Re: Latest Dubbo results

[Guest guest]

This " Dubbo Study " (DUMBO study?) is nothing new under the Australian sun. The

authors of the infamous 2002 Chronic fatigue syndrome guidelines (incl Ian

Hickie) cited these 1996 studies below.

IMHO, just trying to re-cycle old obvious stuff that basically says: If you have

an infection you'll feel tired for a while afterwards and it doesn't mean you're

still infected=> bottom line: You don't require antimicrobial treatment, you

need ...GRADED EXERCISE!!!

You Rich and Yasko chose to look at genes and methylation cycles as " root

cause " . I'm glad I looked at " infections " as mine, as I was nearly dead when I

started treating my bacterial infections in 99-2000. My genes are my genes, but

my bacterial infections were killing me!!!!!

Nelly

In the Australian context it appears that infections such as Q fever and Ross

River virus infection may also trigger CFS.68-71

1.. Marmion BP, M, Maddocks I, et al. Protracted debility and fatigue

after acute Q fever [letter]. Lancet 1996; 347: 977-978.

2.. Eltumi M, Mathieson DM, Brueton MJ, Kovar IZ. Protracted fatigue and

debility after acute Q fever [letter]. Lancet 1996; 347: 978-979.

3.. Selden SM, Cameron AS. Changing epidemiology of Ross River virus disease

in South Australia. Med J Aust 1996; 165: 313-317.

Latest Dubbo results and glutathione

depletion--methylation cycle block hypot.

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.

It is so wonderful that you found your way before croaking! What bacteria were

getting you? Are you currently on long-term abx?

Thanks,

Adrienne

Latest Dubbo results and glutathione

depletion--methylation cycle block hypot.

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.

I'm also very glad that you treated your infections and kept

yourself alive. Please don't misunderstand me. I'm not opposed to

treating infections directly, and in fact I think that's probably

the only thing one can do when things have gotten totally out of

hand with infections.

What I am talking about is, as you said, root causes. I suspect

that the infections are not the root cause of your illness, since

treating them has not cured your illness, but fortunately it has

bought you time, so that you can continue to search for the root

causes and hopefully deal with them.

It may be that if you were able to deal with your root causes more

dierectly, you would achieve total victory, rather than a holding

action. Don't get me wrong, I'm glad you have been able to achieve

a holding action, but I want it all for you!

Rich

>

> This " Dubbo Study " (DUMBO study?) is nothing new under the

Australian sun. The authors of the infamous 2002 Chronic fatigue

syndrome guidelines (incl Ian Hickie) cited these 1996 studies

below.

>

> IMHO, just trying to re-cycle old obvious stuff that basically

says: If you have an infection you'll feel tired for a while

afterwards and it doesn't mean you're still infected=> bottom line:

You don't require antimicrobial treatment, you need ...GRADED

EXERCISE!!!

>

> You Rich and Yasko chose to look at genes and methylation cycles

as " root cause " . I'm glad I looked at " infections " as mine, as I was

nearly dead when I started treating my bacterial infections in 99-

2000. My genes are my genes, but my bacterial infections were

killing me!!!!!

>

> Nelly

>

[Guest guest]

I think it may be all of the above. Some have infections, some methylation

issues, genes for others, but what a fantastically wonderful thing that we're

getting to the crux of the problem finally. It's been a long time coming and

there's a ways to go, and unfortunetly for some of us it took most of lives, but

those that follow will benefit.

Nelly Pointis <janel@...> wrote: This " Dubbo Study " (DUMBO

study?) is nothing new under the Australian sun. The authors of the infamous

2002 Chronic fatigue syndrome guidelines (incl Ian Hickie) cited these 1996

studies below.

IMHO, just trying to re-cycle old obvious stuff that basically says: If you have

an infection you'll feel tired for a while afterwards and it doesn't mean you're

still infected=> bottom line: You don't require antimicrobial treatment, you

need ...GRADED EXERCISE!!!

You Rich and Yasko chose to look at genes and methylation cycles as " root

cause " . I'm glad I looked at " infections " as mine, as I was nearly dead when I

started treating my bacterial infections in 99-2000. My genes are my genes, but

my bacterial infections were killing me!!!!!

Nelly

In the Australian context it appears that infections such as Q fever and Ross

River virus infection may also trigger CFS.68-71

1.. Marmion BP, M, Maddocks I, et al. Protracted debility and fatigue

after acute Q fever [letter]. Lancet 1996; 347: 977-978.

2.. Eltumi M, Mathieson DM, Brueton MJ, Kovar IZ. Protracted fatigue and

debility after acute Q fever [letter]. Lancet 1996; 347: 978-979.

3.. Selden SM, Cameron AS. Changing epidemiology of Ross River virus disease in

South Australia. Med J Aust 1996; 165: 313-317.

