Re: Great LA Times article on CFS

April 25, 2006

When I saw a local doctor suddenly reverse himself after years of

abuse toward CFS and I was told " The reason that the doctor didn't

believe in CFS until now is that YOU failed to present evidence that

was good enough, obviously, or he would have been convinced by now " ,

I got a taste of how " validation " is going to occur.

One day, you expect to hear the usual mistreatment and denial, but

instead, you hear " I have determined that... " and suddenly the very

person who fought you the very hardest is portraying himself as

being the one at the very forefront of science and medicine, and

that HIS enlightenment is based upon REAL technology as opposed to

the " guesswork " or pursuasion that prior illness believers had

employed to reach their specious decision to support the existence

of the illness.

In shock, you ask yourself, " After all this? Is he sorry? Does he

feel any remorse for all that he has done? Why it took him so long? "

You try to find out: " Doctor, what about all those years... " and

the response has already been prepared - " I was just being

scientific and your evidence was not compelling " .

You know this isn't true. You have seen your friends suffer and

die. You wonder if you could just stand toe to toe and look this

doctor in the eye, and ask if he truly believed that everything that

has happened, all the suffering, all the stories - the research, the

evidence, the undeniable measurable abnormalities... that all of it

could just be waved away with a shrug as if none of it meant

anything..., you wonder if perhaps, you looked deep enough into that

doctors eyes - somewhere you might catch a faint glimmer of remorse

and realization of what he has put people through.

But if you push a little harder for an answer, the doctor won't be

the one who stops you. It will be your fellow sufferers who tell

you not to do that. After all, he's on our side now - and we must

be grateful - this is progress.

And just like the history of all illnesses that have been similarly

abused, there is no justice. No investigation of how such a thing

could possible have been allowed to happen. The medical profession

doesn't bother to investigate itself to find out what went wrong -

or what to do so that it won't happen again.

As painful or even counterproductive as it may seem to criticize

under these circumstances, there is one thing that everyone who has

looked at the painful process of illness validation throughout

history has learned. It is that every time this recurring pattern

of abuse toward any emerging illness was repeated, the medical

professsion had learned nothing from its mistakes.

-

April 25, 2006

Hi a,

<< Would these people have gone to the doctor? I don't know. If you

live on a farm or are on welfare you can sort of get along - you don't

think about how you lost your big career if you just lost your job at

Mc's. The disease is tricky and with 80% slow onset you might

not figure anything out. You might start getting treated for RA or

fibro. Or maybe you just think you are depressed. >>

Not to be contrary or ornery, I think it's too easy to dismiss a job

at Mc's -- or anywhere else for that matter, no matter the pay

scale and offering of " benefits. "

People have lots of ways that they use to stay connected with the

community or humanity as a whole. " The world out there. " And just

because we are inexperienced in, or unexposed to, some of the ways is

no reason to discount them.

I think that most of us would be hard-pressed indeed to put into

words the reactions of all of the " greeters " at WalMart if they were

all given the boot, all at once. What would they tell us about how

it feels to have just lost their job?

One person's crumby job with no way out may indeed be another

person's " big career " that at least gives them a few options in life.

the one in Champaign IL

April 25, 2006

Here are some of Reeve's comments in the press conference. He

mentions cognitive behavioral therapy in the third paragraph. I guess

I am suffering too much to see the silver lining in this. The entire

transcript is at

http://www.cdc.gov/od/oc/media/transcripts/t060420.htm

" For the first time ever, we have documented that people with CFS

have certain genes that are related to those parts of brain activity

that mediate the stress response.

And that they have different gene activity levels, this is outside

which genes are there, that are related to their body's ability to

adapt to challenges and stresses that occur throughout life, such as

infections, injury, trauma or various adverse events.

Why is it important? Well, knowing that there is now a biologic

basis for CFS will help us identify better ways to more effectively

diagnose the illness and to come up with more effective treatments,

including ***cognitive behavioral therapy***, medications or a

combination of both. "

>

> But there's already a fairly loaded use of language on his behalf at

> the press conference; compare his comments with Vernon's.

> I'm not interesting in attacking or defending Reeves, all I mean is

> that I'm far more interested in the results that come from the

> Kerr/Gow patients. If both of them manage to talk about their

results

> without mentioning CBT, I have more trust that they are talking

about

> the same disease I have. Not judging which is good science and which

> isn't, just which interests me more.

>

April 25, 2006

Thanks. I dont know how I missed that. Its too bad its in there. Most of the

studies do show CBT is helpful for some CFS patients but I dont think anybody

thinks its a cure. i dont know how a behaviioral intervention is enhanced by

finding a biological basis for CFS (???). Perhaps it has to do with managing

the stress response - I dont know.

.

<christine.emmanuel@...> wrote:

" Well, knowing that there is now a biologic basis for

CFS will help us identify better ways to more effectively diagnose the

illness and to come up with more effective treatments, including

cognitive behavioral therapy, medications or a combination of both. "

http://listserv.nodak.edu/cgi-bin/wa.exe?A2=ind0604d & L=co-cure & T=0 & P=317

>

> THe three studies are very different. The CDC study is far more

complex and ambitious but the Kerr study really focused on immune

genes I believe. The CDC had a large gene set to be sure but their

other laboratory measures were almost entirely focused on the

neuroendocrine system not the immune system - so perhaps its not

surprising we're not hearing about immune stuff.

>

> While I did find the reference to the UK I still have yet to find

any reference to CBT in the briefing, by the way.

>

This list is intended for patients to share personal experiences with each

other, not to give medical advice. If you are interested in any treatment

discussed here, please consult your doctor.

April 25, 2006

I think there are only about two or three sentences in the entire press

conference, out of how many? that could give people pause. I dont think its

necessary to look for a silver lining to get something out of this; I think its

more necessary to stop looking for the bad news - for whats negative - for what

reinforces CFS patients persistent belief that the CDC or whoever is against

them. The CDC again and again says 'biologic basis for CFS' - but that

statement - which really is good to hear from an institution as important at

this - unfortunately doesnt get as much press - not here anyway.

Vickie <vickie77077@...> wrote:

Here are some of Reeve's comments in the press conference. He

mentions cognitive behavioral therapy in the third paragraph. I guess

I am suffering too much to see the silver lining in this. The entire

transcript is at

http://www.cdc.gov/od/oc/media/transcripts/t060420.htm

" For the first time ever, we have documented that people with CFS

have certain genes that are related to those parts of brain activity

that mediate the stress response.

And that they have different gene activity levels, this is outside

which genes are there, that are related to their body's ability to

adapt to challenges and stresses that occur throughout life, such as

infections, injury, trauma or various adverse events.

Why is it important? Well, knowing that there is now a biologic

basis for CFS will help us identify better ways to more effectively

diagnose the illness and to come up with more effective treatments,

including ***cognitive behavioral therapy***, medications or a

combination of both. "

>

> But there's already a fairly loaded use of language on his behalf at

> the press conference; compare his comments with Vernon's.

> I'm not interesting in attacking or defending Reeves, all I mean is

> that I'm far more interested in the results that come from the

> Kerr/Gow patients. If both of them manage to talk about their

results

> without mentioning CBT, I have more trust that they are talking

about

> the same disease I have. Not judging which is good science and which

> isn't, just which interests me more.

>

This list is intended for patients to share personal experiences with each

other, not to give medical advice. If you are interested in any treatment

discussed here, please consult your doctor.

April 25, 2006

> cort johnson wrote:

I think its more necessary to stop looking for the bad news - for

whats negative - for what reinforces CFS patients persistent belief

that the CDC or whoever is against them. <

" persistent belief " ?

Is that what you call it?

I could write an entire book in response to that, but it has already

been done.

-

April 25, 2006

>

> I think there are only about two or three sentences in the entire

press conference, out of how many? that could give people

pause.....The CDC again and again says 'biologic basis for CFS' -

but that

statement - which really is good to hear from an institution as

important at

this - unfortunately doesnt get as much press - not here anyway.

>

Hi Cort.

I've been reading the press conference transcript, the news articles,

Rich's post on the study and some of the papers themselves, and I am

trying to find the good news but I have found more that disturbs me

than makes me optimistic. For instance, here is a question and

answer about " the biologic basis for CFS " :

Our next question comes from Rikert from Congress Quarterly.

QUESTION: Thanks. I was curious whether you know anything about how

this particular genetic makeup that you identified as being

associated with the disease occurs.

Is this something that can occur through, you know, environmental

factors?

DR. REEVES: The genetic makeup--no. Our hypothesis that the HPA axis

is involved in this, which is very clear in this allostatic load, is

a physiologic marker of one's accumulated adaptation to stress.

The working hypothesis is that the HPA axis and the brain is a

plastic organ which changes its actual physical architecture

depending on stresses that are accumulated over the lifetime.

Tom again: What this seems to be saying to me is that we have

created the genetic differences by our response to stress, not vice

versa (i.e. the HPA axis and the brain is a platic organ which

changes its actual physical structure...)

So if you or Rich would like to explain to us in simple terms what

the overall good news is in a few sentences, not the details of the

studies, I'm sure many of us would appreciate it.

On another point, about the seeing the CDC as being against us,

remember Incline Village? Remember a few years ago when the CDC

diverted monies appropriated for CFS research to other projects and

then lied to Congress about it? I think that it is understandable

for some of us to be suspicious of the CDC. Yes I know that Dr.

Reeves was the whistleblower in that last incident, but I haven't

seen any major effort by the CDC to make ammends since then.

Tom

April 26, 2006

> I am

> trying to find the good news but I have found more that disturbs me

> than makes me optimistic.

I agree, and I don't think anyone's looking for the 'negative'. If

it's there, which it is, it deserves scrutiny. It's dangerous not to

approach it this way. You could apply the argument of looking for the

'positive' in something to anything, eg Wessely. I'm see hardly any

reactionary criticism of this, people are responding to what's there.

There may only be a couple of sentences there, but how many are they

out of sentences talking about treatment? And this is where I'm

extremely skeptical, about how this will be applied to development of

treatments.

We all know knowledge does not exist in a vacuum; I'm suspicious of

the paradigm under which this research was conducted, and suspicious

of its interpretation.

Erring on the side of skepticism does no harm and leaves the

possibility to change your mind when you see positive results, but

leaning toward optimism means not being vigilant about the possible

harm this could do.

Schweitzer's report elucidates my instincts that there is cause

for concern here. If anyone can debunk her points, I'd be happy to

listen, but right now this seems spot-on:

http://listserv.nodak.edu/cgi-bin/wa.exe?A2=ind0604d & L=co-cure & T=0 & P=3051

April 26, 2006

Hi, Tom.

Bill Reeve's response to this question wasn't very clear. There

were other questions to which he seemed to miss the point entirely.

I think he was probably under quite a bit of stress himself, during

the press conference! After all, Gerberding was involved,

too, and she's the boss at the CDC. In addition, my experience in

listening to Bill speak at conferences in the past is that he has a

way of selecting his words that tends to get people antagonized

sometimes. There have been a lot of misunderstandings. And

afterward, he honestly seems to be surprised that people took what

he said in a different way than he meant it. An example from the

past was the term " medically unexplained illnesses. " What he seemed

to actually mean was simply that so far the medical science

establishment had not yet figured these illnesses out. What some

people assumed he meant was that these illnesses could never be

explained medically, because they were " all in their heads. " My

impression at the time was that he really didn't mean that, but

there has been so much water under the bridge by now that he gets up

to speak with two strikes against him. Don't get me wrong. I think

that Bill probably does have some preconceived notions that aren't

totally correct, but don't we all?

Now, with regard to the particular question you asked about, Bill's

answer was " No, " and that was the correct answer. But then he went

on to say some other things that weren't expressed very clearly, and

some people got the impression that he was still addressing Rikert's

original question, but he wasn't. He was not talking about genes

when he got into their hypothesis about the HPA axis. What he meant

was that if a person has the particular genetic makeup that

influences their stress response system in the way that occurs in

CFS, and then that person is subjected to stress over an extended

period of time, their HPA axis components and parts of their brains

will actually be changed in response to the stress. He didn't

actually say this, but what I think he was referring to is that if

the cortisol level remains high for an extended time, it causes

changes in the cortisol receptors in parts of the brain such as the

hippocampus and the hypothalamus, and these changes can affect the

function of these parts. I discussed the hippocampal aspects in my

poster paper on glutathione depletion, which I think is involved in

the hippocampal changes.

I covered what I think the good news was in message number 96249,

which I will paste below:

I would like to make some comments about this CDC collaborative

work. One of the best things about it, in my view, is that some of

the researchers started looking at polymorphisms (also called SNPs

or genetic variations). I think this is where the real paydirt lies

in the genomics, not so much in gene expression, which has gotten

much of the attention up to now. The SNPs will help us to

understand root causes, so that we can try to address them.

I'm not sure yet whether these researchers looked at SNPs throughout

the whole 20,000 genes that were characerized, or whether it was

just a limited set of genes involved with the HPA axis and the

neurotransmitters. I expect that it was the latter, but I'll have

wait until I get the full papers to find outfor sure. There are

over 10 million different SNPs in the approximately 35,000 genes of

human genome.

In any case, both the groups who looked at SNPs found that SNPs in

the genes for neuronal tryptophan hydroxylase (TPH2) and nuclear

receptor subfamily 3, group C, member 1 glucocorticoid receptor

(NR3C1) are important in CFS. In addition, one group identified

SNPs in the gene for catechol-O-methyltransferase as being

important, and the other group identified SNPs in the genes for

proopiomelanocortin (POMC), monoamine oxidase A (MAOA) and monoamine

oxidase B (MAOB) as being important.

Why is this significant? Well first, some of these SNPs are in

genes that code for enzymes that are involved in the body's stress

response systems. We have known for a long time that a variety of

stressors (physical, chemical, biological and

psychological/emotional) are involved in the pre-onset of many cases

of CFS, and that was one of the things I emphasized in my 2004

poster paper on glutathione depletion in CFS:

http://www.cfsresearch.org/cfs/research/treatment/15.htm.

The fact that genes that code for enzymes involved with stress

response have significantly different mutations in PWCs than in

others is in line with these observations.

Second, others are involved with neurotransmitters, such as

serotonin and dopamine, and we have known for a long time that these

neurotransmitter levels are often abnormal in PWCs, too.

Third, two of these SNPs are part of the Economy Basic Panel offered

by Dr. Amy Yasko for studying autism, which I have emphasized that I

think also applies to CFS, namely the COMT and MAOA.

Third, one of the molecules involved, namely POMC, figures very

prominently in Dr. Ritchie Shoemaker's biotoxin pathway. It's

located in the hypothalamus, and among other things, it supplies

melanocyte stimulating hormone (MSH) and also ACTH, which drives the

secretion of cortisol.

The monoamine oxidases (MAOs) and COMT control the rate of breakdown

of neurotransmitters such as serotonin and dopamine.

Tryptophan hydroxylase (TPH2), also known as tryptophan 5-

monooxygenase, is the rate-controlling enzyme in the synthesis of

serotonin from tryptophan. Actually, it converts tryptophan to 5-HTP.

The glucocorticoid receptor is the receptor used by cortisol to

influence the nuclei of cells.

