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Patient News 

  

Annual Patient Workshop

 

Save the date:

Sunday

 February 16, 2014

Hilton Dallas-Fort Worth Lakes Executive Conference Center

 

 

 

Therapy Tip

  

The most widely used test to screen for osteoporosis is a bone mineral density (BMD) test. Inflammation Therapy resolves the inflammatory process that causes the bone metabolism abnormalities commonly seen in chronic inflammatory diseases. But remodeling bone mass is a slow

process (the skeleton regenerates approximately every ten years) so BMD test scores may take some time to improve.

 

 

Recovery Reports

 

We are contacted daily by people with chronic illnesses who are looking for an effective treatment. Many ask us to provide evidence of efficacy in the form of statistics or stories. If you have recovered your health or had significant symptom improvement with Inflammation Therapy (or a similar treatment), please help us 'pay it forward' by telling your story. We will post it in the public section of our website to encourage others. Any report, short or long, with or without objective data (e.g., lab results, imaging reports) would be helpful. Please

send your story to

our email .

Thank you!  

To see the latest recovery reports,

click here. 

 

CIR Library Access

 

Access to our free, extensive, easy-to-read Library of Information

 (see this sample page)

and Physicians' Reference Library is available to anyone, without enrollment in our counseling program. If you're interested in using this resource, please send a request to our email

 address along with your doctor's name and fax number (in the US or Canada) or his/her email address, so we can notify your doctor that you have access to this information.

A list of the articles in our libraries is available at this link.

 Physicians may use CIR libraries even if they don't have a patient enrolled in our counseling program. Interested medical practitioners should contact CIR and ask to register.

 

 CIR is an IRS-recognized 501(c)3 non-profit charitable organization. 

Donate to CIR

 in support of our educational and research efforts. 

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Issue: 45
August 2013
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Greetings,

 

We hope you make plans to attend the CIR annual patient workshop on February 16, 2014, in Dallas, Texas.  We will be presenting The Role of Vitamin D Deficiency and Persistent Infection in Auto/Inflammatory Diseases. Topics will explore the relationship of vitamin D, the immune system, intracellular infection and systemic inflammation.  Continuing medical education seminar for physicians is scheduled on the 15th including an evening reception for both patients and physicians.

 

CIR staff   

         

About Inflammation Therapy 
   

Vitamin D and Osteoporosis

 

Osteoporosis is a bone disease characterized by a decrease in bone mineral density and the appearance of small holes in bones due to loss of minerals.1 Vitamin D is an important factor in maintaining bone health to avoid osteoporosis.2 Precise maintenance of the physiologic levels of both extracellular and intracellular ionized calcium is essential to life.3 The vitamin D metabolite 1,25-dihydroxyvitamin D (1,25-D) maintains calcium homeostasis between blood, cells and bones by stimulating calcium absorption from the intestines, reabsorption in the kidneys, and resorption in bones. 1,25-D up-regulates vitamin D receptors (VDR) in the small intestine, which then transcribes genes that shuttle calcium and phosphorus through the intestinal epithelium. However, mucosal response and calcium/phosphorus absorption is dependent on a competent VDR and elevated 1,25-D reduces VDR competence.4 Thus, calcium and phosphorus absorption may be inhibited if VDR function is impaired by elevated 1,25-D.

 

Although some studies show vitamin D and calcium supplements increase bone density slightly and decrease the risk of falls and fractures in certain populations, the quality of evidence is poor.5 A 2013 report by the U.S. Preventive Services Task Force recommends against vitamin D supplementation for the primary prevention of fractures in non-institutionalized, pre or post-menopausal women or older men.6 The 2005 RECORD study concluded, "...routine supplementation with calcium and vitamin D3, either alone or in combination, is not effective in the prevention of further fractures in people who had a recent low-trauma fracture." 7 A similar study stated, "We found no evidence that calcium and vitamin D supplementation reduces the risk of clinical fractures in women with one or more risk factors for hip fracture." 8 A 2008 study found, "Vitamin D supplementation adds no extra short-term skeletal benefit to calcium citrate supplementation even in women with vitamin D insufficiency." 9 And a study at the Bone Mineral Research Center, Winthrop University Hospital, Mineola, NY showed that "Additional intake of 100 mcg vitamin D3 did not lower PTH or markers of bone turnover." 10

In fact, there is ample evidence that elevated 1,25-D leads to bone loss. In 1999, Brot et al found "...elevated levels of 1,25-D were strongly associated with decreased bone mineral density and content, and increased bone turnover." 11 "When levels are above 42 pg/ml 1,25-D stimulates bone osteoclasts. This leads to osteoporosis, dental fractures and calcium deposition into the soft tissues: lungs, breasts, muscle bundles, kidneys." 12 An earlier study warned, "Vitamin D is a toxic compound, and excessive amounts can cause soft-tissue calcification. There is a narrow leeway between the amount required and that initiating tissue damage." 13 Kawamori et al found that, "Elevated 1,25-D induces increased production of osteoclasts from stem cells." 14 And the EMAS study found that "A combination of high 1,25-D and low 25-D is associated with the poorest bone health." 15 This significant evidence regarding bone loss should motivate medical practitioners and researchers to measure both 25-D and 1,25-D to determine vitamin D status. 
 
1. Insel PM, Turner ER, Ross D. Discovering nutrition. 2nd ed. 

    Boston: Jones and Bartlett; 2006.

2. Ross AC, Taylor CL, Yaktine AL, Del Valle HB. Dietary Reference

    Intakes for Calcium and Vitamin D. Washington, D.C.: National

    Academy of Sciences; 2010.0-309-16394-3.  

