Re: Latest Dubbo results and glutathione depletion--methylation cycle block hypothes

[Guest guest]

Rich

I don't know if your paying attention to what is the best treatment

for cfs/fibro? I think the polls kept showing the hydration salts

blasi/salt C where the best treatments out there.. for the past 10

years plus IV glutathiones been done till the cows come home ..But if

your missing the dehydration, come low blood volume aspect of

possible glutathione depletion, you may as well send me a copy of

that last article in brail as well.

I don't think you payed too much attention to what Ken was

describing got him well on the experimental list.. it sounded like-

fix the coagulation and take antimicrobials. Your allowing people to

follow you up a garden path which may mean many will get so diseased

there's no road back, so what you do is foolish without taking the

whole picture into consideration.Remember also, many supplements and

medicines may benefit you from the fact that they are suspended in

potassium salts rather than there active ingredients.cheers

>

> Hi, all.

>

> Today another paper from the Dubbo, Australia, infection outcomes

> study was published (Hickie, I, et al., " Post-infective and chronic

> fatigue syndromes precipitated by viral and non-viral pathogens:

> preospective cohort study, " BMJ,doi:10.1136/bmj.38933.585764.AE).

>

> As you may know, this study is involved with following people who

> develop infectious diseases over time to try to understand why some

> of them do not recover, but instead continue to be ill with a

> disorder that meets the criteria of chronic fatigue syndrome.

>

> This paper compared the percentage of people who had cases of

> mononucleosis (glandular fever), Q fever, and Ross River virus,

> respectively, who later met the criteria for chronic fatigue

> syndrome. It's interesting to note that Q fever is caused by an

> intracellular bacterium, while the other two are viral diseases.

>

> The authors found that the percentage who went on to have CFS was

> the same for the three infectious diseases (11% at 6 months). This

> common result is very significant, because it suggests that the

> reason these people develop CFS is not associated with the

> particular pathogen, but rather with their host response.

>

> Here's a quotation from the paper: " Examination of outcomes after

> the three distinctive acute infections reported here strongly

> implicates aspects of the host response to infection (rather than

> the pathogen itself) as the likely determinants of post-infective

> fatigue syndrome, as the case rates after infection with Epstein--

> Barr virus (a DNA virus), Ross River virus (an RNA virus), and C.

> burnetii (an intracellular bacterium) were comparable, and the

> symptom characteristics progressively merged over time. "

>

> I would like to submit that this is the type of result that would

be

> predicted by the glutathione depletion--methylation cycle block

> hypothesis for the pathogenesis of chronic fatigue syndrome. This

> hypothesis holds that CFS onset is caused by a combination of a

> genetic predisposition (a set of polymorphisms) that particular

> people are born with, and a sufficient load of stressors to lower

> the glutathione level enough to trigger a vicious circle mechanism,

> involving the methylation cycle, and facilitated by the genetic

> predisposition. One of the classes of possible stressors is the

> biological stressors, and infectious agents are one category of

> these biological stressors. According to this model, it does not

> matter what the particular infectious agent is. What matters is

> whether the infection (combined with any other stressors that might

> be present in the particular person) is sufficient to lower the

> glutathione level enough to trigger the vicious circle mechanism.

> It seems clear that the results of this study confirm that this is

> the way onset of CFS behaves when triggered by pathogens.

>

> Please note that this study does not tell us what needs to be done

> for treatment, only what the characteristics are of the category of

> CFS that is post-infectious in origin.

>

> Rich

>

[Guest guest]

Rich,

Ian Hickie is a psychiatrist (of the nastiest kind) who's been set for decades on proving CFS is a psychiatric condition (a kind of Australian Wessely if you like). If he puts his name on a study it is to "prove" that pathogens are not important in the aetiology of CFS. The next step in his reasoning has been the same for years, i e CFS hits the psychiatricly weak and the pathogens are only triggers. You on the other hand will say "it's the glutathione and the "vicious circle mechanism, involving the methylation cycle, and facilitated by the genetic predisposition. ".

I have no way of assessing whether you're right re glutathione depletion being at the root of much of our probs, but I certainly know that I would not go down ANY path with Ian Hickie!!

Nelly

[infections] Latest Dubbo results and glutathione depletion--methylation cycle block hypothes

Hi, all.Today another paper from the Dubbo, Australia, infection outcomes study was published (Hickie, I, et al.,"Post-infective and chronic fatigue syndromes precipitated by viral and non-viral pathogens: preospective cohort study," BMJ,doi:10.1136/bmj.38933.585764.AE).As you may know, this study is involved with following people who develop infectious diseases over time to try to understand why some of them do not recover, but instead continue to be ill with a disorder that meets the criteria of chronic fatigue syndrome.This paper compared the percentage of people who had cases of mononucleosis (glandular fever), Q fever, and Ross River virus, respectively, who later met the criteria for chronic fatigue syndrome. It's interesting to note that Q fever is caused by an intracellular bacterium, while the other two are viral diseases.The authors found that the percentage who went on to have CFS was the same for the three infectious diseases (11% at 6 months). This common result is very significant, because it suggests that the reason these people develop CFS is not associated with the particular pathogen, but rather with their host response. Here's a quotation from the paper: "Examination of outcomes after the three distinctive acute infections reported here strongly implicates aspects of the host response to infection (rather than the pathogen itself) as the likely determinants of post-infective fatigue syndrome, as the case rates after infection with Epstein--Barr virus (a DNA virus), Ross River virus (an RNA virus), and C. burnetii (an intracellular bacterium) were comparable, and the symptom characteristics progressively merged over time."I would like to submit that this is the type of result that would be predicted by the glutathione depletion--methylation cycle block hypothesis for the pathogenesis of chronic fatigue syndrome. This hypothesis holds that CFS onset is caused by a combination of a genetic predisposition (a set of polymorphisms) that particular people are born with, and a sufficient load of stressors to lower the glutathione level enough to trigger a vicious circle mechanism, involving the methylation cycle, and facilitated by the genetic predisposition. One of the classes of possible stressors is the biological stressors, and infectious agents are one category of these biological stressors. According to this model, it does not matter what the particular infectious agent is. What matters is whether the infection (combined with any other stressors that might be present in the particular person) is sufficient to lower the glutathione level enough to trigger the vicious circle mechanism. It seems clear that the results of this study confirm that this is the way onset of CFS behaves when triggered by pathogens.Please note that this study does not tell us what needs to be done for treatment, only what the characteristics are of the category of CFS that is post-infectious in origin.Rich

[Guest guest]

Hi, Nelly.

