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Is inflammaging an auto[innate]immunity subclinical syndrome?

Sergio Giunta email

Immunity & Ageing 2006, 3:12doi:10.1186/1742-4933-3-12

We have a lot to learn about 'diseases of the aging'

Trevor Marshall   (19 December 2006)  Autoimmunity Research Foundation email

In 2004 we described how the chronic inflammatory disease, sarcoidosis, is caused by a life-long accumulation of intra-phagocytic bacterial pathogens[1]. We recently published an update[2], reporting that many chronic inflammatory diseases result from a similar pathogenesis. Our Phase 2 clinical trial has already been demonstrating recovery from some of the diseases of aging, particularly arthritis, osteopenia, and even diabetes[3].

Interestingly, those patients who have recovered from terminal inflammatory conditions, such as sarcoidosis and rheumatoid arthritis, report that recovery feels like "being 20 years younger." We are also observing that the body has an amazing ability to regenerate after inflammatory damage which is currently considered to be 'permanent' (eg, fibrosis and peripheral neuropathy). Clearly we still have a lot to learn about the processes which society categorizes as 'aging'.

Our research points towards Th1 inflammation, the innate immune response to intraphagocytic pathogens, as being the cause of so many "disease of the aging," ranging from atherosclerosis, cardiomyopathy and arthritis through to many neurological conditions, and even to dementia.

We have shown much chronic inflammation results from the body's innate immune response, and we agree it seems likely that 'Inflammaging' may also result from this same pathogenesis.

References:

1. Marshall TG, Marshall FE: Sarcoidosis succumbs to antibiotics - implications for autoimmune disease. Autoimmunity Reviews,2004; 3(4):295-3001

2. Marshall TG: VDR Nuclear Receptor Competence is the Key to Recovery from Chronic Inflammatory and Autoimmune Disease. Abstract presentation, Days of molecular medicine, 2006.

Copy available from URL http://autoimmunityresearch.org/karolinska-handout.pdf

3. Waterhouse JC, Marshall TG, Fenter B, Mangin M, Blaney G: High levels of active 1,25-dihydroxyvitamin D despite low levels of the 25-hydroxyvitamin D precursor - Implications of dysregulated vitamin D for disgnosis and treatment of Chronic Disease. In Vitamin D: New Research. Volume 1. Edited by: Stoltz VD. New York: Nova Science Publishers; 2006. ISBN: 1-60021-000-7

4. Marshall TG: Are statins analogs of vitamin D?. Correspondence to Grimes, DS. The Lancet 2006; 368:1234 doi:10.1016/S0140-6736(06)69509-3

Copy available from URL http://www.thelancet.com/journals/lancet/article/PIIS0140673606695093/fulltext

5. Marshall TG: A New Approach to Treating Intraphagocytic CWD Bacterial Pathogens in Sarcoidosis, CFS, Lyme and other Inflammatory Diseases. American Academy of Environmental Medicine; 2006, Plenary Sessions Syllabus, 41st Annual Meeting.

Copy available from URL http://autoimmunityresearch.org/aaem_2006.ram

6. Marshall TG: Molecular genomics offers new insight into the exact mechanism of action of common drugs - ARBs, Statins, and Corticosteroids. FDA CDER Visiting Professor presentation, FDA Biosciences Library, Accession QH447.M27 2006

Copy available from URL http://autoimmunityresearch.org/fda-visiting-professor-7mar06.ram

7. Marshall TG, Lee RE, Marshall FE: Common angiotensin receptor blockers may directly modulate the immune system via VDR, PPAR and CCR2b. Theor Biol Med Model. 2006 Jan 10;3(1):1. Available from URL http://www.tbiomed.com/content/3/1/1

8.Marshall TG, Fenter BJ, Marshall FE: Antibacterial Therapy Induces Remission in Sarcoidosis (in English). JOIMR 2005;3(1):2 Available from URL http://www.joimr.org/phorum/read.php?f=2&i=107&t=107

Competing interests

There are no competing interests.

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