immunity in CFS

[Guest guest]

> Even if there really are some triggers that can cause the immune

system to self attack, at least the claim can't be made that it's

" underactive " .

I see different meanings that should be separated. One might say it's

" specifically underactive " in eradicating a certain causal persistent

microbe (though that would be stating the obvious).

There also may be a generalized T cell hypoactivity. I have heard

reference to this in CFS but not scrutinized any data. However, a

generalized T cell anergy is common in states like sarcoidosis, RA,

etc, and can be pretty pronounced. I'm guessing this phenomenon is

probably just a prioritization thing due to chronic inflammation (if

that guess is correct, the phenomenon should be found in almost all

the immune diseases). Since immunoactivations of all sorts generate

(or at least risk) disruptions of the body, any given immune stimulus

X tends to thin out the reaction to other stimuli, and also thin the

activity level in the parts of the immune system that do not respond

to X. The immune system is always repressing itself, metering its own

activity, and trying not to impair your physiology unless it

calculates (rightly or no) that risky levels of disruption are in your

best interest.

[Guest guest]

But it shouldn't be considered "underactive" if it's doing the best any human immune system can do against a particularly resistant bug. This is the part that gets me, how everyone always leaves out the bug's remarkable abilities to beat our immune systems, no matter how healthy they might be. Just because bugs are getting more resistant doesn't mean that our immune systems are getting weaker. We simply have a hard time holding our own against some bugs. Always have. Sometimes we gradually adapt, but in the process a lot of people die first. I don't want to be one of the first fallen. I'd have no problem if people would discuss how these bugs are messing with our immune systems, as long as the focus would stay on the bugs. But what always comes through to the average person is..."your immune system isn't good enough, or is malfunctioning", with no talk at all about how resistant the organisms are. It has just not gotten through

yet to people that the bugs need to be understood and taken seriously if we've got any hope of beating them. Focusing on the immune system so much takes attention away from the bugs, when people actually need to be giving the bugs a lot MORE attention. Most people who go on and on about immune system theory actually know very little about the adversaries they're trying to fight. That just seems illogical, and to be honest, downright idiotic. penny <usenethod@...> wrote: > Even if there really are some triggers that can cause the immunesystem to self attack, at least the claim can't be made that it's"underactive". I see different meanings that should be separated. One might say it's"specifically underactive" in eradicating a certain causal persistentmicrobe (though that would be stating the obvious). There also may be a generalized T cell hypoactivity. I have heardreference to this in CFS but not scrutinized any data. However, ageneralized T cell anergy is common in states like sarcoidosis, RA,etc, and can be pretty pronounced. I'm guessing this phenomenon isprobably just a prioritization thing due to chronic inflammation (ifthat guess is correct, the phenomenon should be found in almost allthe immune diseases). Since immunoactivations of all sorts generate(or at least risk) disruptions of the body, any

given immune stimulusX tends to thin out the reaction to other stimuli, and also thin theactivity level in the parts of the immune system that do not respondto X. The immune system is always repressing itself, metering its ownactivity, and trying not to impair your physiology unless itcalculates (rightly or no) that risky levels of disruption are in yourbest interest.

[Guest guest]

> But it shouldn't be considered " underactive " if it's doing the best

any human immune system can do against a particularly resistant bug.

But who's to say that it is? More likely, IMO, that is far from true.

Part of the reason an organism (might have) gotten stuck with some

nonresolving infection could be stochastic - ie, it could easily have

gone otherwise but just didn't (for no single reason or few simple

reasons, just as a dice rolls a 2 one time and a 6 another time for no

simple reason).

But much of it could also very well be genetic. How would you know?

Well, look at twin concordances. Identical twins are very likely to be

concordant for things like TB and leprosy (concordant meaning, either

they both get it, or neither does; if only one gets it they are

discordant).

Of course, since TB is quite communicable and leprosy somewhat so,

it's hard to say whether one simply gave it to the other, or they both

got it from a third source. If so, one could explain the concordance

without recourse to genetic disposition.

Thus, it's hard to prove genetic predispositions to infectious disease

in an airtight way. I can't say that I definitely disagree with your

statement " because of A therefore B therefore C therefore D,

airtight. " But I do think the balance of evidence suggests that

certain persons have a very significant disposition to certain

infections and/or to certain outcomes of certain infections.

> Focusing on the immune system so much takes attention away from the

bugs, when people actually need to be giving the bugs a lot MORE

attention. Most people who go on and on about immune system theory

actually know very little about the adversaries they're trying to

fight. That just seems illogical, and to be honest, downright idiotic.

Well, it's true, immunologists tend to want to find some kind of

immunopathy, and microbiologists look to see infection. The

traditional boundaries of disciplines certainly are not a boon to deep

thinking. Infection and immunity in particular deserve to be studied

together - they created each other and still are creating each other.

A serious inquiry further requires that they both together be put in

evolutionary context. Personally I'm certain I'd rather err on the

side of the big picture than make the opposite error.

