EXPLAINING IMMUNE DYSFUNCTION SYNDROMES
Chronic Fatigue Syndrome, Fibromyalgia, Multiple Chemical Sensitivity, Lyme Disease, Thyroid Disease, Dental Amalgams (mercury)
From a talk by Paul Cheney, MD
Chronic Fatigue Immune Dysfunction Syndrome (CFIDS) patients are Th2 activated. This means they over-respond to toxins, allergens, normal bacteria and parasites, and under-respond to viruses, yeast, cancer and intracellular bacteria. Dr. Cheney explains that the immune system has two different modes of attack, based on the type of invader. One is Th1 (T Helper 1). It goes after organisms that get inside our cells, intracellular pathogens. It is also known as cell-mediated immunity. The other is Th2 (T Helper 2). It attacks extracellular pathogens‚ organisms that are found outside the cells in blood and other body fluids. Some call this humoral or antibody-mediated immunity.
Th0 are the naive, or unformed, cells of the immune system. They are resting, just waiting for an invader. When infection occurs, they convert to either Th1 or Th2, depending on the type of threat. When the resting cell is exposed to a virus, cancer, yeast, or intracellular bacteria (like mycoplasma or chlamydia pneumonia), the Th1 response is initiated. The weapons of the Th1 system include cytotoxic T cells and Natural Killer (NK) cells.
On the other side are normal bacteria, parasites, toxins, and allergens. These trigger a predominately Th2 response. Its weapons include eosinophiles (Eos), polymononuclear cells (PMN), and antibody secreting cells (Ab).
How does the naive cell know which pathway to take? It depends on the cytokine information received. The presence of any organism from the left side triggers production of a cytokine called Interleukin 12. IL-12 causes the Th0 cell to move down the Th1 path. On the other hand, organisms on the right side trigger the production of Interleukin 10 (IL-10), which causes the Th0 cell to move down the Th2 path.
Cheney said this is the point where it gets very interesting. Viruses, especially herpes viruses like EBV, CMV and HHV6, make proteins that mimic IL-10. The virus deceives the immune system into thinking that the threat is coming from the opposite side! So the immune system shifts from the Th1 mode that attacks viruses to the Th2 mode that does not. The virus increases its chances of survival by diverting the immune system. It is now thought that many, if not most, pathogens have this ability.
Researchers have demonstrated that most CFIDS patients end up stuck in Th2 mode. This has several consequences. When the Th2 system activates, it blocks the Th1 system. This suppresses the Th1 weapons, particularly NK function. Accordingly, there is also an increase in the Th2 weapons - the white cells and antibodies. Most notable is increased antibody production. Dr. Cheney said that if you measure antibodies to anything a CFIDS patient has ever been exposed to, they will very likely be elevated.
Cheney notes that other problems ensue. Patients get into trouble on both sides: they overreact to things on the right side and under-react to those on the left. When they are Th2 activated, they no longer have the defence mechanisms to keep dormant all the things they caught in the past. They cannot suppress or control them anymore, and the EBV, chlamydia pneumonia, CMV, etc. reactivate. The yeast also begins to appear.
The only defence against being eaten alive at this point is RNase L. RNase-L cannot kill any of these things. It only stops them from reproducing. According to Cheney, "It's a line in the sand saying 'No more replication', and it waits for Th1 to come and kill them. But Th1 never comes. RNase L sits there and grinds away, possibly going up and down as the pathogens activate and reactivate. But they never get wiped out. RNase L holds the line, waiting for the cavalry that never arrives."
While it is valiantly trying to hold the line, it is also chewing up human messenger RNA, inhibiting all the enzymes in the body, disrupting protein synthesis, and generally making patients miserable. As RNase-L grinds away, it eventually shifts into "after-burner" desperation mode.
Cheney commented "RNase-L is a very good anti-cancer defence. So as long as you're involved in this scenario, you don't get cancer. But a lack of growth hormone will wipe out RNase-L, and we now know there is profound loss of growth hormone in CFIDS. Growth hormone is responsible for protein synthesis, and RNase L is a protein. So if you lose growth hormone, you lose protein synthesis, including RNase L. That may explain why, as the disease wears on and you get more injury, you stop seeing high levels of RNase L. You can't make it anymore."
He believes this is a very scary situation. Patients are Th2 activated and Th1 suppressed. The things on the left come out and there is nothing to stop them. There is no Th1, and eventually no Rnase L. He also believes patients need to balance the immune system - to push it a little more towards Th1. That way they will lose some of the overreaction on the right and gain some control on the left.
Cheney recommends pine cone extract to help shift the immune system from one mode to another. Cheney said, "They make a tea from this in Southern Japan and they have significantly reduced cancer rates. It's thought to work at the gene level in lymphocytes, where it turns on IL-12. It also shuts down IL-10 at the gene level, and that causes a shift towards Th1. Next Blog – What is pine cone extract?
Unformed cells of the immune system convert to either Th1 or Th2 cells when infection occurs: