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

September 2, 2006

Hi, Rich.

This is interesting and reminds me of the only other relative in my family

history to come down with CFS as far as I've been able to determine from stories

told by living relatives. This was my grandfather's mother, my great

grandmother, on my mother's side of the family.

She got an acute infection in about 1920, which some speculated was a less

virulent strain of the Spanish Flu that had crossed the globe a few years

earlier(though I think it may have just as easily been a latent viral

activation, from stress of some sort, being attributed to this major pandemic

given the close proximity of time). Anyway, she was never the same after this

infection though she lived on for two and a half more decades.

After her infection, she no longer went on weekend excursions with the rest of

the family, no longer traveled to family events such as during holidays and all

around stopped being active in life, spending most of her time in bed or in her

bedroom and not feeling well. Doctors didn't know what was wrong with her and

were never able to help.

Also, there was no mention of meloncholy or depression as a description of her

and from another story that my grandfather(deceased since 1999) told me, she

sounded like a fairly rational person(not psychotic or peculiar in character),

giving him some sound advice at a very difficult moment in his young adult life.

" rvankonynen " <richvank@...> wrote:

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

>

September 2, 2006

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

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

September 2, 2006

Did it ever occur to you that she may have had Myalgic Encephalomyelitis

( " atypical,nonparalytic polio " ?)

Did anyone tell you that she was under stress when she bacame ill?

> 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

> >

>

September 2, 2006

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

treatment<<<<<

I predict that this study will be in the arsenal of evidence that the CFS

treatment of choice is CBT to change the person's " unhelpful beliefs " , and

dysfunctional response to stressors.

If they ever incorporate Glutathione, it will be that one's " thinking " they are

ill (or the resulting de-conditioning) is what lowers it.

>

> 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

>

September 2, 2006

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

September 2, 2006

You all would be shocked at how often in Santa Cruz I have come across this

idea. It's a version of blame the patient and we get a lot of that I think. I

used to call it the " Hipper than Thou " syndrome, but I now think if one blames

the patient or person then the scary chronic illness won't happen to them

because they're doing something right and you aren't.

kattemayo <kattemayo@...> wrote: