Suhadolnik's Factor

[Guest guest]

Note: I've sort of made this name up myself .....

What I call Suhadolnik's Factor is the DEFECTIVE RnaseL protein that we

PWC's produce.

In his preliminary studies, he had samples from Cheney and (and

I think some from Bell too). Over 95 percent of those samples tested

positive for the abnormal RnaseL.

He was really puzzled by it (when I asked a local biochemist about it --

I live in the land of duPont; you can't walk across a soccer field

without tripping over a biochemist ...) -- so he took some samples he

ALREADY had in his lab of patients with AIDS and some other diseases --

NONE of those samples showed the defect. He tested his lab assistants

(which I find hilarious). None of them had it either.

I know enough about statistics to know that when you have a sample of

100 patients, which he did, and over 95 percent of them test positive

for something that over 95 percent of normals (even if they are graduate

students) DON'T have -- that's statistically significant. that's MORE

statistically significant than Straus's study involving cortisone

supplements (which he said failed). Straus only used 65 patients, and

he weeded them out from a preliminary group of 200 references!!! NOT

sound statistical methodology.

But the CDC/NIH et al don't TALK about statistical methodology -- at

least not to the public. If it is an " outside-the-campus " study, then

it is suspect. If one of THEM does it, why then, it's significant.

Even if it's cooked.

What is " Suhadolnik's Factor " ? Read his own description, from a talk

given on Capitol Hill, here:

http://pweb.netcom.com/~schweit2/temple.html

Unfortunately, I don't have a copy of the slides he showed -- that's

what was so impressive.

Picture a price code bar. You know what they look like. Remember the

O.J. Simpson trial? remember the DNA strips that looked like price code

bars? Well, RNA strips can look like that too. What Suhadolnik had was

a picture of an RNA strip -- specifically, the RnaseL protein in a

normal person, and in a person with CFS.

The picture of the RnaseL strip was BLANK for HALF it's length! That

is, when you put it side by side with the NORMAL version, HALF WAS

MISSING!!! Thus, the DEFECTIVE version of the protein only weighs 37kDa

(whatever the heck a kDa is!), which is less than half what a NORMAL

version weighs -- 80 kDa.

Imagining it weighing half was not nearly as persuasive as SEEING that

slide of a PWC's RnaseL -- which was literally blank for half of its

length. THAT was mindboggling. (If anybody does have a picture of

this, I'd love to upload it onto a website.)

This is a significant abnormality. The CDC said -- eh, so what? It

doesn't PROVE anything. If everybody diagnosed with CFS doesn't have

it, then it can't be a marker for CFS. (But that's part of the problem

-- how are we diagnosing people for " CFS " ? What IS " CFS " anyway?)

Suhadolnik's co-author and younger colleague, Dr. , has made a great

deal of progress showing what it MEANS to have the defective RnaseL

marker. Conversely, clinical research by De Meirleir and others (and

evidence from the Ampligen studies) continues to confirm the

relationship between the presence of the marker, and a person's

symptoms.

What's exciting to me is that the 37kDa offers an EXPLANATION, an

ETIOLOGY, beyond " somehow the immune system gets out of whack " or

" there's a virus that we haven't discovered yet " or " these people aren't

really sick; it's learned behavior " (gack).

The theory -- really the first NEW theory we've had for this disease --

suggests that for some subset of people diagnosed with CFS/M.E. (and De

Meirleir believes MOST people formally diagnosed with M.E. or PVDS --

Post-Viral Disease Syndrome), the major piece of the puzzle has to do

with the way we fight viruses.

When the body tries to kill a virus, it manufactures an RNA specific to

that virus. The defective RNaseL interferes with that process (and this

is the part that I don't understand well enough to explain to other

people) -- such that this critical final stage, creation of an RNA that

binds with the virus and takes it out of your system (after the virus

has been weakened with antibodies) -- NEVER HAPPENS.

So the disease IS viral -- but it's viruses that we should have gotten

rid of a long time ago. We don't show antibodies to anything anybody

else hasn't had -- but in our cases, these viruses have reactivated

because they were never properly " done in. " (This is my best stab at

explaining it.) So the CDC's obsession with antibodies as the sole

measure of whether an active disease is present DOESN'T WORK FOR US. We

DO have a viral disease -- several viral diseases. And we DO pick up

opportunistic diseases very easily because our battered immune system is

trying to beat down those viruses, but our disease-killing RNA never

moves in to do its job. Whew. Best I can do to explain it.

Having too much RnaseL is a sign that this is going on -- but there are

other diseases that will lead to too much RnaseL, and there are CFS

patients who don't have abnormal amounts of RNaseL.

WHEN DIAGNOSED by or Cheney -- relying more on a viral

definition of the disease -- at least 20 percent of patients DIDn'T have

the abnormal amount of RnaseL. BUT -- using the same samples --

Suhadolnik found that they all had the abnormal marker.

The thing is, diagnosis of CFS is subjective, even when the CDC criteria

is used. So samples from OTHER doctors vary widely in the presence of

the RnaseL factor. But that says more about how the disease is

diagnosed -- and whether the diagnosis is picking up more than one

condition -- than it does about the " insignificance " of the RnaseL

factor.

The proper way to really go about finding this all out would be to take

a sample of the normal population and test for the RnaseL factor. But

there's not enough RESEARCH MONEY.

I talked to Lenny about testing the subjects of his most recent

demographic study at De -- perhaps just limiting the testing to the

ones with chronic fatigue, ideopathic chronic fatigue, and chronic

fatigue syndrome. He'd LOVE to do it. But it costs MONEY.

So in the meantime, do you discard the information you have? guess

what? STATISTICAL THEORY says that you USE all the information that

you've gained so far -- it is more " scientifically " accurate to pay

attention to Suhadolnik's Factor than to NOT pay attention to it, just

because you haven't had a larger study yet. (Another reason Straus's

cortisol study was flawed: he posited a univariate model when this

disease is clearly multivariate -- you should have seen the look on his

face when I said that, too -- <g> -- it means all his tests of

statistical significance are worthless ... another way of saying that,

is that if Teitlebaum and Goldstein have found that a little cortisol IN

COMBINATION WITH OTHER MEDICATIONS, specifically sleep meds, HELPS

PATIENTS and does not seem to trigger the adverse effects -- then

STRAUS's study, which used ONLY cortisone and nothing else, is too

flawed to be able to draw the conclusion he did: cortisone

supplemenation is too dangerous and not effective.)

Uh oh, babbling again. But I find this research so EXCITING. What

Suhadolnik found is just the tip of the iceberg, and is going to lead to

a whole new way of looking at many conditions and diseases. It's on the

cutting edge. It is DAMN good research!

But it's complicated. So the public knows about Wessely and Sharpe and

about cognitive behavior therapy. But they don't know about the 37kDa

RnaseL.

(I have an essay ruminating about all of this here:

http://www.cfids-me.org/marys/redd.html

and a page of links to R.E.D.D. information here:

http://www.cfids-me.org/redd/

R.E.D.D. means RnaseL Enzyme Dysfunction Disease, and TECHNICALLY, since

I tested positive for it, I can discard the name CFS altogether and tell

people, accurately, " I have R.E.D.D., a hereditary immunological

defect. " I wonder how many others of us out there could say that.

Schweitzer

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