Latest Dubbo results and glutathione

depletion--methylation cycle block hypot.

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]

You are an angel.

rvankonynen <richvank@...> wrote: Hi, Nelly.

I'm also very glad that you treated your infections and kept

yourself alive. Please don't misunderstand me. I'm not opposed to

treating infections directly, and in fact I think that's probably

the only thing one can do when things have gotten totally out of

hand with infections.

What I am talking about is, as you said, root causes. I suspect

that the infections are not the root cause of your illness, since

treating them has not cured your illness, but fortunately it has

bought you time, so that you can continue to search for the root

causes and hopefully deal with them.

It may be that if you were able to deal with your root causes more

dierectly, you would achieve total victory, rather than a holding

action. Don't get me wrong, I'm glad you have been able to achieve

a holding action, but I want it all for you!

Rich

>

> This " Dubbo Study " (DUMBO study?) is nothing new under the

Australian sun. The authors of the infamous 2002 Chronic fatigue

syndrome guidelines (incl Ian Hickie) cited these 1996 studies

below.

>

> IMHO, just trying to re-cycle old obvious stuff that basically

says: If you have an infection you'll feel tired for a while

afterwards and it doesn't mean you're still infected=> bottom line:

You don't require antimicrobial treatment, you need ...GRADED

EXERCISE!!!

>

> You Rich and Yasko chose to look at genes and methylation cycles

as " root cause " . I'm glad I looked at " infections " as mine, as I was

nearly dead when I started treating my bacterial infections in 99-

2000. My genes are my genes, but my bacterial infections were

killing me!!!!!

>

> Nelly

>

[Guest guest]

>I suspect

that the infections are not the root cause of your illness, since

treating them has not cured your illness,

Rich,

How long is a piece of string?

What length of treatment is required for any given infectious cocktail? How long

for TB? How long for leprosy? For Aids? How long for Chronic C.burnetii (the

cause of your friend's Hickie's Q-fever)?

When is an infection complex " treated " ?

>It may be that if you were able to deal with your root causes more

>dierectly, you would achieve total victory, rather than a holding

>action.

Rich, I am well aware of how much you do to help us sort out as much as

possible, but at the end of the day, it's the abx and maybe more importantly the

anti-protozoans that have made a huge difference for me, not the zillions of

supplements I have taken (and continue to take).

I am trying to intervene from all sides, I see plenty of value in dealing with

all kinds of detox issues, poor methylation processes, identifying and

unblocking whatever is blocked, but I can't afford to pay for Amy Yasko to do

her research, just like I could not afford to finance the Newcastle guys (yet I

did I had all the tests done urinary markers, stools tests, serum tests, then I

did what they suggested took the amino-acids and the rest and it got me nowhere

at all ).

I nearly financed KdM's and his RnaseL tests but I saw the light after 2 or 3

trips to Brussels.

Wish I could keep on financing all these people but I can't, yet I am reading it

all with interest, as long as it's not on my money any longer.

BTW, whey protein never did a thing for me except gave me the runs. I take Sparx

and I hope it helps some.

The nattokinase and the lauricidin appear to also be of value for me, the whole

lemon drink helps my gut.

>Don't get me wrong, I'm glad you have been able to achieve

>a holding action, but I want it all for you!

Thanks Rich, I want it all for myself too but I don't think the genetics hold it

all. BTW my husband has gradually developed the very same symptoms as myself,

and apart from being both Caucasians we are not at all related (different

ancestry, I am part Swiss German part Meditarrenean, he is pure French not at

all mediterranean). He has the Factor V Leiden coagulation defect and I don't

yet we both appear to benefit from taking nattokinase, so I suspect that our

hypercoag issues are most likely due to the infections, maybe

I've been ill 25 years (after tick-bites, a sore knee and an EM rash), I

recovered about 50% then got bitten by several dozens of ticks in 92 with my

present husband, I got iller (heart, vertigo, very severe neuro problems) than

him at first but he seemed to gradually deteriorate as well, at this point in

time we are both struggling still, although abx and anti-protozoan treatments

are keeping things at bay.

As I often say: many of my symptoms have improved but I haven't (if that makes

sense), I'm still almost housebound and have to spend most of my time resting

but at least I am not in agony from headaches, not throwing up from the vertigo,

not scared my heart will stop any minute now, not feeling like I have the 'flu

all the time (only some times)

Nelly

Re: Latest Dubbo results

Hi, Nelly.

I'm also very glad that you treated your infections and kept

yourself alive. Please don't misunderstand me. I'm not opposed to

treating infections directly, and in fact I think that's probably

the only thing one can do when things have gotten totally out of

hand with infections.

What I am talking about is, as you said, root causes. I suspect

that the infections are not the root cause of your illness, since

treating them has not cured your illness, but fortunately it has

bought you time, so that you can continue to search for the root

causes and hopefully deal with them.

It may be that if you were able to deal with your root causes more

dierectly, you would achieve total victory, rather than a holding

action. Don't get me wrong, I'm glad you have been able to achieve

a holding action, but I want it all for you!

Rich

>

> This " Dubbo Study " (DUMBO study?) is nothing new under the

Australian sun. The authors of the infamous 2002 Chronic fatigue

syndrome guidelines (incl Ian Hickie) cited these 1996 studies

below.

>

> IMHO, just trying to re-cycle old obvious stuff that basically

says: If you have an infection you'll feel tired for a while

afterwards and it doesn't mean you're still infected=> bottom line:

You don't require antimicrobial treatment, you need ...GRADED

EXERCISE!!!

>

> You Rich and Yasko chose to look at genes and methylation cycles

as " root cause " . I'm glad I looked at " infections " as mine, as I was

nearly dead when I started treating my bacterial infections in 99-

2000. My genes are my genes, but my bacterial infections were

killing me!!!!!

>

> Nelly

>

[Guest guest]

Nelly/Rich etc

It always scares me to read or hear of stories like this, because I

know that antibiotics/antimalarials/antiprotozoals/antifungals as

drugs in high amounts for months or years is not an option for me. And

I know in some other cases it did not help others enough--either

because they couldn't tolerate them and it broke down their system

(toxic drugs, and/or toxic metabolites of drugs overhwelming certain

systems) or it was the wrong drug perhaps? The key organism going

unidentified? And the soup of others mostly opportunistic?

Every time I read a story (newspaper, I am on a list that posts them

all from around the country) it seems like I'm reading about someone

who took IV and orals for YEARS, and they are " improved " or " greatly

improved " . Nobody ever says " well. "

This isn't even the case with tb, so...what could be the cause? I can

only imagine a combination of: exposure to toxins in the environment

screwing up all kinds of pathways, bioweaponized bugs from the 60's

and 70's now at large in the environment, a soup of bugs in ticks,

mosquitoes and maybe other vectors, a soup that could overwhelm many

systems, and...antibiotic resistance in general.

I'm glad you're better. I'm sorry it's not better than it is (still

housebound). I've heard of other husband/wife situations or family

scenarios where the whole family fell sick...the family next door not.

How could that be? I have no explanation as ticks in wooded back yards

can't possibly stop at one house and ignore the next. Or is it

possible the family next door all had mild ailments they didn't know

where tickborne? But why mild, when the family I know was

incapacitated (wife, husband, kids). Yet I know of some families where

for instance the wife (usually it's the female, not always,w hich

makes Rich's estrogen hypothesis interesting) is really sick, the

husband okay...

I am not sure we can ever sort out the truth. So many tickbites, who

knows what soup of worms, bacteria, fungi and virii you and hubby got.

It might overwhelm any system. I tend to think when both husband and

wife get sick, but in a different time frame (as you and husband) that

they have different but substantial underlying genetic vulnerabilities.

I cannot find any coherent theory to explain the wide variety of

reactions to tickborne or should I say vector borne illness (some get

stuff from mosquitos these days).

I *have* begun thinking methylation could explain a lot of things--in

terms of vulnerability. Maybe Rich is right and maybe this approach

could now help you make further gains. It *is* expensive though and

that's a problem.

It is probably true that, once over the line, once globally disabled,

you're going to have to somehow reduce the thriving bug population.

You could also probably do serious naturopathic measures, and that

would work too-----cleansing every organ system, the whole gut, even

fasting at times to starve the bugs, but then you'd still have to

repair the underlying vulnerabilities. Why? Because the bugs may

flourish again someday otherwise, or new bugs will come your way.

> >

> > This " Dubbo Study " (DUMBO study?) is nothing new under the

> Australian sun. The authors of the infamous 2002 Chronic fatigue

> syndrome guidelines (incl Ian Hickie) cited these 1996 studies

> below.

> >

> > IMHO, just trying to re-cycle old obvious stuff that basically

> says: If you have an infection you'll feel tired for a while

> afterwards and it doesn't mean you're still infected=> bottom line:

> You don't require antimicrobial treatment, you need ...GRADED

> EXERCISE!!!

> >

> > You Rich and Yasko chose to look at genes and methylation cycles

> as " root cause " . I'm glad I looked at " infections " as mine, as I was

> nearly dead when I started treating my bacterial infections in 99-

> 2000. My genes are my genes, but my bacterial infections were

> killing me!!!!!