Now - I have seen *very* well respected people say that genetics *is*

" the major " determinant of something like lupus. That pisses me off

probably just as much as it would you. As Ewald is always pointing

out, we can all see very clearly that the identical twin concordance

for lupus is only about 35-45% (as I recall). So, looking at genes one

is AT MOST 35-45% " destined " to get lupus (and it could be a lot less,

since those identical twins share environment as well as all their

genes). Lupus must be at least 55-65% (but perhaps more)

environmental/stochastic. Now, the people writing these hasty

sentences know that is the case. What they *really* mean is that

genetics is the " the major " determinant of lupus *not counting the

other 55-70%, because it must just be stochastic, since no one can

figure out what it is.* Well, they don't know that! That is NOT a

fact! Or if they really believe current science is so wonderful that

everything it can't explain must just be stochastic, then they should

explain that quite clearly - rather than misleading the 90% of their

readers who don't think very carefully about this.

[Guest guest]

Bob,

Several things you posted here are worth noting. I think the twin

study in the northwest -forget the name of the woman researcher - was

flawed based on someone I knew who was a twin and in the study.

Your point on the complexity of genetic study is excellent.

And then there is the problem that folks in the same house not only

share genes, but they share pathogens. Lenny 's work in Wichita

revealed this when he demonstrated that spouses and non-blood folks

under the same roof also got cfs. Seems to me that would throw the

genetics as cause right out the window - not that genetics doesn't

increase suceptibility.

But even there, it would seem that figuring out why women demonstrate

more SYMPTOMS might be a fruitful area of study. I must hasten to add

that in my family I am the only female and APPEAR much sicker than

the males, but they are also carrying borrelia at least and do have

symptoms. So perhaps we are just missing the men who are also sick.

a Carnes

>

> One of the most bogus studies out there regarding CFS, in my view,

is

> the " twins study " that tries to draw conclusions about CFS by

starting

> from the misleading assumption that identical twins completely

> eliminates genetic influences.

>

> It's true that your friend and her twin sister have identical DNA

but

> that doesn't mean their genes will express the same. In the case

of

> your friend, I suspect the only reason she hasn't gone down the

same

> path as her sister is that she hasn't yet encountered the right

> environmental trigger. That might be a particular infection

combined

> with the right kind of physical stressors, or a particular food or

> additive, a particular toxin for a sufficiently sustained period of

> time, etc.

>

> To me, the problem with genetic research is not that it's looking

at the

> wrong thing, but that the field way under-estimates the complexity

of

> the problems they are tackling. The mentality seems to be that

it's

> possible to find one defective gene, enzyme or protein that

corresponds

> to one disease state. As if diseases were nice, cooperative little

guys

> with single causes. To continue with the example of your friend's

> identical twin, the trigger may have been not only multi-factorial

but

> those multiple factors would have to happen in a certain way. Now

that

> she has the disease state, those factors may well no longer matter

and

> have been replaced by a completely different chaotic, complex

system of

> interweaved causes and effects that sustain the disease state.

>

> Chronic illness is going to require a multi-disciplanary approach

to

> research, not people in their isolated silos and ivory towers

wasting

> energy debunking those with " competing " theories. I know a CFS

> clinician who understands this well enough that, with the help of a

> wealthy patient, is bringing together CFS researchers from all over

the

> world in a few weeks, to a retreat where they can get to know each

other

> and cross-pollinate. That's how progress is made with disease

states

> like this.

>

> --Bob

[Guest guest]

I almost forgot - this is wonderful - a group of experts sharing. But

I wonder how much money over the years the NIH has spent on so-

called " state of the science " meetings where MDs and scientists were

flown to Washington to discuss cfs - the one I attended in 2000 was a

gathering of about 20 docs who, with possibly 3 exceptions KNEW

NOTHING ABOUT CFS AND HAD ONLY READ THE WORK SENT THEM A COUPLE OF

DAYS BEFORE THE CONFERENCE. To my knowledge not even Cheney has

ever been included in such an NIH session. So I hope this

knowledgable group will put some pieces together. I have to wonder if

they included any Lyme specialists. Bob, do you know????

a Carnes

I know a CFS

> clinician who understands this well enough that, with the help of a

> wealthy patient, is bringing together CFS researchers from all over

the

> world in a few weeks, to a retreat where they can get to know each

other

> and cross-pollinate. That's how progress is made with disease

states

> like this.

>

> --Bob

[Guest guest]

>>>>>>>>>>>>>>>>path as her sister is that she hasn't yet encountered

the right

> environmental trigger. That might be a particular infection

combined

> with the right kind of physical stressors, or a particular food or

> additive, a particular toxin for a sufficiently sustained period of

> time, etc.<<<<<<<<<<<<<<<<<<<<<<<<<<<<<<<<<<<<<<<<<<<<

Bob I found it interesting that you understood all this. I would now

go back and study the parts about bacterial communication and

switches if I was you...This is the whole disease cycle in a nutshell

IMO. What occurs as an after effect to the body-is irrelevamt to

study IMO.