All in all, I think they are working in the right ballpark. I

suspect that if they had looked at genes associated with enzymes and

other proteins involved in the detox system and in the sulfur

metabolism, including the methylation cycle and the glutathione

system, and also in the immune system, they would have found some

more interesting SNPs.

I'm very happy to see that this work was done, and I expect that

there will be more work along these lines, hopefully looking at SNPs

in genes in these other suspect areas. I think this work will

provide the basis for understanding why there are subsets within the

CFS population as well.

Rich

--- In , " Tomcy6 " <tomcy6@...>

> Our next question comes from Rikert from Congress Quarterly.

> QUESTION: Thanks. I was curious whether you know anything about

how

> this particular genetic makeup that you identified as being

> associated with the disease occurs.

> Is this something that can occur through, you know, environmental

> factors?

> DR. REEVES: The genetic makeup--no. Our hypothesis that the HPA

axis

> is involved in this, which is very clear in this allostatic load,

is

> a physiologic marker of one's accumulated adaptation to stress.

> The working hypothesis is that the HPA axis and the brain is a

> plastic organ which changes its actual physical architecture

> depending on stresses that are accumulated over the lifetime.

>

> Tom again: What this seems to be saying to me is that we have

> created the genetic differences by our response to stress, not

vice

> versa (i.e. the HPA axis and the brain is a platic organ which

> changes its actual physical structure...)

>

> So if you or Rich would like to explain to us in simple terms what

> the overall good news is in a few sentences, not the details of

the

> studies, I'm sure many of us would appreciate it.

> Tom

>

April 26, 2006

The British studies into CBT used very woolly criteria for admitting

patients to the trial. Unless very specific criteria (such as the

Canadian Guidelines) are used, I feel the conclusions made are

valueless.

Rosie

Thanks. I dont know how I missed that. Its too bad its in there. Most

of the studies do show CBT is helpful for some CFS patients but I dont

think anybody thinks its a cure. i dont know how a behaviioral

intervention is enhanced by finding a biological basis for CFS (???).

Perhaps it has to do with managing the stress response - I dont know.

.

<christine.emmanuel@...> wrote:

" Well, knowing that there is now a biologic basis for

CFS will help us identify better ways to more effectively diagnose the

illness and to come up with more effective treatments, including

cognitive behavioral therapy, medications or a combination of both. "

http://listserv.nodak.edu/cgi-bin/wa.exe?A2=ind0604d & L=co-cure & T=0 & P=317

>

> THe three studies are very different. The CDC study is far more

complex and ambitious but the Kerr study really focused on immune

genes I believe. The CDC had a large gene set to be sure but their

other laboratory measures were almost entirely focused on the

neuroendocrine system not the immune system - so perhaps its not

surprising we're not hearing about immune stuff.

>

> While I did find the reference to the UK I still have yet to find

any reference to CBT in the briefing, by the way.

>

This list is intended for patients to share personal experiences with

each other, not to give medical advice. If you are interested in any

treatment discussed here, please consult your doctor.

April 26, 2006

Hello Rich,

With all due respect, I hardly think B/W Reeves is the victim here. A number of

things he is quoted as saying are pretty clear, and not good news for our

healing.

The only treatment I saw that he finds as a promising result of these studies is

Cognitive Behavioral Therapy and " medications " . This is the party line of CFS

Psychologizers for many years now. And usually is accompanied by GET (Graded

Exercise Therapy), capable of causing severe damage to ME/CFS patients,

including children. And in the CFS/ME Clinics in the UK, increasingly forced on

sufferers in order to continue their benefits neede for survival.

I did not hear the Press Conference or read every word, or every paper. I do

find it extremely curious (make that...disturbing) that even the press itself

was not given access to all of the studies in time to read them before going to

press with the big Global " Announcement " .

Reeves has never been seen by advocates as a friend to the CFS

Community,but quite the opposite. This is based on quotes and attitudes

eye-witnessed and straight from

the horses mouth (his) by many.

And includes a personal friend of mine, who was the founder of a National

Organization for families of Gulf War veterans with GWS.

She told me that she heard Reeves, speaking on a GWS panel in Houston in

the 90s state adamantly that CFS is not a real disease.

Dumbfounded at the time, I asked her several times to repeat that and was she

positive. Yes, yes, and yes, was the answer.

There are numerous people with much (and repeated) experience with him that can

state all of his CDC/ CFS history in more detail than I.

You say that when he gets up to speak on CFS, he has " 2 strikes " against him.

Are you blaming patients for that?

My experience with the phrase " 2 strikes " is

A) Baseball...the Batter misses the ball...twice...once more and he/she is OUT.

Ca Criminal Justice System...Person has committed 2 major felonies...a 3rd

will send them to prison for Life.

Katrina

>

> Hi, Tom.

>

> Bill Reeve's response to this question wasn't very clear. There

> were other questions to which he seemed to miss the point entirely.

