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How autoimmune studies are mis-characterized
patientadvocate Views: 2,299
Published: 15 years ago

How autoimmune studies are mis-characterized

There are many,many studies that are very complicated which address autoimmunity.

Many immune studies exist where the findings are mischaracterized in my opinion of course.

Many studies exist where overproduction of TNF, INFG, anitbodies, and TH1 helper cells are mischaracterized. Statements from scientists exist like this,

Pub Med:

" In autoimmune diseases the ratio of TH1 cells to TH2 cells is increased."

What does this mean? It appears to say that autoimmunity stems from overproduction of TH1 cells. (Helper cells)

Then further down in the research article we see where the exact same condition exists for viral infections. Yet, oddly enough, the correlation is never made between the two. Why is this?

Here are some examples:

Out of Natural Genetics, a Scientific publication,... on how to treat autoimmunity.

"Immunization with proactive TH2 regulatory peptides appears to regulate the production of TH1 cells and their proinflamatory enzymes, suspected to be the cause of autoimmune symptoms."

Yet in the same article we see that viral infections causes TH1 overproduction anyway.

"Since INF-gamma is a cytokine that is released by TH1 lymphocytes, this increased production is commonly found when cellular immune system is activated by viral infections and/or autoimmunity."

Yet, oddly enough, never is there a correlation between the two diseases once again.

Pub Med:

A scientist concluded after technical analysis of blood,

"Over production of these specific cytokines appears to be the route cause of autoimmunity and should provide us with a target for drug therapy in the future."

In the same article by the same scientist:

"These same interferons and cytokines are identical to those found in severe viral infections such as hepatitis c and viral leukemia."

Yet, still the correlation is never made between the different diseases.

In fact, everywhere we look, TH1 overproduction exists in every single severe viral infection ever documented.

Everytime this comparison exists in scientific articles, the relationship is never explained or even explored, and the mimcry is mischaracterized, sometimes as "autoimmune mimicry."

Is this not misleading?

Because these articles are so technical, people who read them automatically assume that autoimmunity is a defect and not an infection, technical articles are very persuasive and so are the people who write them. We believe the conclusions.

But if we read between the lines we see consistently a relationship between autoimmunity and viral immunity. Only this relationship is repeatedly ignored by those scientific studies that research such.

Never mind studies are currently pouring forth revealing more and more associations to viral infections.

SO, the next time you see scientific mumbo jumbo and fancy terminology, don't lose sight of the fact that the same immunological responses attributed to autoimmune diseases are identical to the immunological responses attributed to viral infections as well. The immune changes, (sometimes called mutations,)found in autoimmune are also found in viral infections and therefore should not be so readily characterized as mutations. Genes switch off and on all the time depending on stressors, toxic responses, level of hypoxia, changes in ph.

The proof is in the pudding alright but you have to read between the lines.

Anybody who disagrees with this can find dozen more studies with identical paradoxes contained right in the middle of the articles. Here is one more!

Bentham Science:

" We have found that these antibodies and their proteins that are overproduced in several autoimmune diseases are identical to the antibodies and proteins also found in several kinds of viral infections. As of yet, we have not found the reason why autoimmunes engage in this viral immune mimicry, however, the over abudance of these antibodies and proteins should provide us a good target for developing pharmocological treatments in the future."

I got a good reason for viral immune mimicry! How about the obvious for a change!

But my goal is not to sell viral immune vs autoimmune. My goal is to point out the inconsistencies in reporting and to point out the stark, real, and consistent associations to viral infections. We are trying to get people to think, ask questions, and wonder why!

I surely have formed an opinion, I may be wrong! But let us all see the big picture when seeking to treat the untreatable.

Thanks for your time.

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