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Researchers Identify Factor In Pathogenesis Of Graves' Disease

Science Daily — Investigators at the Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center (LA BioMed) have found evidence that continues to implicate insulin-like growth factor receptor (IGF-1R) in the development of Graves' disease.

In previous research published in the Journal of Immunology, Terry J. Smith, M.D. and Raymond Douglas, M.D., Ph.D. have identified the interaction between immunoglobulins and IGF-1R as a cause of inflammation and lymphocyte infiltration in both Graves' disease and rheumatoid arthritis. The discovery of these mechanisms in a similar class of autoimmune diseases supports the belief that a single biological mechanism is activating a variety of autoimmune diseases. The identification of such a mechanism may lead to a common therapeutic strategy for these conditions.

According to Dr. Smith, "We continue to build a body of evidence that suggests that a single biological mechanism can activate a variety of autoimmune diseases. It is possible that these findings will allow us for the first time to interrupt the disease process before any lasting damage is done. It could be involved in other autoimmune disorders as well; we're thinking about a large number of diseases."

In the article appearing in the March 1, 2007 issue of the Journal of Immunology, Dr. Smith and his colleagues report that a disproportionately large fraction of peripheral blood T cells express IGF-1R in patients with Graves' disease. The results support a potential role for IGF-1R as a determinant of immune responses through fibroblast and lymphocyte activation and expansion. This further implicates IGF-1R in the pathogenesis of patients with Graves' disease.

Graves' disease, the most common cause of hyperthyroidism, can lead to severe swelling around the eye sockets. It is part of a class of autoimmune disorders in which cellular defense mechanisms mistakenly identify the body's own tissues as foreign and seek to destroy them. Other autoimmune disorders in the same class include rheumatoid arthritis, multiple sclerosis, and lupus. 37,000 new patients per year are diagnosed with Graves' disease in the United States.

"Autoimmune diseases are among the most insidious and debilitating of human ailments," said LA BioMed President and CEO Kenneth P. Trevett, J.D. "We are working closely with Dr. Smith and his colleagues to facilitate this work and promote its transfer to the patient bedside."

The Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center (LA BioMed) is one of the largest independent, not-for-profit biomedical research institutes in Los Angeles County. Affiliated with both the David Geffen School of Medicine at UCLA and the Harbor-UCLA Medical Center, the Institute has an annual budget of over $75 million and currently supports more than 1,000 research studies in areas such as cardiology, emerging infections, cancer, women's health, reproductive health, vaccine research, respiratory physiology, dermatology, neonatology, molecular biology, and genetics.

Note: This story has been adapted from a news release issued by Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center (LA BioMed).

Please be sure to note that this concerns Insulin-like Growth Factor!!!

LyndaCarol, that's one on the reasons I posted it. I figured at least you would be interested

This was an old article, but I am bumping it back up because I now think BOTH insulin and insulin-like growth factor (IGF-1) are important in MS.

Scoobyjude initially posted this article on February 18, 2007:


Researchers Identify Factor In Pathogenesis Of Graves' Disease

Science Daily — Investigators at the Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center (LA BioMed) have found evidence that continues to implicate insulin-like growth factor receptor (IGF-1R) in the development of Graves' disease.

In previous research published in the Journal of Immunology, Terry J. Smith, M.D. and Raymond Douglas, M.D., Ph.D. have identified the interaction between immunoglobulins and IGF-1R as a cause of inflammation and lymphocyte infiltration in both Graves' disease and rheumatoid arthritis. The discovery of these mechanisms in a similar class of autoimmune diseases supports the belief that a single biological mechanism is activating a variety of autoimmune diseases. The identification of such a mechanism may lead to a common therapeutic strategy for these conditions.

According to Dr. Smith, "We continue to build a body of evidence that suggests that a single biological mechanism can activate a variety of autoimmune diseases. It is possible that these findings will allow us for the first time to interrupt the disease process before any lasting damage is done. It could be involved in other autoimmune disorders as well; we're thinking about a large number of diseases."

In the article appearing in the March 1, 2007 issue of the Journal of Immunology, Dr. Smith and his colleagues report that a disproportionately large fraction of peripheral blood T cells express IGF-1R in patients with Graves' disease. The results support a potential role for IGF-1R as a determinant of immune responses through fibroblast and lymphocyte activation and expansion. This further implicates IGF-1R in the pathogenesis of patients with Graves' disease.

Graves' disease, the most common cause of hyperthyroidism, can lead to severe swelling around the eye sockets. It is part of a class of autoimmune disorders in which cellular defense mechanisms mistakenly identify the body's own tissues as foreign and seek to destroy them. Other autoimmune disorders in the same class include rheumatoid arthritis, multiple sclerosis, and lupus. 37,000 new patients per year are diagnosed with Graves' disease in the United States.

"Autoimmune diseases are among the most insidious and debilitating of human ailments," said LA BioMed President and CEO Kenneth P. Trevett, J.D. "We are working closely with Dr. Smith and his colleagues to facilitate this work and promote its transfer to the patient bedside."

The Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center (LA BioMed) is one of the largest independent, not-for-profit biomedical research institutes in Los Angeles County. Affiliated with both the David Geffen School of Medicine at UCLA and the Harbor-UCLA Medical Center, the Institute has an annual budget of over $75 million and currently supports more than 1,000 research studies in areas such as cardiology, emerging infections, cancer, women's health, reproductive health, vaccine research, respiratory physiology, dermatology, neonatology, molecular biology, and genetics.

Note: This story has been adapted from a news release issued by Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center (LA BioMed).

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My hypothesis: excess insulin (hyperinsulinemia) plays a major role in MS, as developed in my initial post: http://www.thisisms.com/forum/general-discussion-f1/topic1878.html "Insulin – Could This Be the Key?"

And I believe this article in Momentum magazine (NMSS application) is important and belongs here for its mention that IGF-1 actually worsened MS:

This idea was expressed (page 67)in the Winter 08-09 issue of the MS Society publication named Momentum,



Here is the abstract of the work mentioned:


1: J Neuroimmunol. 2005 Nov;168(1-2):40-5. Epub 2005 Aug 24. Links
Targeted expression of IGF-1 in the central nervous system fails to protect mice from experimental autoimmune encephalomyelitis.Genoud S, Maricic I, Kumar V, Gage FH.
Laboratory of Genetics, The Salk Institute, 10010 N Torrey Pines Rd, La Jolla, CA 92037, USA.

Insulin-like growth factor 1 (IGF-1) has been identified as a critical molecule in the induction of myelination in the central nervous system (CNS). Systemic injection of IGF-1 has been shown to have a varied and transiently protective effect on the clinical course of experimental autoimmune encephalomyelitis (EAE). Since systemic IGF-1 can also modulate peripheral immune lymphocytes, we examined whether a sustained and local delivery of IGF-1 into the spinal cord would have any influence on the chronic course of EAE in C57/BL6 mice. The capability of adeno-associated virus (AAV) to be retrogradely transported efficiently from muscle to motor neurons of the spinal cord was used to overcome the difficulty routinely encountered when attempting chronic delivery of molecules into the CNS. We demonstrate that AAV-mediated delivery of IGF-1 in CNS did not have any beneficial effect on the clinical course of EAE. Injection of AAV-IGF1 after induction of the disease worsened the clinical symptoms. Furthermore, CNS expression of IGF-1 did not affect the pathogenic anti-MOG T cell response, as examined by proliferation and cytokine secretion. Thus, enhanced expression of IGF-1 in the CNS during inflammation does not have a significant effect on myelination. These data have important implications for the potential use of IGF-1 in the treatment of multiple sclerosis.

PMID: 16120466 [PubMed - indexed for MEDLINE]

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My hypothesis: excess insulin (hyperinsulinemia) plays a major role in MS, as developed in my initial post: http://www.thisisms.com/forum/general-discussion-f1/topic1878.html "Insulin – Could This Be the Key?"

Thanks for resurrecting the thread, gave me some extra info on GD,

In addition I posted a link to a Vid by Loren Cordain (Paleo) discussing a possible pathogenesis of MS via diet and the Gut sponsored by Direct MS,
In this presentation he discusses the role of EGF and it's receptor in this pathway.
It basically suggests WGA (wheat agluttenin) may combine with a bacteria to produce a mega size Glycoprotein that crosses the gut barrier using the EGFr as a doorway and presents the immune system with what one may term a "mothership" size antigen that has receptors which are also common to the human body, this causes an autoimmune cascade.
The information I am seeing in this area of molecular mimicry and the potential pathways which are coming to light add more weight to the gut health and diet pathogenesis of chronic disease.

Video is in 4 parts, part 1 below, he goes on a bit about the Paleo diet at the start, but it gets more meaty as you get further in:
http://www.dailymotion.com/video/x59iwc ... _lifestyle

Edit: Corrected from IGFr to EGFr, had my wires crossed, but still think the hypothesis has validity.

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I am just an interested individual trying to crack the autoimmune nut.
Partner has Graves Disease, 5 years, showing good test results, looking forward to potential remission in the near future.
3 friends have MS, 1 just recently diagnosed, severity 7/10.