> I think he was probably under quite a bit of stress himself, during

> the press conference! After all, Gerberding was involved,

> too, and she's the boss at the CDC. In addition, my experience in

> listening to Bill speak at conferences in the past is that he has a

> way of selecting his words that tends to get people antagonized

> sometimes. There have been a lot of misunderstandings. And

> afterward, he honestly seems to be surprised that people took what

> he said in a different way than he meant it. An example from the

> past was the term " medically unexplained illnesses. " What he seemed

> to actually mean was simply that so far the medical science

> establishment had not yet figured these illnesses out. What some

> people assumed he meant was that these illnesses could never be

> explained medically, because they were " all in their heads. " My

> impression at the time was that he really didn't mean that, but

> there has been so much water under the bridge by now that he gets up

> to speak with two strikes against him. Don't get me wrong. I think

> that Bill probably does have some preconceived notions that aren't

> totally correct, but don't we all?

>

> Now, with regard to the particular question you asked about, Bill's

> answer was " No, " and that was the correct answer. But then he went

> on to say some other things that weren't expressed very clearly, and

> some people got the impression that he was still addressing Rikert's

> original question, but he wasn't. He was not talking about genes

> when he got into their hypothesis about the HPA axis. What he meant

> was that if a person has the particular genetic makeup that

> influences their stress response system in the way that occurs in

> CFS, and then that person is subjected to stress over an extended

> period of time, their HPA axis components and parts of their brains

> will actually be changed in response to the stress. He didn't

> actually say this, but what I think he was referring to is that if

> the cortisol level remains high for an extended time, it causes

> changes in the cortisol receptors in parts of the brain such as the

> hippocampus and the hypothalamus, and these changes can affect the

> function of these parts. I discussed the hippocampal aspects in my

> poster paper on glutathione depletion, which I think is involved in

> the hippocampal changes.

>

> I covered what I think the good news was in message number 96249,

> which I will paste below:

>

> I would like to make some comments about this CDC collaborative

> work. One of the best things about it, in my view, is that some of

> the researchers started looking at polymorphisms (also called SNPs

> or genetic variations). I think this is where the real paydirt lies

> in the genomics, not so much in gene expression, which has gotten

> much of the attention up to now. The SNPs will help us to

> understand root causes, so that we can try to address them.

>

> I'm not sure yet whether these researchers looked at SNPs throughout

> the whole 20,000 genes that were characerized, or whether it was

> just a limited set of genes involved with the HPA axis and the

> neurotransmitters. I expect that it was the latter, but I'll have

> wait until I get the full papers to find outfor sure. There are

> over 10 million different SNPs in the approximately 35,000 genes of

> human genome.

>

> In any case, both the groups who looked at SNPs found that SNPs in

> the genes for neuronal tryptophan hydroxylase (TPH2) and nuclear

> receptor subfamily 3, group C, member 1 glucocorticoid receptor

> (NR3C1) are important in CFS. In addition, one group identified

> SNPs in the gene for catechol-O-methyltransferase as being

> important, and the other group identified SNPs in the genes for

> proopiomelanocortin (POMC), monoamine oxidase A (MAOA) and monoamine

> oxidase B (MAOB) as being important.

>

> Why is this significant? Well first, some of these SNPs are in

> genes that code for enzymes that are involved in the body's stress

> response systems. We have known for a long time that a variety of

> stressors (physical, chemical, biological and

> psychological/emotional) are involved in the pre-onset of many cases

> of CFS, and that was one of the things I emphasized in my 2004

> poster paper on glutathione depletion in CFS:

>

> http://www.cfsresearch.org/cfs/research/treatment/15.htm.

>

> The fact that genes that code for enzymes involved with stress

> response have significantly different mutations in PWCs than in

> others is in line with these observations.

>

> Second, others are involved with neurotransmitters, such as

> serotonin and dopamine, and we have known for a long time that these

> neurotransmitter levels are often abnormal in PWCs, too.

>

> Third, two of these SNPs are part of the Economy Basic Panel offered

> by Dr. Amy Yasko for studying autism, which I have emphasized that I

> think also applies to CFS, namely the COMT and MAOA.

>

> Third, one of the molecules involved, namely POMC, figures very

> prominently in Dr. Ritchie Shoemaker's biotoxin pathway. It's

> located in the hypothalamus, and among other things, it supplies

> melanocyte stimulating hormone (MSH) and also ACTH, which drives the

> secretion of cortisol.

>

> The monoamine oxidases (MAOs) and COMT control the rate of breakdown

> of neurotransmitters such as serotonin and dopamine.

>

> Tryptophan hydroxylase (TPH2), also known as tryptophan 5-

> monooxygenase, is the rate-controlling enzyme in the synthesis of

> serotonin from tryptophan. Actually, it converts tryptophan to 5-HTP.

>

> The glucocorticoid receptor is the receptor used by cortisol to

> influence the nuclei of cells.

>

> All in all, I think they are working in the right ballpark. I

> suspect that if they had looked at genes associated with enzymes and

> other proteins involved in the detox system and in the sulfur

> metabolism, including the methylation cycle and the glutathione

> system, and also in the immune system, they would have found some

> more interesting SNPs.

>

> I'm very happy to see that this work was done, and I expect that

> there will be more work along these lines, hopefully looking at SNPs

> in genes in these other suspect areas. I think this work will

> provide the basis for understanding why there are subsets within the

> CFS population as well.

