Amongst the BII community there is much discussion of ladies having an autoimmune reaction to silicone We already know that the percentage of autoimmune illnesses in women with breast implants is much higher than average. Many of us were diagnosed with numerous autoimmune illnesses such as Hashimoto’s, Graves Disease, MS, Interstitial Cystitis, Colitis, Fibromyalgia, etc. etc. In my practice and work with Know the Cause I have seen many people who give us testimonies of wellness from autoimmune when on the antifungal protocol. We have already established the significant amount of research that silicone degrades to fungi in the article “The Chemistry of Fungi and Silicone”, so now we want to ask “what is the role of fungi in autoimmune disease?” Why are SO many women with breast implants being diagnosed with a string of autoimmune illnesses? When you put the science presented here along with testimonies of wellness from women following our 4-step protocol it is hard to deny that there is a fungal link to autoimmune..........and silicone degrades to fungi.
This article will be in 3 parts. Part 1: Excerpts from “The Fungus Link Volume 2” from Doug Kaufmann Part 2: Excerpts from “The Fungus Link Volume 2” David Holland M.D. Part 3: A very technical scientific research paper that essentially supports all of the above. The heading on this article is from same research paper and explains it in it’s simplicity.
Part 1: Doug Kaufmann:
“Scientists called mycotoxicologists have studied the ability of fungal toxins to alter DNA for more than 30 years. In support of this, notice that Bantam’s definition cites inflammation as playing a major role in autoimmune disease. Inflammation is swelling. We know that yeast also makes bread swell. Connect the dots, and it’s not hard to argue that yeast could be involved in all cases of inflammation. Remember, the first autoimmune disease was identified almost 50 years ago. I believe it isn’t a coincidence that antibiotics were discovered at about the same time. As we’ve said throughout this book, antibiotics are mycotoxins produced by fungi. Dr. Holland and I believe that mycotoxins cause several of the autoimmune disorders, including cancer.”
Part 2 Dr. Holland M.D.
“Penicillamine, a fungal metabolite is suspect in drug induced lupus. Moreover, I suspect that SLE may also be a drug-induced disease. We have yet to identify what that drug might be, but I have an idea it just might be antibiotics. If the mycotoxin penicillamine can cause drug-induced lupus, I believe that nothing prevents another mycotoxin or fungus from causing the same disease. The autoimmune disease in the chart are coupled with the anti fungal treatments that have been shown to work against them, and with mycotoxins or fungi that scientists believe may cause them in the first place. Some scientists tell us that fungi alter and subsequently mimic cells, and that their toxins can alter the DNA of their hosts. I believe that our immune systems sense that trouble is afoot and steps in for the cleanup. The result is inflammation, pain and more damage. In some cases, our immune systems are powerless to act effectively. All the while, the fungus or the mycotoxin continues its invasion via what we eat and breathe. If people fail to change their diets, there is no hope that the source of the disease will ever be shut off. Meanwhile, on the medical end, doctors are taught to suppress autoimmune symptoms with glucocorticosteriods and immune modulators. This is similar to fighting a fire by trying to limit the amount of available oxygen, without ever removing the fuel.
Here are the antifungals that Doug and Dr. Holland used in their practice with success. This book of course was written in 2003 and since then we have found that diet and herbal antifungal rotations bring wellness also.
Disease Antifungal remedy Linked mycotoxin
MS Nystatin ergot and glitoxin
IBS ketoconazole/nystatin aflatoxin
Rheumatoic Arthrits Colchicine
Raynaud’s Syndrome griseofulvin
There is more on the list, but you get the idea. If we have the science that silicone degrades to fungi and the heavy metals in implants attract fungi, the success of these antifungal meds with diet serve as a guide as to what causes autoimmune disease.
Part 3: Autoimmunity Reviews : journal homepage: www.elsevier.com/locate/autrev Parasites and autoimmunity: The case of fungi Luigina Romani ⁎ Microbiology Section, Department of Experimental Medicine and Biochemical Sciences, University of Perugia, Via del Giochetto, 06122 Perugia, Italy Available online 12 August 2008
Keywords: Fungi Inflammation Tolerance Autoimmunity
Infections and autoimmunity . . . . .
Fungalinfectionsanddiseasesasexamplesofimmune-relatedpathology. . . . . . . . . . . . . . . . . . . . . . . . . . 130
IDOattheintersectionbetweenimmunityandtolerance ................................. 132
Take-homemessages..................................................... 132 Acknowledgment....................................................... 133 References.......................................................... 133
Infectious agents can induce autoimmune diseases in several experimental settings, some of which have clinical counterparts. A variety of mechanisms have been invoked to explain these observations, including molecular mimicry and an increase in the immunogenicity of autoantigens caused by inflammation in the target organ. Paradoxically, infectious agents can also suppress allergic and autoimmune disorders. A central question is to determine whether immune dysregulation precedes, if not promotes, infection or alternatively, but not mutually exclusive, the extent to which microbial exposure/colonization contributes to the burst of pathogenic autoimmunity. Here we discussed recent evidence with fungi that help to accommodate microbes, either commensals or ubiquitous, within the immune homeostasis and its dysregulation.
1. Infections and autoimmunity
Infections are major players in the environmental factors which modulate the development of autoimmune diseases, both on positive and negative ways
. The underlying mechanisms are multiple and complex, probably different according to pathogens [2–4].
Mimicry of host antigens by infectious agents may induce cross-reactive autoimmune responses to epitopes within host proteins which, in susceptible individuals, may tip the balance of immunological response versus tolerance toward response and subsequently lead to autoimmune disease. Chronic diseases, such as inflammatory bowel diseases and rheumatoid arthritis, are characterized by a robust immune response resulting in unresolved inflammation .
Despite clear evidence that vaccination with mimetic microbial antigens has the potential to activate autoreactive T cells, crucial evidence for triggering of autoimmunity by mimetic sequences in natural pathogens remains lacking, although they may provoke a prolonged inflammatory response when occurring on a susceptible immunological background. Considering that activation rather than the presence of autoreactive T cells and antigen spreading are the hallmarks of autoimmune disease, the creation of an environ- ment resulting in failure of tolerance and regulatory mechan- isms, rather than emergence of novel microbial antigenic determinants, may well be at the root of autoimmunity. Because microbial degradation products, and even bacterial DNA, are present at sites of autoimmunity, this has led to the speculation that the continuous seeding of bacterial products from the gut may eventually favour, on a permissive genetic background, onset of inflammatory autoimmunity. As the vast majority of infections pertain to our resident microbiota, focus has been given toward understanding the mechanisms underlying transition from healthy carrier state to infectious syndromes, including autoimmune diseases .
More surprisingly, infections may also protect from auto- immune diseases . Western countries are being confronted with a disturbing increase in the incidence of most immune disorders, including autoimmune and allergic diseases, inflam- matory bowel diseases, and some lymphocyte malignancies. Epidemiological and clinical data support the hygiene hypoth- esis according to which the decrease of infections observed over the last three decades is the main cause of the incessant increase in immune disorders. The hypothesis does not exclude an etiological role for specific pathogens in a given immune disorder as might notably be the cas