Yes, I'm aware of some of the positions that Dr. Hickie has taken on

CFS in the past. However, I would like to cite some specific

quotations from this new study, of which he is the lead author:

" Importantly, premorbid and intercurrent psychiatric disorder did

not show predictive power for post-infective fatigue syndrome at any

time point. "

" Severity of the acute illness, and not demographic or psychological

factors, was predictive of post-infective fatigue syndrome. "

There is no mention of cognitive behavioral therapy or graded

exercise therapy in this paper at all.

Maybe it's time to give Dr. Hickie another chance.

Rich

>

> Rich,

>

> Ian Hickie is a psychiatrist (of the nastiest kind) who's been set

for decades on proving CFS is a psychiatric condition (a kind of

Australian Wessely if you like). If he puts his name on a study it

is to " prove " that pathogens are not important in the aetiology of

CFS. The next step in his reasoning has been the same for years, i e

CFS hits the psychiatricly weak and the pathogens are only triggers.

You on the other hand will say " it's the glutathione and

the " vicious circle mechanism, involving the methylation cycle, and

facilitated by the genetic predisposition. " .

>

> I have no way of assessing whether you're right re glutathione

depletion being at the root of much of our probs, but I certainly

know that I would not go down ANY path with Ian Hickie!!

>

> Nelly

> [infections] Latest Dubbo results and

glutathione depletion--methylation cycle block hypothes

>

>

> Hi, all.

>

> Today another paper from the Dubbo, Australia, infection

outcomes

> study was published (Hickie, I, et al., " Post-infective and

chronic

> fatigue syndromes precipitated by viral and non-viral pathogens:

> preospective cohort study, " BMJ,doi:10.1136/bmj.38933.585764.AE).

>

> As you may know, this study is involved with following people

who

> develop infectious diseases over time to try to understand why

some

> of them do not recover, but instead continue to be ill with a

> disorder that meets the criteria of chronic fatigue syndrome.

>

> This paper compared the percentage of people who had cases of

> mononucleosis (glandular fever), Q fever, and Ross River virus,

> respectively, who later met the criteria for chronic fatigue

> syndrome. It's interesting to note that Q fever is caused by an

> intracellular bacterium, while the other two are viral diseases.

>

> The authors found that the percentage who went on to have CFS

was

> the same for the three infectious diseases (11% at 6 months).

This

> common result is very significant, because it suggests that the

> reason these people develop CFS is not associated with the

> particular pathogen, but rather with their host response.

>

> Here's a quotation from the paper: " Examination of outcomes

after

> the three distinctive acute infections reported here strongly

> implicates aspects of the host response to infection (rather

than

> the pathogen itself) as the likely determinants of post-

infective

> fatigue syndrome, as the case rates after infection with Epstein-

-

> Barr virus (a DNA virus), Ross River virus (an RNA virus), and

C.

> burnetii (an intracellular bacterium) were comparable, and the

> symptom characteristics progressively merged over time. "

>

> I would like to submit that this is the type of result that

would be

> predicted by the glutathione depletion--methylation cycle block

> hypothesis for the pathogenesis of chronic fatigue syndrome.

This

> hypothesis holds that CFS onset is caused by a combination of a

> genetic predisposition (a set of polymorphisms) that particular

> people are born with, and a sufficient load of stressors to

lower

> the glutathione level enough to trigger a vicious circle

mechanism,

> involving the methylation cycle, and facilitated by the genetic

> predisposition. One of the classes of possible stressors is the

> biological stressors, and infectious agents are one category of

> these biological stressors. According to this model, it does not

> matter what the particular infectious agent is. What matters is

> whether the infection (combined with any other stressors that

might

> be present in the particular person) is sufficient to lower the

> glutathione level enough to trigger the vicious circle

mechanism.

> It seems clear that the results of this study confirm that this

is

> the way onset of CFS behaves when triggered by pathogens.

>

> Please note that this study does not tell us what needs to be

done

> for treatment, only what the characteristics are of the category

of

> CFS that is post-infectious in origin.

>

> Rich

>

[Guest guest]

Hi, Tony.

Yes, the hydration salts have helped quite a few people, I think

particularly those with fibromyalgia. This treatment hasn't been so

good for many PWCs, though. It may be that those with the ACE

deletion polymorphism already have a problem with too much sodium

retention, because of the higher aldosterone this polymorphism

causes. In any case, I don't think people are finding these salts

to be a cure, but only a help in improving the quality of life.

That's certainly important, but I want to find root causes and

achieve cures.

With regard to IV glutathione infusions, I agree that that is also

temporarily helpful for some, but doesn't usually break the vicious

circle so that glutathione comes up and stays up permanently at a

normal level. I don't know if you've been following closely what

I've been saying lately, but it amounts to going after the root

causes of the vicious circle. If a person fixes those, the

glutathione will come back up automatically. That's where the

genetic testing and targeted treatments with supplements to bypass

genetic problems at the biochemical level come in.

It looks to me as though the low blood volume, a consequence of

the " mild " diabetes insipidus in many PWCs, is actually caused by

glutathione depletion as well. We've had a couple of cases of

people whose dehydration went away when they built their

glutahione. I suspect that the mechanism is that antidiuretic

hormone (ADH), being a secretory protein that incorporates

disulfides in its structure, requires glutathione for its correct

synthesis in the cells of the hypothalamus. When glutathione is low

there, the cells can't make enough ADH, and that causes the kidneys

to dump more water into the urine than they should, producing

dehydration and low blood volume.

Yes, genetic problems in the coagulation proteins are definitely an

issue for a subset of PWCs, and when that is the case, it is

important to deal with it, as Ken did.

Yes, potassium depletion can be a problem as well, and it also needs

to be dealt with. There was some good work in Australia on potassium

in CFS.

Well, I certainly hope I'm not leading people to their destruction,

Tony. That's definitely not my goal. I do think we need to keep

our eyes open to the possibility of various subsets. One size

doesn't fit all.

Rich

> >

> > Hi, all.

> >

> > Today another paper from the Dubbo, Australia, infection

outcomes

> > study was published (Hickie, I, et al., " Post-infective and

chronic

> > fatigue syndromes precipitated by viral and non-viral pathogens:

> > preospective cohort study, " BMJ,doi:10.1136/bmj.38933.585764.AE).