>

> Rich

>

> --- In , " Tomcy6 " <tomcy6@>

>

> > Our next question comes from Rikert from Congress Quarterly.

> > QUESTION: Thanks. I was curious whether you know anything about

> how

> > this particular genetic makeup that you identified as being

> > associated with the disease occurs.

> > Is this something that can occur through, you know, environmental

> > factors?

> > DR. REEVES: The genetic makeup--no. Our hypothesis that the HPA

> axis

> > is involved in this, which is very clear in this allostatic load,

> is

> > a physiologic marker of one's accumulated adaptation to stress.

> > The working hypothesis is that the HPA axis and the brain is a

> > plastic organ which changes its actual physical architecture

> > depending on stresses that are accumulated over the lifetime.

> >

> > Tom again: What this seems to be saying to me is that we have

> > created the genetic differences by our response to stress, not

> vice

> > versa (i.e. the HPA axis and the brain is a platic organ which

> > changes its actual physical structure...)

> >

> > So if you or Rich would like to explain to us in simple terms what

> > the overall good news is in a few sentences, not the details of

> the

> > studies, I'm sure many of us would appreciate it.

>

> > Tom

> >

>

April 26, 2006

God knows I'm not a expert on CBT. I'm sure there have been problems with the

studies - those that used the Oxford criteria are bad I'm sure - but there have

been quite a few studies now, I dont think they can all be bad, and why CBT

would work in AIDS patients (to raise their immune measures) and heart patients

and kidney dialysis patients and not CFS patients - I dont know. I know it

worsens some patients but I think people with more moderate CFS can probably be

helped by it.

We're also dealing with a different context in the US than in the UK; there is

a good deal of government sponsored research into CFS pathophysiology, they

psychological interpretation that dominates governmental reserach there is not

as prevalent here. We dont have to worry as much about CBT here - perhaps thats

why it doesnt bother me so much.

I was incredibly helped by a transformational program called EST in the early

1990's. I assume its kind like a very intensive CBT program. It enabled and

still does enable people to get their attention off their 'story' and their

thoughts and feelings. Nobody expects to have their health, job, career etc

taken from, everyone expects to be healthy etc. - to all of a sudden have that

taken away for no reason is a gut wrenching experience - nobody's prepared for

it., nobody deals with it well I'm -its a tough row to hoe. All sorts of well

people came out of that program with increased vitality and so did I, suffering

on my bed with CFS. I want to acknowledge that my case of CFS is much more

moderate than some of those on this list.

One of our real champions for two decades now, Klimas, says CBT helps

her patients and the woman who wrote Seabiscuit said she got help from it. If

the CDC's conclusion was that CFS was a behavioral disorder characterized by

poor coping and that CBT was the only appropriate treatment for it I would be

all over them. THey didnt say that though - they did a huge study that

concentrated mostly on biological factors, they said they had evidence that CFS

was a real disease but then someone mentioned CBT once or twice and some people

just went nuts - an inappropriate response I believe.

I dont think the study was perfect; in a perfect world I would have had some

different investigators and I would have focused more on the immune system. I

wouldnt have had idiopathic fatigue patients in there but those are all judgment

calls. I havent read them but I think theres probably ALOT more bad than good

in these papers and that in the end they will probably be an asset to us all.

Thats my opinion!

Rosie <rosiecox@...> wrote:

The British studies into CBT used very woolly criteria for admitting

patients to the trial. Unless very specific criteria (such as the

Canadian Guidelines) are used, I feel the conclusions made are

valueless.

Rosie

Thanks. I dont know how I missed that. Its too bad its in there. Most

of the studies do show CBT is helpful for some CFS patients but I dont

think anybody thinks its a cure. i dont know how a behaviioral

intervention is enhanced by finding a biological basis for CFS (???).

Perhaps it has to do with managing the stress response - I dont know.

.

<christine.emmanuel@...> wrote:

" Well, knowing that there is now a biologic basis for

CFS will help us identify better ways to more effectively diagnose the

illness and to come up with more effective treatments, including

cognitive behavioral therapy, medications or a combination of both. "

http://listserv.nodak.edu/cgi-bin/wa.exe?A2=ind0604d & L=co-cure & T=0 & P=317

>

> THe three studies are very different. The CDC study is far more

complex and ambitious but the Kerr study really focused on immune

genes I believe. The CDC had a large gene set to be sure but their

other laboratory measures were almost entirely focused on the

neuroendocrine system not the immune system - so perhaps its not

surprising we're not hearing about immune stuff.

>

> While I did find the reference to the UK I still have yet to find

any reference to CBT in the briefing, by the way.

>

This list is intended for patients to share personal experiences with

each other, not to give medical advice. If you are interested in any

treatment discussed here, please consult your doctor.

April 26, 2006

Hi, Katrina.

Your points are well taken. I'm certainly not going to defend

everything Bill Reeves has said and done. However, I do think that

their decision to look at the genetics over the past few years has

been a good one, particularly the polymorphisms. I do hope that

they extend their search to polymorphisms in enzymes that affect

other systems involved in the early pathogenesis of CFS, as I have

said.

