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

[Guest guest]

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