(Editor’s Note: What follows are the first of several transcripts of an appointment that Carol Sieverling had with Dr. Cheney. Cheney discussed a broad range of subjects related to CFS. Carol has kindly decided to make the details of her discussions with Cheney publicly available, for the benefit of all CFS patients. They are republished here with her permission. Please remember to discuss all suggestions with your own healthcare provider. For further information, please contact Carol at firstname.lastname@example.org)
Carol’s Note: Here are the transcripts of tapes from my October 23 & 24 appointment with Dr. Cheney. Statements in quotes are of course from Cheney; statements in parentheses are my own comments; statements not in quotes or parentheses are my own paraphrase/summary of Cheney.
Please bear with the somewhat technical beginning and hang in there – it lays the foundation for some very, very important topics.
Cheney TH1/TH2 – Part I: the two modes of the immune system
The immune system seems to have two different modes of attack, based on the type of invader. One is called TH1, the other TH2. (The numbers are supposed to be in subscript.) As I reflect on my notes, I think Cheney implies that a healthy person’s immune system should be dynamic – meaning it should be able to switch back and forth as the situation demands, or do some of both simultaneously. Nancy Klimas and other researchers have clearly demonstrated that most CFIDS patients end up stuck in TH2 mode. We are TH2 activated.
CFS Patients are TH2 Activated
How that happens, what its implications are, and how to treat it are some of the things Cheney addresses. Cheney began with a diagram. On the top half of a page he drew an inverted “V”. At the top of it is “TH0”. (TH with zero as a subscript.) The left line ends in an arrow pointing at “TH1”, and the right one points at “TH2”. The arrow on the right is thicker and darker, indicating that CFIDS patients are TH2 activated. “TH0 are the naive cells of the immune system, mostly harbored in the lymph nodes. They are naive, just resting, waiting for something to happen, ‘Waiting for Godot’ (Cheney humor for the literate!).
What happens is an infection ensues and then they convert to either TH1 or TH2. These are activator forms – T Helper 1 and T Helper 2. So if you expose this resting cell up here to antigens of a viral class, yeast class, or cancer class, you’re going to initiate TH1 response. Viruses, cancer, yeast, and intracellular bacteria (like mycoplasma and chlamydia pneumonia) initiate the TH1 response. The effector cells of the TH1 system are cytotoxic T cells and Natural Killer (NK) cells. They “effect” or execute the TH1 response.”
Cheney continues: “On the other side of the coin you have bacteria (extracellular), parasites, toxins, and allergens. They tend to inaugurate a predominately TH2 response. The effector cells for TH2 are eosinophiles (Eos), polymononuclear cells (PMN), and antibody secreting cells (Ab).”
Cheney is drawing all this as he speaks: he’s written “virus, cancer, yeast, bacteria (intra)” vertically, on top of each other, beside the TH1 arrow. On the other side in the same fashion he writes “bacteria (extracellular), parasites, toxins, allergens.” A small inverted “V” is added below TH1 and below TH2. He writes “Tc” and “NK” below TH1. Below TH2 on the left he writes “Eos”, and under it “PMN”; on the right side “Ab”.
“Now, you might ask how does this naive cell know which pathway to take? Well, it depends on the cytokine information instructing it. Interleukin 12 (IL-12) makes it go down the TH1 path. Interleukin 10 (IL-10) makes it go down the TH2 path.” Now Cheney has drawn a dotted line straight up from “virus” to “IL-12”, which is written at the top, to the left of “TH0”. On the right side is a similar dotted line going up from “bacteria” to “IL-10”. Little arrows point from IL-12 and IL-10 inwards toward TH0.
So, one scenario based on this info: a virus invades your body; IL-12 appears, causing the naive, resting TH0 cell to convert to TH1; that calls up the troops in the form of T cells and NK cells, and they go to work attacking the virus.
