letterhead
Patient News 

  

Annual Patient Workshop

 

Treating

Autoimmune and

Inflammatory

Diseases with

Inflammation

Therapy

 

When: Sunday

February 16, 2014

Where: Hilton

Dallas-Ft. Worth

Lakes Executive

Conference Center

 

For details and

registration 

information

click here

 

 

 

Therapy Tip

  

Chronic Illness Recovery recommends that patients on Inflammation Therapy maintain a level of 25-D between 10-20ng/ml. This level ensures adequate stores of vitamin D and isn't so high as to suppress immune system function. Immunosuppression is contraindicated in the presence of persistent infection.


 

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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Have you enjoyed this newsletter?

  

 

 

 

 

 

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.  

 

 

 

Issue: 49
December 2013
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Holiday Greetings!

 

Chronic fatigue syndrome, fibromyalgia, rheumatoid arthritis and other chronic diseases make life miserable for millions of people throughout the world. Generous donations from people like you to support Chronic Illness Recovery can make a difference for those dealing with these challenges. During this holiday season, there are many ways you can help with the fight: an annual gift, a monthly credit card donation, a tribute to a friend or caretaker.  

 

When you support CIR, you can make a difference in people's lives and help change the future. As a nonprofit organization, gifts of all sizes are needed to build a strong base of financial support. Every gift, no matter the size, is important!

 

Please support us by making a donation to CIR, either through a secure online transaction or by sending a check or money order via regular mail to: Chronic Illness Recovery, P.O. Box 10756, Ft. Worth, TX 76114

You may call our toll-free number 1-888-846-2474 for assistance with any gift. Thank you in advance for your thoughtful financial support.

 

Sincerely looking forward to a healthy New Year,

 

 signature       

Belinda

Patient Workshop - Sunday, February 16, 2014

Featured Speaker, Dr. Neil Hirschenbein, MD, PhD
La Jolla Institute of Comprehensive Medicine

Hirschenbein

Dr. Neil Hirschenbein has been in the East County, San Diego area for 18 years. He is board certified in internal medicine and gastroenterology. He also has a PhD in clinical psychology from Boston University. Dr. Hirschenbein attended medical school at the University of Illinois, Chicago and completed his residency and fellowship at UCSD. He is committed to the high quality care of his patients and professional and personal growth through on-going education to more fully serve his patients and their families in the ever-changing health care environment of San Diego County.

 

Dr. Hirschenbein's most recent certification came from UCSD for his participation in Health Care leadership. He is a member of the American Medical Association, the California Medical Association, and the San Diego County Medical Society. He is also a member of the San Diego GI Society, American College of Physicians, American College of Physician Executives, American College of Managed Care Medicine, American Society of Bariatric Physicians, American Academy of Anti-Aging Medicine and the El Cajon, La Mesa and Santee Chambers of Commerce. He was named a Steering Committee Physician for Shared Performance Groups, California Medical Advantage. He resides with his wife Mary Anne in Blossom Valley. They have five children.

Dr. Hirschenbein will be presenting the topic Antibiotic Protocols and a case report on Chronic Fatigue Syndrome.

 

 

About Inflammation Therapy 

Putative Etiology of Low Vitamin D

 

Vitamin D proponents use a disease deficiency model to explain low levels of 25(OH)D. Their hypothesis states low 25(OH)D causes chronic diseases; however, a pathogenesis has not been elucidated. Low serum 25(OH)D in the presence of disease can also be explained with a dysregulated vitamin D metabolism model. This hypothesis proposes that low vitamin D is the consequence of a chronic inflammatory process caused by persistent infection.

 

The bacterial pathogenesis theorizes that intracellular bacteria cause abnormal vitamin D endocrine function, resulting in low vitamin D. Specifically, cell wall deficient (CWD) bacteria invade nucleated cells and use strategies to avoid destruction. Excess 1,25(OH)2D is produced in an effort to up-regulate the VDR to transcribe AMPs; and 25(OH)D is rapidly metabolized in the process, resulting in a low serum level. The resulting elevated 1,25(OH)2D causes chronic, systemic inflammation and its accompanying symptoms. Gerald J Domingue, Professor Emeritus of Tulane University School of Medicine commented, "This might translate into an etiology for chronic inflammatory diseases, when the stressed bacteria increase in numbers and overwhelm the normal biological functions of the host." [1] Gabriel Nunez, M.D., [2] Professor of Pathology at the University of Michigan Medical School, was quoted in the university newsletter, "In our study, the presence of bacterial microbes inside the cell is what triggers the immune response." In 2007 French researchers observe that the presence of pathogenic invasive bacteria could be the link between an innate immune response to invasive bacteria and the development of the inflammation. [3] Dr. Siobhan O'Connor, [4] assistant to the director of the National Center for Infectious Diseases, stated, "The epidemiologic, clinical, and pathologic features of many chronic inflammatory diseases are consistent with a microbial cause. Infectious agents likely determine more cancers, immune-mediated syndromes, neurodevelopmental disorders, and other chronic conditions than currently appreciated."

 

A known effect of vitamin D is suppression of the immune system. [5] In a study of a pro-inflammatory molecule, lipopolysaccharide (LPS), Lemire [6] found elevated 25(OH)D reduced the inflammatory cascade. Low levels (below 30ng/ml) failed to inhibit the LPS inflammatory cascade but higher levels (30ng/ml) inhibited inflammatory signaling. The highest levels of inflammatory inhibition occurred at 50ng/ml. 25(OH)D can also be indirectly immuno-suppressive by being converted to excess 1,25(OH)2D. A 2007 study concluded, "On the whole, vitamin D confers an immunosuppressive effect." [7] Theoretically, immune system suppression allows parasitic microbes to persist and proliferate in host phagocytes, successfully compete for nutritional resources, and displace commensal organisms from their niche. [8]

 

  1. Domingue GJ. Demystifying pleomorphic forms in persistence and expression of disease: Are they bacteria, and is peptidoglycan the solution? Discov Med. Sep 2010;10(52):234-46.
  2. Rueter A. Microbes start immune response by sneaking inside cells. University of Michigan Health System. Apr 16, 2007. http://www2.med.umich.edu/prmc/media/newsroom/details.cfm?ID=577. Accessed May 8, 2013.
  3. Rolhion N, Darfeuille-Michaud A. Adherent-invasive Escherichia coli in inflammatory bowel disease. Inflamm Bowel Dis. Oct 2007;13(10):1277-83.
  4. O'Connor SM, Taylor CE, Hughes JM. Emerging infectious determinants of chronic diseases. Emerg Infect Dis. Jul 2006;12(7):1051-7.
  5. Zhang Y, Leung DY, Richers BN, et al. Vitamin D inhibits monocyte/macrophage proinflammatory cytokine production by targeting MAPK phosphatase-1. J Immunol. Mar 2012;188(5):2127-35.
  6. Lemire J. 1,25-Dihydroxyvitamin D3--a hormone with immunomodulatory properties. Z Rheumatol. 2000;59 Suppl 1:24-7.
  7. Arnson Y, Amital H, Shoenfeld Y. Vitamin D and autoimmunity: new aetiological and therapeutic considerations. Ann Rheum Dis. Sep 2007;66(9):1137-42.
  8. Domingue G, Turner B, Schlegel JU. Cell-wall deficient bacterial variants in kidney tissue. Detection by immunofluorescence. Urology. Mar 1974;3(3):288-92.

Scientific Articles

 

Vitamin D status and ill health: a systematic review

Vitamin D supplementation is ill-advised above a threshold of 30ng/ml 25-D. Inflammatory processes involved in disease occurrence and clinical course would reduce 25(OH)D, which would explain why low vitamin-D status is reported in a wide range of disorders. It would be wiser to seek reasons underlying the low vitamin-D level, such as inflammatory processes or undiagnosed cardiovascular diseases, and fix them.

 

Isolation of Clostridium perfringens Type B

in an Individual at First Clinical Presentation of Multiple SclerosisProvides Clues for Environmental Triggers of the Disease.  

Researchers have identified a bacterial toxin that they believe may be a trigger for multiple sclerosis (MS).

 

Infection and Autoimmunity 

The editors of Infection and Autoimmunity boldly state that reading the chapters in this book brings one to the conclusion that all autoimmune diseases are infectious, until proven otherwise.  

 

Quotes 

  

"Thanks for the personalized service. I'm impressed always on the thoroughness, knowledgeable, and quickness of your responses to my and other patients concerns and need for information." Jean

 

"Thanks for your great work and support." John

 
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