> >

> > Nelly

> >

>

>

>

>

>

>

[Guest guest]

Hi,

You know Edy, this is a nice thought, really. It's depressing to go

year after year being sick, and wasting our lives. But if it will help

others, if some good can come of it, then that is most comforting.

Michele G

>

It's been a long time coming and there's a ways to go, and

unfortunetly for some of us it took most of lives, but those that

follow will benefit.

[Guest guest]

HI Rich,

I just wanted to comment on something I learned from watching the

presentations from the April DAN! Conference. In Jill second

presentation, she suggested that the methylation cycle is not

malfunctioning in girls b/c of the effects of estrogen in upregulating

the enzymes. She said she doesn't know yet what the cause is in girls.

This is consistent with my normal creatinine. A friend who is very sick

just found out her creatinine is normal, after 6+ years of CFS.

Re: Latest Dubbo results

Hi, Nelly.

I'm also very glad that you treated your infections and kept

yourself alive. Please don't misunderstand me. I'm not opposed to

treating infections directly, and in fact I think that's probably

the only thing one can do when things have gotten totally out of

hand with infections.

What I am talking about is, as you said, root causes. I suspect

that the infections are not the root cause of your illness, since

treating them has not cured your illness, but fortunately it has

bought you time, so that you can continue to search for the root

causes and hopefully deal with them.

It may be that if you were able to deal with your root causes more

dierectly, you would achieve total victory, rather than a holding

action. Don't get me wrong, I'm glad you have been able to achieve

a holding action, but I want it all for you!

Rich

[Guest guest]

HI Rich,

I just wanted to comment on something I learned from watching the

presentations from the April DAN! Conference. In Jill second

presentation, she suggested that the methylation cycle is not

malfunctioning in girls b/c of the effects of estrogen in upregulating

the enzymes. She said she doesn't know yet what the cause is in girls.

This is consistent with my normal creatinine. A friend who is very sick

just found out her creatinine is normal, after 6+ years of CFS.

Re: Latest Dubbo results

Hi, Nelly.

I'm also very glad that you treated your infections and kept

yourself alive. Please don't misunderstand me. I'm not opposed to

treating infections directly, and in fact I think that's probably

the only thing one can do when things have gotten totally out of

hand with infections.

What I am talking about is, as you said, root causes. I suspect

that the infections are not the root cause of your illness, since

treating them has not cured your illness, but fortunately it has

bought you time, so that you can continue to search for the root

causes and hopefully deal with them.

It may be that if you were able to deal with your root causes more

dierectly, you would achieve total victory, rather than a holding

action. Don't get me wrong, I'm glad you have been able to achieve

a holding action, but I want it all for you!

Rich

[Guest guest]

Nelly wrote:

" I nearly financed KdM's and his RnaseL tests but I saw the light

after 2 or 3 trips to Brussels. "

Can you share what light you saw? Did you decide the RnaseL tests

are not worth doing? Thanks!

>

> >I suspect

> that the infections are not the root cause of your illness, since

> treating them has not cured your illness,

>

> Rich,

>

> How long is a piece of string?

>

> What length of treatment is required for any given infectious

cocktail? How long for TB? How long for leprosy? For Aids? How long

for Chronic C.burnetii (the cause of your friend's Hickie's Q-fever)?

>

> When is an infection complex " treated " ?

>

> >It may be that if you were able to deal with your root causes more

> >dierectly, you would achieve total victory, rather than a holding

> >action.

>

> Rich, I am well aware of how much you do to help us sort out as

much as possible, but at the end of the day, it's the abx and maybe

more importantly the anti-protozoans that have made a huge difference

for me, not the zillions of supplements I have taken (and continue to

take).

>

>

> I am trying to intervene from all sides, I see plenty of value in

dealing with all kinds of detox issues, poor methylation processes,

identifying and unblocking whatever is blocked, but I can't afford to

pay for Amy Yasko to do her research, just like I could not afford to

finance the Newcastle guys (yet I did I had all the tests done

urinary markers, stools tests, serum tests, then I did what they

suggested took the amino-acids and the rest and it got me nowhere at

all ).

>

> I nearly financed KdM's and his RnaseL tests but I saw the light

after 2 or 3 trips to Brussels.

>

> Wish I could keep on financing all these people but I can't, yet I

am reading it all with interest, as long as it's not on my money any

longer.

>

> BTW, whey protein never did a thing for me except gave me the runs.

I take Sparx and I hope it helps some.

>

> The nattokinase and the lauricidin appear to also be of value for

me, the whole lemon drink helps my gut.

>

> >Don't get me wrong, I'm glad you have been able to achieve

> >a holding action, but I want it all for you!

>

> Thanks Rich, I want it all for myself too but I don't think the

genetics hold it all. BTW my husband has gradually developed the very

same symptoms as myself, and apart from being both Caucasians we are

not at all related (different ancestry, I am part Swiss German part

Meditarrenean, he is pure French not at all mediterranean). He has

the Factor V Leiden coagulation defect and I don't yet we both appear

to benefit from taking nattokinase, so I suspect that our hypercoag

issues are most likely due to the infections, maybe

>

> I've been ill 25 years (after tick-bites, a sore knee and an EM

rash), I recovered about 50% then got bitten by several dozens of

ticks in 92 with my present husband, I got iller (heart, vertigo,

very severe neuro problems) than him at first but he seemed to

gradually deteriorate as well, at this point in time we are both

struggling still, although abx and anti-protozoan treatments are

keeping things at bay.

>

> As I often say: many of my symptoms have improved but I haven't (if

that makes sense), I'm still almost housebound and have to spend most

of my time resting but at least I am not in agony from headaches, not

throwing up from the vertigo, not scared my heart will stop any

minute now, not feeling like I have the 'flu all the time (only some

times)

>

> Nelly

>

>

[Guest guest]

I won't go into great details but a couple of things made me realise KdM was

only using us (at least me and a few other French patients I knew) and that he

was not interested in treating us, just interested in gaining a career for

himself.

eg: I was interviewed by one of his assistants (she was nice but just learning

how to take down a patient's history, great for her, nothing in it for me),

blood was taken (about a dozen vials) and I was told it would be tested for

various viruses and bacteria as well as for the RnaseL, then I was seen by the

Master for 5 minutes approx. and when I said I had a zillion ventricular extra

systoles per day, he quickly wrote a script for a calcium-channel blocker and

sent me on my way, I was told if the RnaseL was positive I would be offered a

trial with Ampligen.

I went back about a month later (from Paris to Brussels) and the second time, I

didn't even get to see him at all, and I got no results, more blood was taken

(never got any results, except the RnaseL which was positive). I had been told I

would be tested for intracellular bacteria by PCR (never done or no results

given to me).

The calcium-channel blocker nearly killed me, BP dropped so dramatically I spent

months lying down, couldn't stand at all, and the number of ES increased, my

heart was all over the place, my vertigo increased.

I rang KdM and he fobbed me off on all counts (fobbed me off re any test

results, fobbed me off re Ampligen-at the time, 99, I thought it might be

interesting-, fobbed me off BIG TIME when I mentioned the possibility of an

intracellular bacteria causing the abnormal RnaseL test- KdM screamed at me on

the phone that only a VIRUS could cause this abnormal RnaseL to be present, not

a BACTERIA, he has completely changed his tune since.

As you can see, I am not of of his most fervent fans.

Nelly

Re: Latest Dubbo results

Nelly wrote:

" I nearly financed KdM's and his RnaseL tests but I saw the light

after 2 or 3 trips to Brussels. "

Can you share what light you saw? Did you decide the RnaseL tests

are not worth doing? Thanks!

>

> >I suspect

> that the infections are not the root cause of your illness, since

> treating them has not cured your illness,

>

> Rich,

>

> How long is a piece of string?

>

> What length of treatment is required for any given infectious

cocktail? How long for TB? How long for leprosy? For Aids? How long

for Chronic C.burnetii (the cause of your friend's Hickie's Q-fever)?

>

> When is an infection complex " treated " ?

>

> >It may be that if you were able to deal with your root causes more

> >dierectly, you would achieve total victory, rather than a holding

> >action.

>

> Rich, I am well aware of how much you do to help us sort out as

much as possible, but at the end of the day, it's the abx and maybe

more importantly the anti-protozoans that have made a huge difference

for me, not the zillions of supplements I have taken (and continue to

take).

>

>

> I am trying to intervene from all sides, I see plenty of value in

dealing with all kinds of detox issues, poor methylation processes,

identifying and unblocking whatever is blocked, but I can't afford to

pay for Amy Yasko to do her research, just like I could not afford to

finance the Newcastle guys (yet I did I had all the tests done

urinary markers, stools tests, serum tests, then I did what they

suggested took the amino-acids and the rest and it got me nowhere at

all ).

>

> I nearly financed KdM's and his RnaseL tests but I saw the light

after 2 or 3 trips to Brussels.

>

> Wish I could keep on financing all these people but I can't, yet I

am reading it all with interest, as long as it's not on my money any

longer.

>

> BTW, whey protein never did a thing for me except gave me the runs.

I take Sparx and I hope it helps some.

>

> The nattokinase and the lauricidin appear to also be of value for

me, the whole lemon drink helps my gut.

>

> >Don't get me wrong, I'm glad you have been able to achieve

> >a holding action, but I want it all for you!