Part II: how viruses, bacteria, cancer, etc deceive the immune system
“This is where it gets rather interesting. Viruses, especially herpes viruses, and especially HHV6, make proteins that mimic IL-10.” The result – the virus deceives the immune system into thinking that the threat is coming from the other side, like a bacteria or a parasite. So the immune system shifts from the TH1 mode that goes after viruses, to the TH2 mode that doesn’t. The virus has found a way to divert the immune system and survive. Very sneaky and deceptive – and a great survival mechanism for the virus. This has all been published, by the way.
It is now thought that many, if not most, pathogens have this ability. Take a scenario from the right side of the diagram. You get a parasite. It produces an IL-12 like molecule, which fools your immune system into thinking the threat is coming from the left side. The fake IL-12 causes your immune system to shift from the TH2 response that would go after the parasite, to the TH1 response, which does little if anything to parasites. “It’s suspected that cancer ultimately defeats your immune system by (a variation of) this mechanism. The cancer cell (actually) turns on the gene that makes (real) IL-10, and then you’ve lost your immune system against cancer.”
Cheney has added two horizontal arrows to his drawing by this time. A third of the way down the TH1 line is a small circle with a line coming out of it and pointing toward, but not quite touching, the TH2 line. Above and below this arrow is written “IL-10 like peptides”. Half way down the TH2 line is a small circle with a line coming out of it and pointing toward, but not touching the TH1 line. Under this arrow is written “IL-12 like peptides”.
Part III: Consequences of TH2 activation
Topics include: NK function, elevated antibodies, reactivated viruses, cancer risk, RNase L, growth hormone.
It’s well documented that CFIDS patients tend to be TH2 activated. This has several consequences. “When the TH2 system activates, it blocks the TH1 system.” You get suppression of the TH1 weapons, particularly NK function. Accordingly, you also get an increase in the TH2 weapons – the white cells, especially eosinophiles, and antibodies.
Increased Antibody Production Causes More Problems
“But the biggest thing you see is increased antibody production. Measure antibodies to anything a CFIDS patient has ever been exposed to and they’ll be elevated.” On the diagram Cheney draws arrows pointing downwards by “Tc” and “NK”, and arrows pointing upwards beside “Eos” and “Ab”. (Suppressed on the left, over activated on the right.) “Other problems ensue. Patients tend to over react to these things (points to right side: bacteria, parasites, toxins and allergens) and under react to viruses, cancer, yeast, and intracellular bacteria. You get into trouble on both sides: a lack of response to viruses, etc, and going overboard responding to bacteria, toxins, allergens, etc.”
When you under-react to the pathogens on the TH1 side, you no longer have the defense mechanisms to keep dormant all those things you caught long ago. You can’t control them anymore. The EBV, chlamydia pneumonia, CMV, etc., that you caught long ago all reactivate. “The yeast begins to come out and possibly, at some future date, cancer might come out. Cancer takes a longer evolutionary … it takes a lot longer for cancer to come out than herpes viruses. Your only defense against this situation – your only defense against being eaten alive – is RNase L. So if these (pathogens) do activate, your RNase L system is your only defense.”
“You must remember that RNase L cannot kill any of these things. It only inhibits their replication (stops them from reproducing). 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 you activate and reactivate. But you never get clearance. RNase L holds the line, waiting for the cavalry that never arrives. But of course while it’s valiantly trying to hold the line (against viruses and intracellular bacteria), it’s also messing up human messenger RNA.”
As RNase L “grinds” away, it eventually shifts into “after-burner” desperation mode – the more powerful and more deadly 80kDa low molecular weight form of RNase L. “RNase is a very good anti-cancer defense. So as long as you’re involved in this scenario, you don’t get cancer. By the way, something that will inhibit RNase L is growth hormone deficiency. A lack of growth hormone will wipe out RNase L. RNase L is a protein and growth hormone is responsible for protein synthesis, so if you lose GH, you lose protein synthesis, including RNase L. And we now know CFIDS involves significant growth hormone deficiency – often profound. So that may explain why, as the disease wears on and you get more injury, you stop seeing lots of RNase L – because you can’t make it anymore.”
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