No, I'm certainly not blaming the patients for the negative bias

that I think often prevails against Bill Reeves when he stands up to

talk publicly about CFS. I don't totally blame him for it, either,

though. He inherited some history at the CDC that he did not have

control over, and he has a bureaucracy in which he has to work. As

I've said, I don't think his choice of words is always the best, and

when there is uncertainty about what he is saying, which is often

the case because it is not clearly expressed, there is a wide

tendency to interpret his remarks in a way that suggests that he is

a bit of an ogre, because of all the past history of CFS at the

CDC. I think it should be remembered that Bill Reeves was the

whistle blower on the CDC management about the misappropriation of

CFS research funds a few years ago. I think that took a lot of guts.

What is very remarkable to me is that he landed on his feet. That's

pretty unusual for whistle blowers in the government. Usually

that's the end of their career. I have some experience with this

type of thing, having worked in government-related institutions

during all of my career.

Concerning CFS not being a " real disease, " again, strictly speaking,

that's true from the standpoint of the way the term " disease " is

defined at the CDC. CFS is a syndrome, or collection of symptoms.

In order to be classified as a disease, it needs to be better

understood, in terms of at least a clearer means of diagnosis, if

not a better understanding of causes. I think it is likely that the

current CFS case definition actually includes more than one disease,

but they aren't well enough defined yet to be separated out. The

problem with him saying that it isn't a " real disease " is that this

can be interpreted more than one way. With the negative bias that

results from the unfortunate history, many people take that to mean

that he's saying that it doesn't really exist in terms of an organic

or physiological condition, and so it must then be " all in their

heads. " I didn't hear exactly what Bill Reeves said in Houston, but

I suspect that he didn't actually mean that CFS doesn't exist as a

physiological or organic condition. I think he was speaking in

terms of classification as a syndrome rather than as a disease at

present.

At the Wisconsin AACFS conference in 2004, Bill Reeves spoke

candidly about the manner in which the CFS case definition was

developed. I quoted him exactly in my review of that meeting. In

particular, he referred to a bunch of guys sitting around in a smoke-

filled room, and then he caught himself and said, " Well, we weren't

actually smoking--this was at the CDC. " Do you get what I mean? He

should have worded that differently when he first said it. By the

time he corrected himself, people already had a visual image that

they would not forget, and it was not favorable. Now I'm not going

to defend the manner in which the case definition was developed, but

the process could have been described in a less tawdry light.

Honestly, when I have heard him speak, I've always been struck by

his unfortunate choice of words, and I've always thought to

myself, " Bill, do you have any idea how this sounds to people who

have CFS and who are already very suspicious of you? " He needs to

qualify what he says and use a few more words, so that he can take

out the uncertainty about what he is saying, and head off the

consequent tendency of people to choose a negative slant, which

results from the unfortunate history of CFS.

Well, I don't want to continue to be Bill Reeves's apologist, but I

don't believe he is the bete noire that many people seem to believe

he is.

Rich

> >

> > Hi, Tom.

> >

> > Bill Reeve's response to this question wasn't very clear. There

> > were other questions to which he seemed to miss the point

entirely.

> > I think he was probably under quite a bit of stress himself,

during

> > the press conference! After all, Gerberding was involved,

> > too, and she's the boss at the CDC. In addition, my experience

in

> > listening to Bill speak at conferences in the past is that he

has a

> > way of selecting his words that tends to get people antagonized

> > sometimes. There have been a lot of misunderstandings. And

> > afterward, he honestly seems to be surprised that people took

what

> > he said in a different way than he meant it. An example from

the

> > past was the term " medically unexplained illnesses. " What he

seemed

> > to actually mean was simply that so far the medical science

> > establishment had not yet figured these illnesses out. What

some

> > people assumed he meant was that these illnesses could never be

> > explained medically, because they were " all in their heads. " My

> > impression at the time was that he really didn't mean that, but

> > there has been so much water under the bridge by now that he

gets up

> > to speak with two strikes against him. Don't get me wrong. I

think

> > that Bill probably does have some preconceived notions that

aren't

> > totally correct, but don't we all?

> >

> > Now, with regard to the particular question you asked about,

Bill's

> > answer was " No, " and that was the correct answer. But then he

went

> > on to say some other things that weren't expressed very clearly,

and

> > some people got the impression that he was still addressing

Rikert's

> > original question, but he wasn't. He was not talking about

genes

> > when he got into their hypothesis about the HPA axis. What he

meant

> > was that if a person has the particular genetic makeup that

> > influences their stress response system in the way that occurs

in

> > CFS, and then that person is subjected to stress over an

extended

> > period of time, their HPA axis components and parts of their

brains

> > will actually be changed in response to the stress. He didn't

> > actually say this, but what I think he was referring to is that

if

> > the cortisol level remains high for an extended time, it causes

> > changes in the cortisol receptors in parts of the brain such as

the

> > hippocampus and the hypothalamus, and these changes can affect

the

> > function of these parts. I discussed the hippocampal aspects in

my

> > poster paper on glutathione depletion, which I think is involved

in

> > the hippocampal changes.