> >

> > As you may know, this study is involved with following people

who

> > develop infectious diseases over time to try to understand why

some

> > of them do not recover, but instead continue to be ill with a

> > disorder that meets the criteria of chronic fatigue syndrome.

> >

> > This paper compared the percentage of people who had cases of

> > mononucleosis (glandular fever), Q fever, and Ross River virus,

> > respectively, who later met the criteria for chronic fatigue

> > syndrome. It's interesting to note that Q fever is caused by an

> > intracellular bacterium, while the other two are viral diseases.

> >

> > The authors found that the percentage who went on to have CFS

was

> > the same for the three infectious diseases (11% at 6 months).

This

> > common result is very significant, because it suggests that the

> > reason these people develop CFS is not associated with the

> > particular pathogen, but rather with their host response.

> >

> > Here's a quotation from the paper: " Examination of outcomes

after

> > the three distinctive acute infections reported here strongly

> > implicates aspects of the host response to infection (rather

than

> > the pathogen itself) as the likely determinants of post-

infective

> > fatigue syndrome, as the case rates after infection with Epstein-

-

> > Barr virus (a DNA virus), Ross River virus (an RNA virus), and

C.

> > burnetii (an intracellular bacterium) were comparable, and the

> > symptom characteristics progressively merged over time. "

> >

> > I would like to submit that this is the type of result that

would

> be

> > predicted by the glutathione depletion--methylation cycle block

> > hypothesis for the pathogenesis of chronic fatigue syndrome.

This

> > hypothesis holds that CFS onset is caused by a combination of a

> > genetic predisposition (a set of polymorphisms) that particular

> > people are born with, and a sufficient load of stressors to

lower

> > the glutathione level enough to trigger a vicious circle

mechanism,

> > involving the methylation cycle, and facilitated by the genetic

> > predisposition. One of the classes of possible stressors is the

> > biological stressors, and infectious agents are one category of

> > these biological stressors. According to this model, it does

not

> > matter what the particular infectious agent is. What matters is

> > whether the infection (combined with any other stressors that

might

> > be present in the particular person) is sufficient to lower the

> > glutathione level enough to trigger the vicious circle

mechanism.

> > It seems clear that the results of this study confirm that this

is

> > the way onset of CFS behaves when triggered by pathogens.

> >

> > Please note that this study does not tell us what needs to be

done

> > for treatment, only what the characteristics are of the category

of

> > CFS that is post-infectious in origin.

> >

> > Rich

> >

>

[Guest guest]

Rich,

It's not been my experience that these particular leopards change their

spots. Also, it has been my experience that they are very good at

saying things that sound great from time to time. If Dr Hickie has

publicly recanted his past crusade to psychologize CFS, and has

distanced himself from that particular hobby-horse, then, maybe.

Considering the terrible human suffering directly caused by Hickie,

Wessely, et. al., it would take nothing less for me to even

provisionally trust that he doesn't have an ulterior motive.

--Bob

rvankonynen wrote:

Hi, Nelly.

Yes, I'm aware of some of the positions that Dr. Hickie has taken on

CFS in the past. However, I would like to cite some specific

quotations from this new study, of which he is the lead author:

"Importantly, premorbid and intercurrent psychiatric disorder did

not show predictive power for post-infective fatigue syndrome at any

time point."

"Severity of the acute illness, and not demographic or psychological

factors, was predictive of post-infective fatigue syndrome."

There is no mention of cognitive behavioral therapy or graded

exercise therapy in this paper at all.

Maybe it's time to give Dr. Hickie another chance.

Rich

>

> Rich,

>

> Ian Hickie is a psychiatrist (of the nastiest kind) who's been set

for decades on proving CFS is a psychiatric condition (a kind of

Australian Wessely if you like). If he puts his name on a study it

is to "prove" that pathogens are not important in the aetiology of

CFS. The next step in his reasoning has been the same for years, i e

CFS hits the psychiatricly weak and the pathogens are only triggers.

You on the other hand will say "it's the glutathione and

the "vicious circle mechanism, involving the methylation cycle, and

facilitated by the genetic predisposition. ".

>

> I have no way of assessing whether you're right re glutathione

depletion being at the root of much of our probs, but I certainly

know that I would not go down ANY path with Ian Hickie!!

>

> Nelly

> [infections] Latest Dubbo results and

glutathione depletion--methylation cycle block hypothes

>

>

> Hi, all.

>

> Today another paper from the Dubbo, Australia, infection

outcomes

> study was published (Hickie, I, et al.,"Post-infective and

chronic

> fatigue syndromes precipitated by viral and non-viral pathogens:

> preospective cohort study," BMJ,doi:10.1136/bmj.38933.585764.AE).

>

> As you may know, this study is involved with following people

who

> develop infectious diseases over time to try to understand why

some

> of them do not recover, but instead continue to be ill with a

> disorder that meets the criteria of chronic fatigue syndrome.

>

> This paper compared the percentage of people who had cases of

> mononucleosis (glandular fever), Q fever, and Ross River virus,

> respectively, who later met the criteria for chronic fatigue

> syndrome. It's interesting to note that Q fever is caused by an

> intracellular bacterium, while the other two are viral diseases.

>

> The authors found that the percentage who went on to have CFS

was

> the same for the three infectious diseases (11% at 6 months).

This

> common result is very significant, because it suggests that the

> reason these people develop CFS is not associated with the

> particular pathogen, but rather with their host response.

>

> Here's a quotation from the paper: "Examination of outcomes

after

> the three distinctive acute infections reported here strongly

> implicates aspects of the host response to infection (rather

than

> the pathogen itself) as the likely determinants of post-

infective

> fatigue syndrome, as the case rates after infection with Epstein-

-

> Barr virus (a DNA virus), Ross River virus (an RNA virus), and

C.

> burnetii (an intracellular bacterium) were comparable, and the

> symptom characteristics progressively merged over time."

>

> I would like to submit that this is the type of result that

would be

> predicted by the glutathione depletion--methylation cycle

block

> hypothesis for the pathogenesis of chronic fatigue syndrome.

This

> hypothesis holds that CFS onset is caused by a combination of a

> genetic predisposition (a set of polymorphisms) that particular

> people are born with, and a sufficient load of stressors to

lower

> the glutathione level enough to trigger a vicious circle

mechanism,

> involving the methylation cycle, and facilitated by the genetic

> predisposition. One of the classes of possible stressors is the

> biological stressors, and infectious agents are one category of

> these biological stressors. According to this model, it does not

> matter what the particular infectious agent is. What matters is

> whether the infection (combined with any other stressors that

might

> be present in the particular person) is sufficient to lower the

> glutathione level enough to trigger the vicious circle

mechanism.

> It seems clear that the results of this study confirm that this

is

> the way onset of CFS behaves when triggered by pathogens.

>

> Please note that this study does not tell us what needs to be

done

> for treatment, only what the characteristics are of the category

of

> CFS that is post-infectious in origin.

>

> Rich

>

[Guest guest]

Rich

I see your point...BUT as you can observe I went past the mcdonalds

menu board approach to everything's supposedly alright, to

explaining to my doctor that your lab is screwed and is practising

crap.I actually find your maybe selling a song and dance to despertae

people, which may keep them from trying there hardest to get a

<<<<<<<<<real diagnosis>>>>>>>>>>>>>>>.I suppose that is my gripe

with you.Also that you won't go and see 20 of these people to

visualise the real condition, that I know, lived with, and strongly

associate with....

How intelligent would you feel if you observed a 100 people giving

there real life account of the direction there life headed after they

received a sinus infection?I mean it's that simple that it's actually

frightening to have someone skew the real picture of these diseases

because his pants are too high up around his chest.

> > >

> > > Hi, all.

> > >

> > > Today another paper from the Dubbo, Australia, infection

> outcomes

> > > study was published (Hickie, I, et al., " Post-infective and

> chronic

> > > fatigue syndromes precipitated by viral and non-viral

pathogens:

> > > preospective cohort study, "

BMJ,doi:10.1136/bmj.38933.585764.AE).

> > >

> > > As you may know, this study is involved with following people

> who

> > > develop infectious diseases over time to try to understand why

> some

> > > of them do not recover, but instead continue to be ill with a

> > > disorder that meets the criteria of chronic fatigue syndrome.

> > >

> > > This paper compared the percentage of people who had cases of

> > > mononucleosis (glandular fever), Q fever, and Ross River virus,

> > > respectively, who later met the criteria for chronic fatigue

> > > syndrome. It's interesting to note that Q fever is caused by

an

> > > intracellular bacterium, while the other two are viral diseases.

> > >

> > > The authors found that the percentage who went on to have CFS

> was

> > > the same for the three infectious diseases (11% at 6 months).

> This

> > > common result is very significant, because it suggests that the

> > > reason these people develop CFS is not associated with the

> > > particular pathogen, but rather with their host response.

> > >

> > > Here's a quotation from the paper: " Examination of outcomes

> after

> > > the three distinctive acute infections reported here strongly

> > > implicates aspects of the host response to infection (rather

> than

> > > the pathogen itself) as the likely determinants of post-

> infective

> > > fatigue syndrome, as the case rates after infection with

Epstein-

> -

> > > Barr virus (a DNA virus), Ross River virus (an RNA virus), and

> C.

> > > burnetii (an intracellular bacterium) were comparable, and the

> > > symptom characteristics progressively merged over time. "

> > >

> > > I would like to submit that this is the type of result that

> would

> > be

> > > predicted by the glutathione depletion--methylation cycle block

> > > hypothesis for the pathogenesis of chronic fatigue syndrome.

> This

> > > hypothesis holds that CFS onset is caused by a combination of a

> > > genetic predisposition (a set of polymorphisms) that particular

> > > people are born with, and a sufficient load of stressors to

> lower

> > > the glutathione level enough to trigger a vicious circle

> mechanism,

> > > involving the methylation cycle, and facilitated by the genetic

> > > predisposition. One of the classes of possible stressors is

the

> > > biological stressors, and infectious agents are one category of

> > > these biological stressors. According to this model, it does

> not

> > > matter what the particular infectious agent is. What matters

is

> > > whether the infection (combined with any other stressors that

> might

> > > be present in the particular person) is sufficient to lower the

> > > glutathione level enough to trigger the vicious circle

> mechanism.

> > > It seems clear that the results of this study confirm that this

> is

> > > the way onset of CFS behaves when triggered by pathogens.

> > >

> > > Please note that this study does not tell us what needs to be

> done

> > > for treatment, only what the characteristics are of the

category

> of

> > > CFS that is post-infectious in origin.

> > >

> > > Rich

> > >

> >

>

[Guest guest]

I have to agree. I think there are many factors that are allowing these infections to take hold and would swear on a stack of bibles that I believe coagulation is one of them. I don't see how one particular nutrient depletion, when we know we have so many, can be the ultimate causative factor which makes us all susceptible to all kinds of organisms. And besides, if the question is discerning the ultimate cause, then why are we depleted in glutathione in the first place? How are we going to address THAT cause? Or the cause of THAT cause? I think the human body is too complex, and there are too many interdependent physical and environmental factors to pinpoint one particular originating cause. I guess I'm just very cynical when it comes to people becoming so fixated on one small piece of the puzzle. There's always been something that grabs hold

of people's attention for a while, whether it's eppstein barr, or a dysfunctioning HPA-Axis, to building immunity with whey protein. Unfortunatley, I usually see the same results which means eventually moving on to the next big thing (while possibly maintaining some small piece of knowledge from all the previous hooplah). So, when I start seeing people getting some remarkable results from glutathione replenishment, I'll be a lot less skeptical. In the meantime, I wish people with this kind of ability to build a case for a particular theory would spend more time looking at the actual infections and how to stop the damage they do. It's the toxins from the infection, and the ensuing inflammation that's actually killing us right now in this very moment, not our theoretical inherent susceptibilities. Even if it does come down to genetics and something

like glutathione depletion in the end, ignoring the actual killer is not preventing people from getting sicker and sicker. It's like instead of learning how to defend yourself against an attacker, you try to psychoanalyze him first and why he went all aggressive and psycho-killer in the first place. First order of business when your life is at stake. Get the killer under control. Then figure out what went wrong to create a killer in the first place. Don't get me wrong. I'm certainly not opposed to the kind of research Rich is doing. I think it's invaluable. I just think it's early to try to be so persuasive about it when it's not doing real people much good, except maybe diverting their attention from where it needs to be, which is focused on halting the damage being done. I mainly just wish some researcher out there somewhree would be interested

enough to put as much passion and energy into trying to fight this illness in real time, right now. I guess there are some, like Stratton and Wheldon. Unfortunately, they don't come on forums like this with their theories, as excellent as they are. dumbaussie2000 <dumbaussie2000@...> wrote: RichI don't know if your paying attention to what is

