.”

“So what happens in practice is that places exposed to more load put on more bone, while those exposed to less load put on less bone.”

All the intricate central processing takes place in the hypothalamus, a small yet complex region of the brain that links the nervous and hormone systems.

From: We now know that the brain controls the formation of bone

Osteoporosis prevention and nutrition. Tucker KL

Curr Osteoporos Rep Dec 2009; 7(4) :111-7 Full text via publisher | Download citationAffiliation USDA Human Nutrition Research Center on Aging, Tufts University, 711 Washington Street, Boston, MA 02111, USA. Katherine.tucker@tufts.edu Abstract Although calcium and vitamin D have been the primary focus of nutritional prevention of osteoporosis, recent research has clarified the importance of several additional nutrients and food constituents. Further, results of calcium and vitamin D supplementation trials have been inconsistent, suggesting that reliance on this intervention may be inadequate. In addition to dairy, fruit and vegetable intake has emerged as an important modifiable protective factor for bone health. Several nutrients, including magnesium, potassium, vitamin C, vitamin K, several B vitamins, and carotenoids, have been shown to be more important than previously realized. Rather than having a negative effect on bone, protein intake appears to benefit bone status, particularly in older adults. Regular intake of cola beverages shows negative effects and moderate alcohol intake shows positive effects on bone, particularly in older women. Current research on diet and bone status supports encouragement of balanced diets with plenty of fruit and vegetables, adequate dairy and other protein foods, and limitation of foods with low nutrient density.

Another study is out, this one showing that Vitamin D doesn't boost bone strength in aging men. Most of the previous studies have looked only at women: http://jcem.endojournals.org/cgi/content/abstract/jc.2010-2284v1

So why do we continue to 'fortify' our milk? Apparently it is because of people like this:Despite the findings, people still need to get enough calcium and vitamin D to reduce the risk of osteoporosis, or bone thinning, said Dr. Mone Zaidi, an osteoporosis researcher at the Mount Sinai School of Medicine in New York, who was not involved in the study.


IMO Vitamin D will turn out to be the biggest, and most costly, mistake that Medicine has ever made. Worse than Thalidomide. Worse than FenFen. It is just a matter of time until the people taking high doses of Vitamin D find that not only is it harming them, but they cannot even wean from this steroid.

It seems like hardly a week goes by without another study coming back showing Vit D is no help as a supplement. Not for cancer, not for bone, not for anything. Sigh…


Eur J Clin Nutr. 2011 Jan;65(1):132-9. Epub 2010 Oct 13. Diet and hip fractures among elderly Europeans in the EPIC cohort. Benetou V, Orfanos P, Zylis D, Sieri S, Contiero P, Tumino R, Giurdanella MC, Peeters PH, Linseisen J, Nieters A, Boeing H, Weikert C, Pettersson U, Johansson I, Bueno-de-Mesquita HB, Dorronsoro M, Boffetta P, Trichopoulou A. Department of Hygiene, University of Athens Medical School, Athens, Greece. vben@nut.uoa.gr Abstract BACKGROUND/OBJECTIVES: Evidence on the role of diet during adulthood and beyond on fracture occurrence is limited. We investigated diet and hip fracture incidence in a population of elderly Europeans, participants in the European Prospective Investigation into Cancer and nutrition study. SUBJECTS/METHODS: 29, 122 volunteers (10,538 men, 18,584 women) aged 60 years and above (mean age: 64.3) from five countries were followed up for a median of 8 years and 275 incident hip fractures (222 women and 53 men) were recorded. Diet was assessed at baseline through validated dietary questionnaires. Data were analyzed through Cox proportional-hazards regression with adjustment for potential confounders. RESULTS: No food group or nutrient was significantly associated with hip fracture occurrence. There were suggestive inverse associations, however, with vegetable consumption (hazard ratio (HR) per increasing sex-specific quintile: 0.93, 95% confidence interval (CI): 0.85-1.01), fish consumption (HR per increasing sex-specific quintile: 0.93, 95% CI: 0.85-1.02) and polyunsaturated lipid intake (HR per increasing sex-specific quintile: 0.92, 95% CI: 0.82-1.02), whereas saturated lipid intake was positively associated with hip fracture risk (HR per increasing sex-specific quintile: 1.13, 95% CI: 0.99-1.29). Consumption of dairy products did not appear to influence the risk (HR per increasing sex-specific quintile: 1.02, 95% CI: 0.93-1.12). CONCLUSIONS: In a prospective study of the elderly, diet, including consumption of dairy products, alcohol and vitamin D, did not appear to play a major role in hip fracture incidence. There is however, weak and statistically non-significant evidence that vegetable and fish consumption and intake of polyunsaturated lipids may have a beneficial, whereas saturated lipid intake a detrimental effect. PMID: 20948558