>

> Thanks Rich, I want it all for myself too but I don't think the

genetics hold it all. BTW my husband has gradually developed the very

same symptoms as myself, and apart from being both Caucasians we are

not at all related (different ancestry, I am part Swiss German part

Meditarrenean, he is pure French not at all mediterranean). He has

the Factor V Leiden coagulation defect and I don't yet we both appear

to benefit from taking nattokinase, so I suspect that our hypercoag

issues are most likely due to the infections, maybe

>

> I've been ill 25 years (after tick-bites, a sore knee and an EM

rash), I recovered about 50% then got bitten by several dozens of

ticks in 92 with my present husband, I got iller (heart, vertigo,

very severe neuro problems) than him at first but he seemed to

gradually deteriorate as well, at this point in time we are both

struggling still, although abx and anti-protozoan treatments are

keeping things at bay.

>

> As I often say: many of my symptoms have improved but I haven't (if

that makes sense), I'm still almost housebound and have to spend most

of my time resting but at least I am not in agony from headaches, not

throwing up from the vertigo, not scared my heart will stop any

minute now, not feeling like I have the 'flu all the time (only some

times)

>

> Nelly

>

>

[Guest guest]

the Dubbo study is very new and and very important - I

suggest you read it before you jump the gun on this

just because an author you dont like is involved.

These studies - which are trying to elucidate the

cause of post-infective fatigue - could break that

aspect of CFS wide open.

I havent read this latest paper but I cant imagine

theres anything in there on graded exercise - and why

should there be - this is not a paper on therapy.

Cort

--- Nelly Pointis <janel@...> wrote:

> This " Dubbo Study " (DUMBO study?) is nothing new

> under the Australian sun. The authors of the

> infamous 2002 Chronic fatigue syndrome guidelines

> (incl Ian Hickie) cited these 1996 studies below.

>

> IMHO, just trying to re-cycle old obvious stuff that

> basically says: If you have an infection you'll feel

> tired for a while afterwards and it doesn't mean

> you're still infected=> bottom line: You don't

> require antimicrobial treatment, you need ...GRADED

> EXERCISE!!!

>

> You Rich and Yasko chose to look at genes and

> methylation cycles as " root cause " . I'm glad I

> looked at " infections " as mine, as I was nearly dead

> when I started treating my bacterial infections in

> 99-2000. My genes are my genes, but my bacterial

> infections were killing me!!!!!

>

> Nelly

>

> In the Australian context it appears that

> infections such as Q fever and Ross River virus

> infection may also trigger CFS.68-71

>

> 1.. Marmion BP, M, Maddocks I, et al.

> Protracted debility and fatigue after acute Q fever

> [letter]. Lancet 1996; 347: 977-978.

> 2.. Eltumi M, Mathieson DM, Brueton MJ, Kovar IZ.

> Protracted fatigue and debility after acute Q fever

> [letter]. Lancet 1996; 347: 978-979.

> 3.. Selden SM, Cameron AS. Changing epidemiology

> of Ross River virus disease in South Australia. Med

> J Aust 1996; 165: 313-317.

> Latest Dubbo results

> and glutathione depletion--methylation cycle block

> hypot.

>

>

> 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

>

>

>

>

>

> [Non-text portions of this message have been

> removed]

>

>

__________________________________________________

[Guest guest]

the Dubbo study is very new and and very important - I

suggest you read it before you jump the gun on this

just because an author you dont like is involved.

These studies - which are trying to elucidate the

cause of post-infective fatigue - could break that

aspect of CFS wide open.

I havent read this latest paper but I cant imagine

theres anything in there on graded exercise - and why

should there be - this is not a paper on therapy.

Cort

--- Nelly Pointis <janel@...> wrote:

> This " Dubbo Study " (DUMBO study?) is nothing new

> under the Australian sun. The authors of the

> infamous 2002 Chronic fatigue syndrome guidelines

> (incl Ian Hickie) cited these 1996 studies below.

>

> IMHO, just trying to re-cycle old obvious stuff that

> basically says: If you have an infection you'll feel

> tired for a while afterwards and it doesn't mean

> you're still infected=> bottom line: You don't

> require antimicrobial treatment, you need ...GRADED

> EXERCISE!!!

>

> You Rich and Yasko chose to look at genes and

> methylation cycles as " root cause " . I'm glad I

> looked at " infections " as mine, as I was nearly dead

> when I started treating my bacterial infections in

> 99-2000. My genes are my genes, but my bacterial

> infections were killing me!!!!!

>

> Nelly

>

> In the Australian context it appears that

> infections such as Q fever and Ross River virus

> infection may also trigger CFS.68-71

>

> 1.. Marmion BP, M, Maddocks I, et al.

> Protracted debility and fatigue after acute Q fever

> [letter]. Lancet 1996; 347: 977-978.