the best treatment for cfs/fibro? I think the polls kept showing the hydration salts blasi/salt C where the best treatments out there.. for the past 10 years plus IV glutathiones been done till the cows come home ..But if your missing the dehydration, come low blood volume aspect of possible glutathione depletion, you may as well send me a copy of that last article in brail as well.I don't think you payed too much attention to what Ken was describing got him well on the experimental list.. it sounded like- fix the coagulation and take antimicrobials. Your allowing people to follow you up a garden path which may mean many will get so diseased there's no road back, so what you do is foolish without taking the whole picture into consideration.Remember also, many supplements and medicines may benefit you from the fact that they are suspended in potassium salts rather than there active

ingredients.cheers>> Hi, all.> > Today another paper from the Dubbo, Australia, infection outcomes > study was published (Hickie, I, et al.,"Post-infective and chronic > fatigue syndromes precipitated by viral and non-viral pathogens: > preospective cohort study," BMJ,doi:10.1136/bmj.38933.585764.AE).> > As you may know, this study is involved with following people who > develop infectious diseases over time to try to understand why some > of them do not recover, but instead continue to be ill with a > disorder that meets the criteria of chronic fatigue syndrome.> > This paper compared the percentage of people who had cases of > mononucleosis (glandular fever), Q fever,

and Ross River virus, > respectively, who later met the criteria for chronic fatigue > syndrome. It's interesting to note that Q fever is caused by an > intracellular bacterium, while the other two are viral diseases.> > The authors found that the percentage who went on to have CFS was > the same for the three infectious diseases (11% at 6 months). This > common result is very significant, because it suggests that the > reason these people develop CFS is not associated with the > particular pathogen, but rather with their host response. > > Here's a quotation from the paper: "Examination of outcomes after > the three distinctive acute infections reported here strongly > implicates aspects of the host response to infection (rather than > the pathogen itself) as the likely determinants of post-infective > fatigue syndrome, as the case rates after infection with

Epstein--> Barr virus (a DNA virus), Ross River virus (an RNA virus), and C. > burnetii (an intracellular bacterium) were comparable, and the > symptom characteristics progressively merged over time."> > I would like to submit that this is the type of result that would be > predicted by the glutathione depletion--methylation cycle block > hypothesis for the pathogenesis of chronic fatigue syndrome. This > hypothesis holds that CFS onset is caused by a combination of a > genetic predisposition (a set of polymorphisms) that particular > people are born with, and a sufficient load of stressors to lower > the glutathione level enough to trigger a vicious circle mechanism, > involving the methylation cycle, and facilitated by the genetic > predisposition. One of the classes of possible stressors is the > biological stressors, and infectious agents are one category of

> these biological stressors. According to this model, it does not > matter what the particular infectious agent is. What matters is > whether the infection (combined with any other stressors that might > be present in the particular person) is sufficient to lower the > glutathione level enough to trigger the vicious circle mechanism. > It seems clear that the results of this study confirm that this is > the way onset of CFS behaves when triggered by pathogens.> > Please note that this study does not tell us what needs to be done > for treatment, only what the characteristics are of the category of > CFS that is post-infectious in origin.> > Rich>

[Guest guest]

Rich

You're not in a position to comment.

You haven't been brutalized by disease only to be dismissed as

psychologically unfit.

I have. 23 years now.

Psychogenic theories have been used to inflict real harm against

PWCs.

You continue to promote psychological stress as a causative variable

in the onset of some PWCs' illness. I think you are Procrustean in

doing so. But even if stress plays a sufficiently unique role in

CFS (as distinct from, say, the putative role it may play in cancer)

to warrant significant consideration (as distinct from, say, the way

cancer patients are dealt with) you are reckless in the way you

promote this view. You do not preface your comments with caveats

that are commensurate with the historical, and ongoing, use of

psychology as a weapon.

Your omissions are instructive:

You suggest that Hickie be given another chance. No consideration

to the opportunity costs associated with doing so. Hickie isn't

paying for this research himself. The study you cited was funded by

Australian and American taxpayers. When Hickie is funded, someone

else isn't. There are plenty of immunologists, microbiologists,

neuroscientists in need of funding—scientists that haven't

compromised themselves.

I learned a lot about the value I could place in your views when you

posted this:

/message/83535

You acknowledged that Warren and Marshall faced great opposition to

their work on H. pylori. You then proceeded to reserve a causal

role for stress in the onset of ulcers. And you did so with no

apparent cognitive dissonance. After all, it was largely people

like you who opposed their work:

" ….it was a frustrating time for the next 10 years though because

nobody believed us….The idea of stress and things like that was just

so entrenched nobody could really believe that it was bacteria. "

http://www.msnbc.msn.com/id/9576387/

That is, living, breathing human beings continued to suffer real

pain and disease because the psychogenic theory for ulcers prevailed

over science.

You obviously do not use your model with the intent to harm PWCs.

But you know very well that psychogenic theories continue to be used

in this way. You have a responsibility, then, to discuss

your " stress " component in a context that explicitly contrasts your

model from the bigotry that has been deployed against PWCs. You

have a responsibility, that is, to ensure that your audience, no

matter who they are, understands that you believe that psychology

has been used to harm PWCs and that your model does not endorse this.

Whatever contributions you may make to our cause, they do not

compensate for your careless promotion of psychogenic factors.

Matt

>

>

> Maybe it's time to give Dr. Hickie another chance.

>

> Rich

>

[Guest guest]

Matt,

I have never felt that Rich pushed the stress/psycho theory. He is genuinely convinced of a physical root cause behind CFS/ME. He's looking into dysfunctions in various detox pathways for eg, not into stress.

Fascinating how incredibly traumatised we all are, I am amazed myself at the strength of my anger at the sheer notion of giving that war criminal Hickie another chance. I sense a very similar feeling from you, Matt.

We certainly have been brutalised, humiliated, left to rot, dismissed by all as crazy depressives who didn't even want to get better etc. etc. but let's not attack Rich, he works for free and he is on our side. After all he has a right to pursue whatever avenues that are of interest to him.