Cigarette smoking and bone mineral density in older men and women.
Hollenbach KA, Barrett-Connor E, Edelstein SL, Holbrook T
Am J Public Health83p1265-70(1993 Sep)
Importance of Vitamin D receptor for neuronal control of hematopoietic stem cell niche.
Kawamori Y, Katayama Y, Asada N, Minagawa K, Sato M, Okamura A, Shimoyama M, Nakagawa K, Okano T, Tanimoto M, Kato S, Matsui T
Bloodp(2010 Sep 2)
Estrogen receptor-beta modulates synthesis of bone matrix proteins in human osteoblast-like MG63 cells.
Cao L, Bu R, Oakley JI, Kalla SE, Blair HC
J Cell Biochem89p152-64(2003 May 1)
Platelet vitamin D receptor is reduced in osteoporotic patients.
D'Amelio P, Cristofaro MA, De Vivo E, Ravazzoli M, Grosso E, Di Bella S, Aime M, Cotto N, Silvagno F, Isaia G, Pescarmona GP
Panminerva Med54p225-31(2012 Sep)
Treatment of Vitamin D Insufficiency in Postmenopausal Women: A Randomized Clinical Trial.
Hansen KE, Johnson RE, Chambers KR, Johnson MG, Lemon CC, Vo TN, Marvdashti S
JAMA Intern Med175p1612-21(2015 Oct)
Vitamin D does not increase calcium absorption in young women: a randomized clinical trial.
Gallagher JC, Jindal PS, Smith LM
J Bone Miner Res29p1081-7(2014)
The effect of vitamin D on calcium absorption in older women.
Gallagher JC, Yalamanchili V, Smith LM
J Clin Endocrinol Metab97p3550-6(2012 Oct)
Calcium, vitamin D supplementation, and physical function in the Women's Health Initiative.
Brunner RL, Cochrane B, Jackson RD, Larson J, Lewis C, Limacher M, Rosal M, Shumaker S, Wallace R
J Am Diet Assoc108p1472-9(2008 Sep)
12) , 13)
Randomised controlled trial of calcium and supplementation with cholecalciferol (vitamin D3) for prevention of fractures in primary care.
Porthouse J, Cockayne S, King C, Saxon L, Steele E, Aspray T, Baverstock M, Birks Y, Dumville J, Francis R, Iglesias C, Puffer S, Sutcliffe A, Watt I, Torgerson DJ
BMJ330p1003(2005 Apr 30)
Oral vitamin D3 and calcium for secondary prevention of low-trauma fractures in elderly people (Randomised Evaluation of Calcium Or vitamin D, RECORD): a randomised placebo-controlled trial.
Grant AM, Avenell A, Campbell MK, McDonald AM, MacLennan GS, McPherson GC, Anderson FH, Cooper C, Francis RM, Donaldson C, Gillespie WJ, Robinson CM, Torgerson DJ, Wallace WA
Lancet365p1621-8(2005 May 7-13)
15) , 18)
Effect of calcium or 25OH vitamin D3 dietary supplementation on bone loss at the hip in men and women over the age of 60.
Peacock M, Liu G, Carey M, McClintock R, Ambrosius W, Hui S, Johnston CC
J Clin Endocrinol Metab85p3011-9(2000 Sep)
Calcium plus vitamin D supplementation and the risk of fractures.
Jackson RD, LaCroix AZ, Gass M, Wallace RB, Robbins J, Lewis CE, Bassford T, Beresford SA, Black HR, Blanchette P, Bonds DE, Brunner RL, Brzyski RG, Caan B, Cauley JA, Chlebowski RT, Cummings SR, Granek I, Hays J, Heiss G, Hendrix SL, Howard BV, Hsia J, Hubbell FA, Johnson KC, Judd H, Kotchen JM, Kuller LH, Langer RD, Lasser NL, Limacher MC, Ludlam S, Manson JE, Margolis KL, McGowan J, Ockene JK, O'Sullivan MJ, Phillips L, Prentice RL, Sarto GE, Stefanick ML, Van Horn L, Wactawski-Wende J, Whitlock E, Anderson GL, Assaf AR, Barad D
N Engl J Med354p669-83(2006 Feb 16)
17) , 21)
Annual high-dose oral vitamin D and falls and fractures in older women: a randomized controlled trial.
Sanders KM, Stuart AL, Williamson EJ, Simpson JA, Kotowicz MA, Young D, Nicholson GC
JAMA303p1815-22(2010 May 12)
Rapid recovery of bone mass in hypercalciuric, osteoporotic men treated with hydrochlorothiazide.
Adams JS, Song CF, Kantorovich V
Ann Intern Med130p658-60(1999 Apr 20)
Serum vitamin D metabolites and intestinal calcium absorption efficiency in women.
Aloia JF, Chen DG, Yeh JK, Chen H
Am J Clin Nutr92p835-40(2010 Oct)
Large-scale in silico and microarray-based identification of direct 1,25-dihydroxyvitamin D3 target genes.
Wang TT, Tavera-Mendoza LE, Laperriere D, Libby E, MacLeod NB, Nagai Y, Bourdeau V, Konstorum A, Lallemant B, Zhang R, Mader S, White JH
Mol Endocrinol19p2685-95(2005 Nov)
Effect of minocycline on osteoporosis.
Williams S, Wakisaka A, Zeng QQ, Barnes J, Seyedin S, Martin G, Wechter WJ, Liang CT
Adv Dent Res12p71-5(1998 Nov)
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