> 2.. Eltumi M, Mathieson DM, Brueton MJ, Kovar IZ.

> Protracted fatigue and debility after acute Q fever

> [letter]. Lancet 1996; 347: 978-979.

> 3.. Selden SM, Cameron AS. Changing epidemiology

> of Ross River virus disease in South Australia. Med

> J Aust 1996; 165: 313-317.

> Latest Dubbo results

> and glutathione depletion--methylation cycle block

> hypot.

>

>

> 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

>

>

>

>

>

> [Non-text portions of this message have been

> removed]

>

>

__________________________________________________

[Guest guest]

>

> fobbed me off BIG TIME when I mentioned the possibility of an

intracellular bacteria causing the abnormal RnaseL test- KdM screamed

at me on the phone that only a VIRUS could cause this abnormal RnaseL

to be present, not a BACTERIA, he has completely changed his tune since.

>

Hi Nelly,

First of all, I'm sorry to hear you went through this - sounds like a

dreadful experience, and none of us deserve to be treated like that.

Second, I'm curious him having 'changed his tune since' re: bacteria

and RNaseL. Is this true? I realise that he does acknowledge bacteria

can raise elastase but I thought there was something else - I've

forgotten much of what I read, but I think it was abnormal 2-5OAS? -

that had to be triggered by a virus. Maybe someone can clarify? Cort?

Or perhaps there's some new information I don't know about re: bacteria.

Thanks,

[Guest guest]

Well, Cort, you haven't read it and yet you know it is new and important?!!!!

You haven't read it but you " imagine " what's in it and you tell ME " to read it

before I jump the gun " . ROFL

For your info, Cort, I HAVE read it and I am not finding it " new and important " .

It might be " new and important " to Mr Hickie as he might be finally realising

what we have all known for centuries, i e that our fatigue is physiological not

psychological and that some viral and bacterial pathogens can produce in some

people lasting fatigue, wow! I am so impressed!

And you guessed right there is nothing on CGT/GET, I never said there was, it is

not a study on treatment.

I won't write any more on this topic, for fear of being labelled " hysterical "

again by somebody who has not even read the study!!

Nelly

Latest Dubbo results

> and glutathione depletion--methylation cycle block

> hypot.

>

>

> 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

>

>

>

>

>

> [Non-text portions of this message have been

> removed]

>

>

__________________________________________________

[Guest guest]

Hi, and Nelly.

" " <christine.emmanuel@...> wrote:

I'm curious him having 'changed his tune since' re: bacteria

> and RNaseL.

***Dr DeM may be realizing the glutathione(GSH) depletion hypothesis for CFS is

on target here. Both viruses and bacteria as well as other

GSH depleters that result in low glutathione status can be said to activate the

RnaseL enzyme system in CFS, but it is low GSH status that seems to be the

mechanism that does this specifically no matter how it got low to start.

Is this true? I realise that he does acknowledge bacteria

> can raise elastase but I thought there was something else - I've

> forgotten much of what I read, but I think it was abnormal 2-5OAS? -

> that had to be triggered by a virus. Maybe someone can clarify? Cort?

>

> Or perhaps there's some new information I don't know about re: bacteria.

***It's as Rich recently said his motto has become after years of looking at

this in CFS, " Follow the glutathione! " . More specifically, as ones GSH becomes

low enough the suppressive capacity it has over calpain ends and calpain

activates, ie, signaling the activation of the RnaseL enzyme system.

***Again extrapolating from his hypothesis, how GSH gets depleted, ie,

predisposing sets of SNPs for poor methylation, intracellular viruses,

intracellular bacteria, heavy metal toxicity, chemical exposure and/or other

environmental stressors that can deplete ones GSH are important yet they are

secondary to that it is actual low GSH that activates RnaseL.

***Inversely, improving GSH status, by whatever means one needs to do to

accomplish this, deactivates RnaseL.

I think this is exactly what happened with me in improving my GSH status.

***Unfortunately, deactivating RnaseL isn't the whole ball game to coming out of

the CFS hole. It's more like the half way mark for many, IMO, with downstream

issues that have built up over time, like mercury or chemicals or other toxic

sources, that still need to be addressed and effectively eliminated.

> Thanks,

>

>

***

[Guest guest]

I apologize for saying you didnt read the study. For some reason I missed your

appendation of other studies of this ilk. I was probably just too upset to see

someone slam another study I consider very important to look further. You've

obviously looked at this study and I was incorrect about that and I apologize

for that.

I havent gotten the study but I've read the abstract and am very familiar with

the other Dubbo studies.