Nelly

[infections] Re: Latest Dubbo results and glutathione depletion--methylation cycle block hypothes

RichYou're not in a position to comment.You haven't been brutalized by disease only to be dismissed as psychologically unfit.I have. 23 years now.Psychogenic theories have been used to inflict real harm against PWCs.You continue to promote psychological stress as a causative variable in the onset of some PWCs' illness. I think you are Procrustean in doing so. But even if stress plays a sufficiently unique role in CFS (as distinct from, say, the putative role it may play in cancer) to warrant significant consideration (as distinct from, say, the way cancer patients are dealt with) you are reckless in the way you promote this view. You do not preface your comments with caveats that are commensurate with the historical, and ongoing, use of psychology as a weapon.Your omissions are instructive:You suggest that Hickie be given another chance. No consideration to the opportunity costs associated with doing so. Hickie isn't paying for this research himself. The study you cited was funded by Australian and American taxpayers. When Hickie is funded, someone else isn't. There are plenty of immunologists, microbiologists, neuroscientists in need of funding—scientists that haven't compromised themselves.I learned a lot about the value I could place in your views when you posted this:/message/83535You acknowledged that Warren and Marshall faced great opposition to their work on H. pylori. You then proceeded to reserve a causal role for stress in the onset of ulcers. And you did so with no apparent cognitive dissonance. After all, it was largely people like you who opposed their work:"….it was a frustrating time for the next 10 years though because nobody believed us….The idea of stress and things like that was just so entrenched nobody could really believe that it was bacteria."http://www.msnbc.msn.com/id/9576387/That is, living, breathing human beings continued to suffer real pain and disease because the psychogenic theory for ulcers prevailed over science.You obviously do not use your model with the intent to harm PWCs. But you know very well that psychogenic theories continue to be used in this way. You have a responsibility, then, to discuss your "stress" component in a context that explicitly contrasts your model from the bigotry that has been deployed against PWCs. You have a responsibility, that is, to ensure that your audience, no matter who they are, understands that you believe that psychology has been used to harm PWCs and that your model does not endorse this.Whatever contributions you may make to our cause, they do not compensate for your careless promotion of psychogenic factors.Matt>> > Maybe it's time to give Dr. Hickie another chance. > > Rich >

[Guest guest]

Nelly

>

> Matt,

>

> I have never felt that Rich pushed the stress/psycho theory. He is

genuinely convinced of a physical root cause behind CFS/ME. He's

looking into dysfunctions in various detox pathways for eg, not into

stress.

*************I gave a URL in which Rich continued to promote the

theory of pschological stress as a causal variable in the onset of

ulcers, despite the clearest illustration of the practical risks in

doing so.

Here is a URL to a post in which he promotes psychological stress as

a causal variable in the onset of illness for some PWCs:

/message/101355

What do you think (not ) challenges Rich on so often if not

Rich's promotion of the psychological stress component to his theory?

>

> We certainly have been brutalised, humiliated, left to rot,

dismissed by all as crazy depressives who didn't even want to get

better etc. etc. but let's not attack Rich, he works for free and he

is on our side. After all he has a right to pursue whatever avenues

that are of interest to him.

*******Rich has a right to promote his theories. But he is not

entitled to promote them uncontested. Is there something in

my " attack " that was false?

Psychogenicists have successfully prevented the adequate funding of

biomedical research into CFS and have armed our physicians with the

tools they use to undermine us. The ostracism by family members

and " friends " follows. So when Rich said " Maybe it's time

to give Dr. Hickie another chance. " is this statement an

appropriate reflection of the sociopolitical problem we face? He

had the chance to say something like,

" The use of psychological theories to undermine the welfare of PWCs

is deplorable. To the extent that Dr. Hickie participated in that I

must read his publications with some caution. Nonetheless, I think

the research in question may have some merit. Hopefully future

efforts will be carried out by researchers whose motives can not be

questioned. That won't happen until funding agencies take a clear

stance against the abuses of psychology, and earmark grants for the

biologists that can actually make positive contributions unqualified

by past errors. Until then the publications of people like Dr.

Hickie are what we have to work with. "

But he didn't.

His statement doesn't even focus on the publication, but on how we

should respond to Dr. Hickie himself. He seems to advocate

forgiveness. Why else did he frame the statement the way he did?

In the post to that I cited above Rich said, " If you could

bring yourself to forgive and get on with your life... "

Now you may think that Rich is in a position to recommend that PWCs

forgive the people who have done them harm, but I do not believe

Rich has the perspective or wisdom to comment accurately on this.

And I said so. More to the point, there is a sociopolitical goal

that we strive for when we confront the psychogenicists. I believe

that healthy people are the most bigoted people I've encountered.

They are flagrant. They question our character, though not always

with the sophistication of published psychogenicists. This is about

civil rights and at the heart of every peaceful civil rights

movement is the attempt to shame others out of their corrupt

behavior. PWC activism is pathetic and will remain so until PWCs

clearly confront the psychogenicists for the harm they do. How can

PWCs find their voice when people like Rich advocate that

we " forgive and get on with our lives " . Rich may have the mental

health of individual PWCs in mind when he says this, but it

undermines efforts at political change. The abuses of

psychogenicists should be highlighted, not minimized.

It wouldn't take much for Rich to be " on my side " . He wouldn't have

to give up glutathione, mitochondrial dysfunction or even the

psychological component to his model. He brings other genuine

insights to bear. I would like to view him as an ally. We don't

have many. But his continued attempts to diminish PWC outrage is

unacceptable.

It boggles my mind that we are not all unified on this issue. It

would be so easy. It might, believe or not, alleviate a lot

of " stress. "

Matt

[Guest guest]

Rich,

Have you read Mark London's article on Recuperation and why it may

work? So far Recuperation along with antibiotics has worked the best

of anything I have tried. My diagnosis is cfs, Lyme, and quinolone

tendon damage.

Here is a link to his article. I would be interested in your

perspective on it.

http://web.mit.edu/london/www/RRR.htm

a Carnes

>

> Hi, Tony.

>

> Yes, the hydration salts have helped quite a few people, I think

> particularly those with fibromyalgia. This treatment hasn't been

so

> good for many PWCs, though. It may be that those with the ACE

> deletion polymorphism already have a problem with too much sodium

> retention, because of the higher aldosterone this polymorphism

> causes. In any case, I don't think people are finding these salts

> to be a cure, but only a help in improving the quality of life.

> That's certainly important, but I want to find root causes and

> achieve cures.

