Re: Chronic Fatigue Syndrome (CFS) Pharmacogenic Profiling

[Guest guest]

That was very decent of Dr. Shoemaker to title this

subchapter " Vindication for " , and say such nice things about me.

It is very bizarre to say something that is vehemently denied and

ridiculed for so many years, and watch these very same words

become " self evident " .

People used to call moldies crazy and stupid for saying it, and now

society around is changing so that it becomes crazy and stupid to

not already know something which is so blindingly obvious.

When Dr S says " remains bitter that his correct insights were

ignored " , it's true, but even more than bitter, I find myself

absolutely outraged and stunned into disbelief that something which

is suddenly so obvous is the very abnormality that researchers

completely refused to even discuss for twenty years.

When Dr Cheney asked me to volunteer to be in the CDC study for

the " Holmes et al " definition of the illness - which led to the

creation of the term " Chronic Fatigue Syndrome " , he told me that by

participating in this study, not only would I be doing a valuable

service to the cause of CFS, but that special attention would be

given to my case. As a prototypical case for CFS, I thought that

this meant that the clues I presented would be studied.

It is in my medical records that I was implicating mold exposure in

my CFS onset, and was demanding that this important trigger for my

symptoms should be investigated. This has never happened.

I have no idea where Dr De Meirleir could have obtained his data on

mold exposure in the original Incline Village CFS cohort. Not only

did researchers dismiss the mycotoxin connection to CFS, but the

other Incline patients I've discussed mold with attached no

significance to this type of exposure.

If the CDC's genetic studies confirm Dr. Shoemakers HLA DR findings

and lead to pharmacogenic profiling for mold susceptibility, it will

also confirm that the reason they didn't know about the mycotoxin

connection to CFS for twenty years is that they declined to discuss

it after being asked to do so.

-

Mold Warriors by Dr. Ritchie Shoemaker

Chapt. 23 " Mold at Ground Zero for CFS "

Answers from Abroad: " Vindication for "

page 447:

One of the researchers who was well represented at the CFS meetings

was Dr Kenny De Meirleir from Belgium. He had published extensively

on the different mechanisms that contribute to Chronic Fatigue

Syndrome. Before I could talk to him, however, Dr Suhaldonik

presented his data on the enzyme complexity involving RNaase L. He

had been working with Drs. and Cheney for some time.

I asked him about mold and CFS. Making me fall to the floor, he

said, " Oh, yes, we know a lot about mold exposure in the original

cohort in Incline Village. The source of activation of the

endopeptidase that cleaves RNase L is increased response of a

cytokine, alpha interferon.

" Now wait, " I asked, " our data is very clear that alpha interferon

levels are increased like crazy in mold patients compared to

controls. Can we say that mold exposure doesn't change RNase L like

you have reported in putative viral CFS patients? "

Dr. De Meirleir chimed in, " We know that cyokine increases are

important activators of the subsequent increased activity of those

enzymes. Given your data, we need to look again at our data in which

we clearly see changes in innate immune responses in CFS.

Mold could be the common denominator. "

The issue for me was that while De Meirleir knew about MSH, innate

immune response activation, including complement, coagulase negative

Staph and changes in exercise intolerance and reduced VO2 max, he

didn't know about VEGF (Vascular Endothelial Growth Factor).

But he knew about mycotoxins binding to Toll receptors (no one else

did); in fact, he said that a Toll 3 receptor, a mycotoxin receptor,

was critical to teh abnormalities in the innate immune response

abnormalities in CFS. When I said that the interferon and IL-1B

increases induced by mycotoxins, binding to the Toll 3 receptor

activated excessive cytokine responses that then altered genes

expressing autoimmunity, VEGF, and erythropoietin and lowered MSH

with all of its downstream physiologic changes, Kenny just smiled.

" Yes, when we can put the changes in the other findings (increased

elastase is just one example) that I know to be true,

alongside yours, then we just might begin to understand Chronic

Fatigue Syndrome, " he said.

-Dr. Ritchie Shoemker