Kaiser Permanente Researchers Indentified on Lymebusters

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Oh carla you let my secret out.LOL

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Inflammatory chronic autoimmune illnesses have been connected to abnormalities in T-cell responses along with imbalances in the production of cytokines. Parasitic diseases are also being connected to abnormal T-cell responses similar to those found in autoimmune diseases. These abnormal immune responses may partially explain why people with Morgellons become sick and then stay sick for such an extended period of time while others may escape symptoms entirely. There is much yet to be learned about autoimmune diseases and parasitic diseases (to include bacteria, viruses and fungi as well as insects). This next short quote is from an article about SLE (systemic lupus erythematosus), an autoimmune disease:

Correlative Study Of Serum Th1/Th2 Cytokines Levels In Patients With Systemic Lupus Erythematosus With SLEDAI, EDOJ4(1):3

"The abnormality in the T- cell response is manifested by an imbalance in the production of cytokines. Cytokines have been functionally divided into 2 subgroups: Th1, mainly interleukin (IL)-2, IL-12, interferon (IFN)g , and tumor necrosis factor (TNF) a and b, which mainly activate the cellular machinery of the immune system, and Th2 (IL-4, IL-5, IL-10, and IL-13) cytokines, which activate the humoral machinery [4,5,6,7]."

Delayed Immune System Repsonse To Autoimmune Diseases

If indeed Morgellons symptoms are related to impaired immune system response then why does it take so long for symptoms of this disease to manifest? If there is a genetic error then why does Morgellons appear mostly in adults and not as frequently in children? It does seem to be an anomoly until one begins to see that this is often the case with autoimmune diseases. They often show up decades later in life, though the impaired immune response which preceeds them may have been in place since birth. The next quote is from the above link:

“Systemic lupus erythematosus (SLE) is a heterogenous, chronic autoimmune disease characterized by the deposit of immune complexes in different organs. The disease primarily affects women between the third and fourth decades of life.”

Many types of autoimmune diseases make their first appearances later in life (again for the most part), in diseases such as rheumatoid arthritis or Hashimoto’s thyroiditis. There are also other autoimmune disorders which are also mostly adult onset. Some parasitic diseases such as leishmaniasis have an autoimmune component which allows the parasite to hide within the body:

Wiley InterScience :: Session Cookies Sorry this seems to be a URL which does not copy from google but it is an abstract from wiley.com:

“A significant reduction of active TE cells and of OKT 4 positive cells (helper/inducerphenotype) and increase of OKT 8 positive cells (suppressor/ cytotoxic phenotype) was observed in peripheral blood of all patients with persistent active lesions and leishmaniasis recidivans. In patients with highly ulcerated persistent lesions a low proportion of active TE cells was also demonstrated in cellular extracts from dermal tissue. The results support the data obtained in experimental leishmaniasis that lack of helper/inducer cells and generation of suppressor T cells may be responsible for the development of chronic leishmaniasis.”

Restoration of IFN-gamma production and lymphocyte proliferation in visceral leishmaniasis -- Carvalho et al. 152 (12): 5949 -- The Journal of Immunology

“Visceral leishmaniasis is associated with a marked depression of T cell responses, which has been characterized by the absence of IL-2 and IFN- gamma production by lymphocytes on in vitro stimulation with Leishmania Ag.

Zinc Deficiency and Impaired Immune Response

It is quite possible zinc deficiency (whether a genetic problem, one which is caused by low dietary intake or one the parasite itself induces in the host for survival) also enables long term survival of parasites. This article is very long so I will only post a paragraph. This is a good article for anyone interested in the connection between parasites and nutritional status (in this case zinc) which 2manyfibers has discussed in some of his posts as well:

Zinc Deficiency Impairs Immune Responses against Parasitic Nematode Infections at Intestinal and Systemic Sites -- Scott and Koski 130 (5): 1412S -- Journal of Nutrition

”Research on the complex interactions among host nutritional status, parasitic infection and immune responsiveness has focused on the detrimental consequences of parasitic infections on host nutritional status and on mechanisms by which malnutrition impairs immunocompetence. Curiously, relatively few studies have examined the effects of malnutrition on the immune response in the parasite-infected host, and even fewer have considered the events occurring at the intestinal level, where absorption of nutrients occurs, intestinal parasites reside, and the gastrointestinal-associated lymphoid tissues play a role in directing both the local and the more systemic immune responses. Our work using a zinc-deficient nematode-infected mouse model reveals that parasites are better able to survive in the zinc-deficient hosts than in well-nourished hosts; that the production of interleukin-4 in the spleen of zinc-deficient mice is depressed, leading to depressed levels of IgE, IgG1 and eosinophils; and that the function of T cells and antigen-presenting cells is impaired by zinc deficiency as well as by energy restriction. Given the paramount role of the gastrointestinal-associated lymphoid tissues in inducing and regulating immune responses to intestinal parasites and in orchestrating responses in the spleen and peripheral circulation, we conclude that zinc deficiency (in association with energy restriction) exerts profound effects on the gut mucosal immune system, leading to changes in systemically disseminated immune responses and, importantly, to prolonged parasite survival.”

While it may seem strange to think that dysfunctional immune system response may be a connection for all who have Morgellons symptoms this assumption appears to be a valid consideration for research. This is why I believe that Kaiser appointed people who have a background in genetics, even though one of the two seems more interested in other areas of research. Dr. Risch, however, does have an extensive background in genetics (not all of the information about him from the Kaiser site):

“Dr. Risch also has a longstanding collaborative project underway, with Canadian colleagues, on genetic susceptibility to multiple sclerosis.

He is also collaborating on genetics projects of autism and Crohn's Disease as well as genetic disorders in the Jewish population.”

I am not sure how much can be accomplished by such a limited study of Morgellons, but if this particular study unveils a genetic susceptibility to Morgellons symptoms this may be a step in the right direction. It probably will only be an outline study (if that, given Kaiser involvement and limited funding), but at least this study may lead to better and more targeted studies by other researchers. To obtain additional funding it is probably necessary to at least identify Morgellons symptoms as a real disease process. So far this has not been accomplished by any person or organization.