>

> With regard to IV glutathione infusions, I agree that that is also

> temporarily helpful for some, but doesn't usually break the vicious

> circle so that glutathione comes up and stays up permanently at a

> normal level. I don't know if you've been following closely what

> I've been saying lately, but it amounts to going after the root

> causes of the vicious circle. If a person fixes those, the

> glutathione will come back up automatically. That's where the

> genetic testing and targeted treatments with supplements to bypass

> genetic problems at the biochemical level come in.

>

> It looks to me as though the low blood volume, a consequence of

> the " mild " diabetes insipidus in many PWCs, is actually caused by

> glutathione depletion as well. We've had a couple of cases of

> people whose dehydration went away when they built their

> glutahione. I suspect that the mechanism is that antidiuretic

> hormone (ADH), being a secretory protein that incorporates

> disulfides in its structure, requires glutathione for its correct

> synthesis in the cells of the hypothalamus. When glutathione is low

> there, the cells can't make enough ADH, and that causes the kidneys

> to dump more water into the urine than they should, producing

> dehydration and low blood volume.

>

> Yes, genetic problems in the coagulation proteins are definitely an

> issue for a subset of PWCs, and when that is the case, it is

> important to deal with it, as Ken did.

>

> Yes, potassium depletion can be a problem as well, and it also

needs

> to be dealt with. There was some good work in Australia on

potassium

> in CFS.

>

> Well, I certainly hope I'm not leading people to their destruction,

> Tony. That's definitely not my goal. I do think we need to keep

> our eyes open to the possibility of various subsets. One size

> doesn't fit all.

>

> Rich

>

>

>

> > >

> > > Hi, all.

> > >

> > > Today another paper from the Dubbo, Australia, infection

> outcomes

> > > study was published (Hickie, I, et al., " Post-infective and

> chronic

> > > fatigue syndromes precipitated by viral and non-viral

pathogens:

> > > preospective cohort study, "

BMJ,doi:10.1136/bmj.38933.585764.AE).

> > >

> > > As you may know, this study is involved with following people

> who

> > > develop infectious diseases over time to try to understand why

> some

> > > of them do not recover, but instead continue to be ill with a

> > > disorder that meets the criteria of chronic fatigue syndrome.

> > >

> > > This paper compared the percentage of people who had cases of

> > > mononucleosis (glandular fever), Q fever, and Ross River virus,

> > > respectively, who later met the criteria for chronic fatigue

> > > syndrome. It's interesting to note that Q fever is caused by

an

> > > intracellular bacterium, while the other two are viral diseases.

> > >

> > > The authors found that the percentage who went on to have CFS

> was

> > > the same for the three infectious diseases (11% at 6 months).

> This

> > > common result is very significant, because it suggests that the

> > > reason these people develop CFS is not associated with the

> > > particular pathogen, but rather with their host response.

> > >

> > > Here's a quotation from the paper: " Examination of outcomes

> after

> > > the three distinctive acute infections reported here strongly

> > > implicates aspects of the host response to infection (rather

> than

> > > the pathogen itself) as the likely determinants of post-

> infective

> > > fatigue syndrome, as the case rates after infection with

Epstein-

> -

> > > Barr virus (a DNA virus), Ross River virus (an RNA virus), and

> C.

> > > burnetii (an intracellular bacterium) were comparable, and the

> > > symptom characteristics progressively merged over time. "

> > >

> > > I would like to submit that this is the type of result that

> would

> > be

> > > predicted by the glutathione depletion--methylation cycle block

> > > hypothesis for the pathogenesis of chronic fatigue syndrome.

> This

> > > hypothesis holds that CFS onset is caused by a combination of a

> > > genetic predisposition (a set of polymorphisms) that particular

> > > people are born with, and a sufficient load of stressors to

> lower

> > > the glutathione level enough to trigger a vicious circle

> mechanism,

> > > involving the methylation cycle, and facilitated by the genetic

> > > predisposition. One of the classes of possible stressors is

the

> > > biological stressors, and infectious agents are one category of

> > > these biological stressors. According to this model, it does

> not

> > > matter what the particular infectious agent is. What matters

is

> > > whether the infection (combined with any other stressors that

> might

> > > be present in the particular person) is sufficient to lower the

> > > glutathione level enough to trigger the vicious circle

> mechanism.

> > > It seems clear that the results of this study confirm that this

> is

> > > the way onset of CFS behaves when triggered by pathogens.

> > >

> > > Please note that this study does not tell us what needs to be

> done

> > > for treatment, only what the characteristics are of the

category

> of

> > > CFS that is post-infectious in origin.

> > >

> > > Rich

> > >

> >

>

[Guest guest]

Chronic disease caused stress in me- not the other way around.

When I was a child - born spleenless and other with organs in the

wrong place - and always crying and sick-

my mother was investigated for munchausens - and I was looked at as a

baby that just wanted attention (untill I had exploratory surgeryin

1956 and they saw the physical reasons)

When I had a blocked intestine in 1975 at 27 year old, from

adhesionms from that 1956 operationand was being sent home from the

ER day after day with what they called " a case of hysterical

pregnancy " .. that caused stress in me.

Then I got a blood transfusion during THAT operation to save my life

because of their blunder that infused me with tainted blood..Lyme and

Babesia (or maybe Malaria).. and for the next 27 years I was mis dx'd

with autoimmune disorders..

Sooooooo I've had plenty of STRESS caused BY the medical profession's

ineptness.

WHat I realized growing up, and going thru the medical mill- is that

medicine can be like religon to some Drs.- and you 'ain't gonna

change their beliefs and if you speak hersey - they want to burn you

at the stake on way or another.

I've got no use for alot of them - most of them.

Any researcher or Physician that respots to the somatic cause

for something they aren't smart enough to figure out has zero stature

with me- regardless of who they are.

Barb

Matt wrote in part:

It boggles my mind that we are not all unified on this issue. It

would be so easy. It might, believe or not, alleviate a lot

of " stress. "

[Guest guest]

Matt,

I'm sorry I offended you.

Rich

[Guest guest]

Rich,

I have great respect for you and like you. You took up for me on

experimental when I got attacked for simply disagreeing with you.

Please keep studying and posting, especially here. This list is least

likely to agree with you,and that is the very group where you will get

honest disagreement and a challenge for you to support your

perspective.

That is exactly what we need if we are to make progress together

toward healing.

a Carnes

>

> Matt,

>

> I'm sorry I offended you.

>

> Rich

>

[Guest guest]

Hi, a.