> >

> >

> > > But it shouldn't be considered " underactive " if it's doing

the best

> > any human immune system can do against a particularly

resistant bug.

> >

> > But who's to say that it is? More likely, IMO, that is far

from true.

> > Part of the reason an organism (might have) gotten stuck with

some

> > nonresolving infection could be stochastic - ie, it could

easily have

> > gone otherwise but just didn't (for no single reason or few

simple

> > reasons, just as a dice rolls a 2 one time and a 6 another

time for no

> > simple reason).

> >

> > But much of it could also very well be genetic. How would you

know?

> > Well, look at twin concordances. Identical twins are very

likely to be

> > concordant for things like TB and leprosy (concordant

meaning, either

> > they both get it, or neither does; if only one gets it they

are

> > discordant).

> >

> > Of course, since TB is quite communicable and leprosy

somewhat so,

> > it's hard to say whether one simply gave it to the other, or

they both

> > got it from a third source. If so, one could explain the

concordance

> > without recourse to genetic disposition.

> >

> > Thus, it's hard to prove genetic predispositions to

infectious disease

> > in an airtight way. I can't say that I definitely disagree

with your

> > statement " because of A therefore B therefore C therefore D,

> > airtight. " But I do think the balance of evidence suggests

that

> > certain persons have a very significant disposition to certain

> > infections and/or to certain outcomes of certain infections.

> >

> > > Focusing on the immune system so much takes attention away

from the

> > bugs, when people actually need to be giving the bugs a lot

MORE

> > attention. Most people who go on and on about immune system

theory

> > actually know very little about the adversaries they're

trying to

> > fight. That just seems illogical, and to be honest, downright

idiotic.

> >

> > Well, it's true, immunologists tend to want to find some kind

of

> > immunopathy, and microbiologists look to see infection. The

> > traditional boundaries of disciplines certainly are not a

boon to deep

> > thinking. Infection and immunity in particular deserve to be

studied

> > together - they created each other and still are creating

each other.

> > A serious inquiry further requires that they both together be

put in

> > evolutionary context. Personally I'm certain I'd rather err

on the

> > side of the big picture than make the opposite error.

> >

> > Now - I have seen *very* well respected people say that

genetics *is*

> > " the major " determinant of something like lupus. That pisses

me off

> > probably just as much as it would you. As Ewald is always

pointing

> > out, we can all see very clearly that the identical twin

concordance

> > for lupus is only about 35-45% (as I recall). So, looking at

genes one

> > is AT MOST 35-45% " destined " to get lupus (and it could be a

lot less,

> > since those identical twins share environment as well as all

their

> > genes). Lupus must be at least 55-65% (but perhaps more)

> > environmental/stochastic. Now, the people writing these hasty

> > sentences know that is the case. What they *really* mean is

that

> > genetics is the " the major " determinant of lupus *not

counting the

> > other 55-70%, because it must just be stochastic, since no

one can

> > figure out what it is.* Well, they don't know that! That is

NOT a

> > fact! Or if they really believe current science is so

wonderful that

> > everything it can't explain must just be stochastic, then

they should

> > explain that quite clearly - rather than misleading the 90%

of their

> > readers who don't think very carefully about this.

> >

> >

> >

>

[Guest guest]

I don't want to get in a catfight here, but I think Teitlebaum has a better

track record than

Cheney, who is treated like some sort of God. Don't get me wrong, Cheney has

been a

great advocate, a tireless researcher and has probably helped a lot of people,

but even he

admitted when asked how many folks he had " cured " -- he said " none " .

I used to think T-baum was a slick salesman, just in it for the $$. But then I

heard him

speak here in Seattle, and came away with a totally different impression. He

has treated

patients longer than Cheney, he had CFS himself, was homeless for a year, but

eventually

recovered, etc., etc..

That is GREAT that someone is pulling together a group of the top docs/

researchers...hope to hear more about it in the coming weeks...

Dan

> >

> > I almost forgot - this is wonderful - a group of experts sharing. But

> > I wonder how much money over the years the NIH has spent on so-

> > called " state of the science " meetings where MDs and scientists were

> > flown to Washington to discuss cfs - the one I attended in 2000 was a

> > gathering of about 20 docs who, with possibly 3 exceptions KNEW

> > NOTHING ABOUT CFS AND HAD ONLY READ THE WORK SENT THEM A COUPLE OF

> > DAYS BEFORE THE CONFERENCE. To my knowledge not even Cheney has

> > ever been included in such an NIH session. So I hope this

> > knowledgable group will put some pieces together. I have to wonder if

> > they included any Lyme specialists. Bob, do you know????

> >

> > a Carnes

> >

> > I know a CFS

> > > clinician who understands this well enough that, with the help of a

> > > wealthy patient, is bringing together CFS researchers from all over

> > the

> > > world in a few weeks, to a retreat where they can get to know each

> > other

> > > and cross-pollinate. That's how progress is made with disease

> > states

> > > like this.

> > >

> > > --Bob

> >

> >

>