3.  Boden SD, Kaplan FS. Calcium  homestasis. Orthop Clin North

     Am. Jan 1990;21(1):31-42. 

4.  Vidal M, Ramana CV, Dusso AS. Stat1-vitamin D receptor

     interactions antagonize 1,25-dihydroxyvitamin D transcriptional

     activity and nhance stat1-mediated transcription. Mol Cell Biol.

     Apr 2002;22(8):2777-87. 

5.  Cranney A, Weiler HA, O'Donnel S, Puil L. Summary of evidence-

     based review on vitamin D efficacy and safety in relation to bone

     health. Am J Clin Nutr. Aug 2008;88(2):513S-519S. 

6.   Moyer VA. Vitamin D and Calcium Supplementation to Prevent

      Fractures in Adults: U.S. Preventive Services Task Force

      Recommendation Statement. Ann Intern Med. Feb 2013;[Epub

      ahead of print]. 

7.   Grant AM, Avenell A, Campbell MK, et al. Oral vitamin D3 ad

      calcium for secondary prevention of low-trauma fractures in

      elderly people (Randomised Evaluation of Calcium Or vitamin D,

      RECORD): a randomized placebo-controlled trial. Lancet. May

      2005;365(9471):1621-8. 

8.   Porthouse J, Cockayne S, King C, et al. Randomised controlled

      trial of calcium and supplementation with cholecalciferol (vitamin

      D3) for prevention of fractures in primary care. BMJ. Apr 2005;

      330(7498):1003. 

9.   Zhu K, Bruce D, Austin N, Devine A, Ebeling PR, Prince RL.

      Randomized controlled trial of the effects of calcium with or

      without vitamin D on bone structure and bone-related chemistry

      in elderly women with vitamin D insufficiency. J Bone Miner Res.

      Aug 2008;23(8):1343-8. 

10.  Aloia J, Bojadzievski T, Yusupov E, et al. The relative influence

       of calcium intake and vitamin D status on serum parathyroid 

       hormone and bone turnover biomarkers in a double-blind,

       placebo-controlled parallel group, longitudinal factorial design.

       J Clin Endocrinol Metab. Jul 2010;95(7):3216-24.

11.  Brot C, Jorgensen N, Madsen OR, Jensen LB, Sorensen OH.

       Relationships between bone mineral density, serum vitamin D

       metabolites and calcium:phosphorus intake in healthy peri-

       menopausal women. J Intern Med. May 1999;245(5):509-16.

12.  Ishizuka S, Kurihara N, Miura D, et al. Vitamin D antagonist,

       TEI-9647, inhibits osteoclast formation induced by 1alpha,25-

       dihydroxyvitamin D3 from pagetic, bone marrow cells. J Steroid

       Biochem Mol Biol. May 2004;89-90(1-5):331-4.

13.  Holmes RP, Kummerow FA. The relationship of adequate and

       excessive intake of vitamin D to health and disease. J Am Coll

       Nutr. 1983;2(2):173-99.

14.  Kawamori Y, Katayama Y, Asada N, et al. Role fo vitamin D

       receptor in the neuronal control of the hematopoietic stem cell

       niche. Blood. Dec 2010;116(25):5528-35.

15.  Vanderschueren D, Pye SR, O'Neill TW, et al. Active vitamin D

       (1,25-dihydroxyvitamin D) and bone health in middle-aged and

       elderly men: the European Male Aging Study (EMAS). J Clin

       Endocrinol Metab. Mar 2013;98(3):995-1005. 

 

 

Scientific Articles

 

 Angiotensin II accelerates osteoporosis by activating osteoclasts
Hideo Shimizu et al. FASEB Journal. 2008;22:2465-2475.
"Because Ang II caused osteoclast activation, leading to accelerated osteoporosis, angiotensin receptor blockers could lessen the risk of osteoporosis in elderly people, possibly beyond their blood pressure-lowering effect."

 

Angiotensin II Type 2 Receptor Blockade Increases Bone Mass

Yayoi Izu et al. J. Biol. Chem.,Vol. 284,Issue 8, 4857-4864, Feb 2009

"AT2 receptor blockade decreases bone resorption and increases bone formation."

 

The Flip Side of Osteoimmunity: Crosstalk Among Stem Cell, BMP-2 and Innate Immune Cells, and the Control of Osteoblastogenesis� 
Kwan, Shu Ying. Carnegie Mellon University, 7-1-2011, Dissertations, Paper 46.
"Bone morphogenetic protein (BMP-2) can direct both osteoclastogenesis and osteoblastogenesis. The preference toward bone resorption or formation/repair appears to be influenced by the inflammatory microenvironment. When BMP-2 is in a predominately classic inflammatory microenvironment, it tends to promote osteoclastogenesis (bone resorption)."

 

 

Quotes 

  

"Thanks for all of your help. You have no idea how much of a help you (and your service) are to me...just to be able to 'speak the language' of chronic inflammation and to be giving merit to the terrible time I am having with my health (instead of dismissing my confusing symptoms or otherwise normal looking labs) is of great comfort." R.D.

 

"As always I found the site and you all very helpful, kind, etc." RJM

 

 

Survey

 

Volunteers who have a diagnosis of autoimmune or inflammatory disease or are chronically ill but who are not being treated with Inflammation Therapy, the Marshall Protocol or the Stillpoint Protocol are needed to be in the control group of our long-term clinical study.

 

If you meet these criteria and would like to take part in this project (which will only take a few minutes each month), please contact us at our email address.