Lyme and cell wall deficient bacteria:
//www.curezone.org/forums/fm.asp?i=1635162


Let me guess..Dr's want to put you on steroids to shut off your immune system, since it's an "autoimmune disorder", right? And, blood tests show you have Vitamin D deficiency, and they want to make sure you get plenty of Vitamin D.

First things they do with an "autoimmune disorder".
Shut off your immune system with steroids, which Vitamin D is also, and what happens to all the types of pathogens that have no immune system then keeping them in check?

Put in a search on this forum for "Vitamin D" and read.

How are stealth bacterias involved?

http://bacteriality.com/2007/09/15/vitamind/

Most of these researchers are also unaware of a new understanding about the cause of many chronic diseases. As a person falls ill with a chronic disease, L-form bacteria begin to live inside the cells of the immune system and in various tissues.[12][13] These bacteria create proteins that, just like elevated 25-D, are able to bind and block the Vitamin D Receptor.[14] Together, elevated 25-D and bacterial proteins block the ability of the Vitamin D Receptor to turn on the immune system more than either substance alone.


25-D is immunosuppressive.

The Vitamin D Receptor also directly controls the expression of many of the antimicrobial peptides (AMPs).[8][9][17][14] The AMPs are proteins that kill bacteria, viruses, and fungae by a variety of mechanisms including disrupting membranes, interfering with metabolism, and targeting components of the machinery inside the cell. When 25-D reaches the level at which it inactivates the receptor, the AMPs are no longer produced, and bacteria can spread more easily throughout the body.

People infected with L-form bacteria are particularly prone to the effects of 25-D on the Vitamin D Receptor. That is because their L-form bacteria have created proteins which have already bound and deactivated the Vitamin D Receptor to varying degrees. Extra amounts of the steroid 25-D only bind and shut down the receptor even more, further inhibiting the innate immune system, the transcription of thousands of genes, and the production of the AMPs.

“It is when L-form bacteria die that they begin to cause a major increase in symptoms for the host, since as they die they release a large amount of toxins and cytokines, proteins that generate pain and fatigue. ”The above scenario is all too familiar, since L-form bacteria are found everywhere in our environment, from soil, to water, to sperm, to inside the womb.[18] Consequently, it seems that few people will remain free of them for long and most will acquire substantial levels of them as they age.[19]

L-form bacteria have evolved mechanisms that allow them to live for long periods of time within the cells, and when alive, generally persist without generating too many symptoms.[20]

Furthermore, as L-form bacteria die, the cell that they have parasitized dies as well, and cellular debris is released into the bloodstream. These substances cause the tissues to become inflamed, resulting in what is known as “Th1 inflammation.”[21]

As previously discussed, the innate immune system is responsible for killing L-form bacteria and is controlled by the Vitamin D Receptor (VDR). Elevated levels of the steroid 25-D and bacterial proteins bind and inactivate the VDR, causing the immune system to work less effectively.

As the immune system becomes increasingly inhibited, fewer L-form bacteria are killed. Furthermore, the Vitamin D Receptor is no longer able to transcribe the antimicrobial peptides, and fewer bacteria are killed by DNA fragmentation. As fewer bacteria die, fewer inflammatory cytokines are released, and fewer toxins and cellular debris enter the bloodstream. As the level of inflammation temporarily decreases, a patient will start to feel better.

This seeming wellness is illusory. Without the innate immune system and the antimicrobial peptides to keep L-form bacteria in check, the pathogens easily spread to new cells, new tissues, and new organs.