I think you were incorrect when you said this study was really similar to

others. It is an order of magnitude different. This is the first time

researchers are analyzing the physiology of people who come down with CFS after

an infection. The other studies you mentioned just looked at symptoms. You did

say the study suggested graded exercise - it did not. The fact that infections

can cause physiological changes that cause CFS may be self evident to you and

to me but I assure that it is not to the scientific community. The Dubbo studies

could be a very big deal in CFS.

What I believe you did is knock a paper that pushes the science in the

direction we want to go, not one that suggests psychology is at the heart of

CFS. Thats what I was reacting to.

Yours truly, Cort

Nelly Pointis <janel@...> wrote:

Well, Cort, you haven't read it and yet you know it is new and

important?!!!!

You haven't read it but you " imagine " what's in it and you tell ME " to read it

before I jump the gun " . ROFL

For your info, Cort, I HAVE read it and I am not finding it " new and important " .

It might be " new and important " to Mr Hickie as he might be finally realising

what we have all known for centuries, i e that our fatigue is physiological not

psychological and that some viral and bacterial pathogens can produce in some

people lasting fatigue, wow! I am so impressed!

And you guessed right there is nothing on CGT/GET, I never said there was, it is

not a study on treatment.

I won't write any more on this topic, for fear of being labelled " hysterical "

again by somebody who has not even read the study!!

Nelly

Latest Dubbo results

> and glutathione depletion--methylation cycle block

> hypot.

>

>

> 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

>

>

>

>

>

> [Non-text portions of this message have been

> removed]

>

>

__________________________________________________

[Guest guest]

I apologize for saying you didnt read the study. For some reason I missed your

appendation of other studies of this ilk. I was probably just too upset to see

someone slam another study I consider very important to look further. You've

obviously looked at this study and I was incorrect about that and I apologize

for that.

I havent gotten the study but I've read the abstract and am very familiar with

the other Dubbo studies.

I think you were incorrect when you said this study was really similar to

others. It is an order of magnitude different. This is the first time

researchers are analyzing the physiology of people who come down with CFS after

an infection. The other studies you mentioned just looked at symptoms. You did

say the study suggested graded exercise - it did not. The fact that infections

can cause physiological changes that cause CFS may be self evident to you and

to me but I assure that it is not to the scientific community. The Dubbo studies

could be a very big deal in CFS.

What I believe you did is knock a paper that pushes the science in the

direction we want to go, not one that suggests psychology is at the heart of

CFS. Thats what I was reacting to.

Yours truly, Cort

Nelly Pointis <janel@...> wrote:

Well, Cort, you haven't read it and yet you know it is new and

important?!!!!

You haven't read it but you " imagine " what's in it and you tell ME " to read it

before I jump the gun " . ROFL

For your info, Cort, I HAVE read it and I am not finding it " new and important " .

It might be " new and important " to Mr Hickie as he might be finally realising

what we have all known for centuries, i e that our fatigue is physiological not

psychological and that some viral and bacterial pathogens can produce in some

people lasting fatigue, wow! I am so impressed!

And you guessed right there is nothing on CGT/GET, I never said there was, it is

not a study on treatment.

I won't write any more on this topic, for fear of being labelled " hysterical "

again by somebody who has not even read the study!!

Nelly

Latest Dubbo results

> and glutathione depletion--methylation cycle block

> hypot.

>

>

> 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

>

>

>

>

>

> [Non-text portions of this message have been

> removed]

>

>

__________________________________________________

[Guest guest]

cort johnson wrote:

This is the first time researchers are analyzing the physiology of

people who come down with CFS after an infection.

Cort

>

Huh?

-

[Guest guest]

True, if you somehow ignore 50 years of work on ME.

On 9/5/06, erikmoldwarrior <erikmoldwarrior@...> wrote:

> cort johnson wrote:

> This is the first time researchers are analyzing the physiology of

> people who come down with CFS after an infection.

> Cort

> >

>

> Huh?

>

> -

>

>

>

>

>

> 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.

>

[Guest guest]

How do I even reply to a statement like that? I guess I dont - not wanting to

go to the trouble of explaining the history of CFS research - or maybe you didnt

get this paper?

This is the first time researchers are taking a group of people who come down

with one of three infections and then follow them as a subset of those people

come down with CFS. While they're doing that they are assessing their immune

response (in this case) to try and determine what happened to make that one

subset of people come down CFS.

I dont think they were doing that 50 or 25 or 5 or even 3 years ago.

Does that clear that question up?

bob niederman <bobn1955@...> wrote:

True, if you somehow ignore 50 years of work on ME.

On 9/5/06, erikmoldwarrior <erikmoldwarrior@...> wrote:

> cort johnson wrote:

> This is the first time researchers are analyzing the physiology of

> people who come down with CFS after an infection.

> Cort

> >

>

> Huh?

>

> -

>

>

>

>

>

> 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.

>