Thank you. I think you're O.K. yourself! I do appreciate having my

hypotheses challenged. That's what hypotheses are for. You, and

, and Cort, and Matt, and Tony, and Nelly and Penny and others

do me a great service when you work me over. I'm not offended at

all. I really don't want to make people angry in the process

though, or make their lives more difficult than they already are, by

causing them to experience more you-know-what.

Rich

>

> Rich,

> I have great respect for you and like you. You took up for me on

> experimental when I got attacked for simply disagreeing with you.

> Please keep studying and posting, especially here. This list is

least

> likely to agree with you,and that is the very group where you will

get

> honest disagreement and a challenge for you to support your

> perspective.

>

> That is exactly what we need if we are to make progress together

> toward healing.

>

> a Carnes

>

> >

> > Matt,

> >

> > I'm sorry I offended you.

> >

> > Rich

> >

>

[Guest guest]

> >

> > Rich,

> > I have great respect for you and like you. You took up for me on

> > experimental when I got attacked for simply disagreeing with you.

> > Please keep studying and posting, especially here. This list is

> least

> > likely to agree with you,and that is the very group where you

will

> get

> > honest disagreement and a challenge for you to support your

> > perspective.

> >

> > That is exactly what we need if we are to make progress together

> > toward healing.

> >

> > a Carnes

> >

> > >

> > > Matt,

> > >

> > > I'm sorry I offended you.

> > >

> > > Rich

> > >

> >

>

[Guest guest]

Rich,

Freidl made a good point on another email list. She said that

Yasko is not against the use of antibiotics for Lyme. Since she is a

naturopath she cannot prescribe them, but does agree with their use.

I await with interest her treatment of other Lyme patients to see how

they fare. As you know I am already doing things to boost glutathione

etc. So any advances will be welcome.

a

>

> Hi, a.

>

> Thank you. I think you're O.K. yourself! I do appreciate having

my

> hypotheses challenged. That's what hypotheses are for. You, and

> , and Cort, and Matt, and Tony, and Nelly and Penny and others

> do me a great service when you work me over. I'm not offended at

> all. I really don't want to make people angry in the process

> though, or make their lives more difficult than they already are,

by

> causing them to experience more you-know-what.

>

> Rich

>

>

> >

> > Rich,

> > I have great respect for you and like you. You took up for me on

> > experimental when I got attacked for simply disagreeing with you.

> > Please keep studying and posting, especially here. This list is

> least

> > likely to agree with you,and that is the very group where you

will

> get

> > honest disagreement and a challenge for you to support your

> > perspective.

> >

> > That is exactly what we need if we are to make progress together

> > toward healing.

> >

> > a Carnes

> >

> > >

> > > Matt,

> > >

> > > I'm sorry I offended you.

> > >

> > > Rich

> > >

> >

>

[Guest guest]

Hi, a.

Well, you, me, and Dr. Yasko--that makes at least four of us

who are not against antibiotics. I think we're making progress here!

Rich

>

> Rich,

> Freidl made a good point on another email list. She said

that

> Yasko is not against the use of antibiotics for Lyme. Since she is

a

> naturopath she cannot prescribe them, but does agree with their

use.

>

> I await with interest her treatment of other Lyme patients to see

how

> they fare. As you know I am already doing things to boost

glutathione

> etc. So any advances will be welcome.

>

> a

[Guest guest]

Dear Rich

See http://www.mja.com.au/public/issues/177_09_041102/beard_041102.pdf#search=%22%22Ian%20Hickie%22%20BMJ%20CFS%22

Personally, I wouldn't piss on the man if he was on fire.

I feel his reductionist approach has set back the treatment of psychiatric and psychosomatic patients, let alone all of us with severe illnessesses which he categorises as somatiform disorders ( because he won't read the literature on causation or look either) at least a hunderd years. The man is a psychopath !!!

He completely ignores the trenchant criticism of the Australian Guidelines (no doubt that he would see it as a criticism of himself as he had a big hand in compiling the document)

Regards

Windsor (In Aus)

[infections] Latest Dubbo results and glutathione depletion--methylation cycle block hypothes> > > Hi, all.> > Today another paper from the Dubbo, Australia, infection outcomes > study was published (Hickie, I, et al.,"Post-infective and chronic > fatigue syndromes precipitated by viral and non-viral pathogens: > preospective cohort study," BMJ,doi:10.1136/bmj.38933.585764.AE).> > As you may know, this study is involved with following people who > develop infectious diseases over time to try to understand why some > of them do not recover, but instead continue to be ill with a > disorder that meets the criteria of chronic fatigue syndrome.> > This paper compared the percentage of people who had cases of > mononucleosis (glandular fever), Q fever, and Ross River virus, > respectively, who later met the criteria for chronic fatigue > syndrome. It's interesting to note that Q fever is caused by an > intracellular bacterium, while the other two are viral diseases.> > The authors found that the percentage who went on to have CFS was > the same for the three infectious diseases (11% at 6 months). This > common result is very significant, because it suggests that the > reason these people develop CFS is not associated with the > particular pathogen, but rather with their host response. > > Here's a quotation from the paper: "Examination of outcomes after > the three distinctive acute infections reported here strongly > implicates aspects of the host response to infection (rather than > the pathogen itself) as the likely determinants of post-infective > fatigue syndrome, as the case rates after infection with Epstein--> Barr virus (a DNA virus), Ross River virus (an RNA virus), and C. > burnetii (an intracellular bacterium) were comparable, and the > symptom characteristics progressively merged over time."> > I would like to submit that this is the type of result that would be > predicted by the glutathione depletion--methylation cycle block > hypothesis for the pathogenesis of chronic fatigue syndrome. This > hypothesis holds that CFS onset is caused by a combination of a > genetic predisposition (a set of polymorphisms) that particular > people are born with, and a sufficient load of stressors to lower > the glutathione level enough to trigger a vicious circle mechanism, > involving the methylation cycle, and facilitated by the genetic > predisposition. One of the classes of possible stressors is the > biological stressors, and infectious agents are one category of > these biological stressors. According to this model, it does not > matter what the particular infectious agent is. What matters is > whether the infection (combined with any other stressors that might > be present in the particular person) is sufficient to lower the > glutathione level enough to trigger the vicious circle mechanism. > It seems clear that the results of this study confirm that this is > the way onset of CFS behaves when triggered by pathogens.> > Please note that this study does not tell us what needs to be done > for treatment, only what the characteristics are of the category of > CFS that is post-infectious in origin.> > Rich>