> >

> > I covered what I think the good news was in message number

96249,

> > which I will paste below:

> >

> > I would like to make some comments about this CDC collaborative

> > work. One of the best things about it, in my view, is that some

of

> > the researchers started looking at polymorphisms (also called

SNPs

> > or genetic variations). I think this is where the real paydirt

lies

> > in the genomics, not so much in gene expression, which has gotten

> > much of the attention up to now. The SNPs will help us to

> > understand root causes, so that we can try to address them.

> >

> > I'm not sure yet whether these researchers looked at SNPs

throughout

> > the whole 20,000 genes that were characerized, or whether it was

> > just a limited set of genes involved with the HPA axis and the

> > neurotransmitters. I expect that it was the latter, but I'll

have

> > wait until I get the full papers to find outfor sure. There are

> > over 10 million different SNPs in the approximately 35,000 genes

of

> > human genome.

> >

> > In any case, both the groups who looked at SNPs found that SNPs

in

> > the genes for neuronal tryptophan hydroxylase (TPH2) and nuclear

> > receptor subfamily 3, group C, member 1 glucocorticoid receptor

> > (NR3C1) are important in CFS. In addition, one group identified

> > SNPs in the gene for catechol-O-methyltransferase as being

> > important, and the other group identified SNPs in the genes for

> > proopiomelanocortin (POMC), monoamine oxidase A (MAOA) and

monoamine

> > oxidase B (MAOB) as being important.

> >

> > Why is this significant? Well first, some of these SNPs are in

> > genes that code for enzymes that are involved in the body's

stress

> > response systems. We have known for a long time that a variety

of

> > stressors (physical, chemical, biological and

> > psychological/emotional) are involved in the pre-onset of many

cases

> > of CFS, and that was one of the things I emphasized in my 2004

> > poster paper on glutathione depletion in CFS:

> >

> > http://www.cfsresearch.org/cfs/research/treatment/15.htm.

> >

> > The fact that genes that code for enzymes involved with stress

> > response have significantly different mutations in PWCs than in

> > others is in line with these observations.

> >

> > Second, others are involved with neurotransmitters, such as

> > serotonin and dopamine, and we have known for a long time that

these

> > neurotransmitter levels are often abnormal in PWCs, too.

> >

> > Third, two of these SNPs are part of the Economy Basic Panel

offered

> > by Dr. Amy Yasko for studying autism, which I have emphasized

that I

> > think also applies to CFS, namely the COMT and MAOA.

> >

> > Third, one of the molecules involved, namely POMC, figures very

> > prominently in Dr. Ritchie Shoemaker's biotoxin pathway. It's

> > located in the hypothalamus, and among other things, it supplies

> > melanocyte stimulating hormone (MSH) and also ACTH, which drives

the

> > secretion of cortisol.

> >

> > The monoamine oxidases (MAOs) and COMT control the rate of

breakdown

> > of neurotransmitters such as serotonin and dopamine.

> >

> > Tryptophan hydroxylase (TPH2), also known as tryptophan 5-

> > monooxygenase, is the rate-controlling enzyme in the synthesis of

> > serotonin from tryptophan. Actually, it converts tryptophan to 5-

HTP.

> >

> > The glucocorticoid receptor is the receptor used by cortisol to

> > influence the nuclei of cells.

> >

> > All in all, I think they are working in the right ballpark. I

> > suspect that if they had looked at genes associated with enzymes

and

> > other proteins involved in the detox system and in the sulfur

> > metabolism, including the methylation cycle and the glutathione

> > system, and also in the immune system, they would have found some

> > more interesting SNPs.

> >

> > I'm very happy to see that this work was done, and I expect that

> > there will be more work along these lines, hopefully looking at

SNPs

> > in genes in these other suspect areas. I think this work will

> > provide the basis for understanding why there are subsets within

the

> > CFS population as well.

> >

> > Rich

> >

> > --- In , " Tomcy6 " <tomcy6@>

> >

> > > Our next question comes from Rikert from Congress

Quarterly.

> > > QUESTION: Thanks. I was curious whether you know anything

about

> > how

> > > this particular genetic makeup that you identified as being

> > > associated with the disease occurs.

> > > Is this something that can occur through, you know,

environmental

> > > factors?

> > > DR. REEVES: The genetic makeup--no. Our hypothesis that the

HPA

> > axis

> > > is involved in this, which is very clear in this allostatic

load,

> > is

> > > a physiologic marker of one's accumulated adaptation to stress.

> > > The working hypothesis is that the HPA axis and the brain is a

> > > plastic organ which changes its actual physical architecture

> > > depending on stresses that are accumulated over the lifetime.

> > >

> > > Tom again: What this seems to be saying to me is that we have

> > > created the genetic differences by our response to stress, not

> > vice

> > > versa (i.e. the HPA axis and the brain is a platic organ

which

> > > changes its actual physical structure...)

> > >

> > > So if you or Rich would like to explain to us in simple terms

what

> > > the overall good news is in a few sentences, not the details

of

> > the

> > > studies, I'm sure many of us would appreciate it.

> >

> > > Tom

> > >

> >

>

April 26, 2006

Yes we must be vigilant. Theres been so much negative stuff written about this

report , however, that I have felt bound to point out there are positives as

well. I did reply to 's report in a recent e-mail.

<christine.emmanuel@...> wrote: > I am