Glutathione depletion and idiopathic cardiomyopathy in CFS

[Guest guest]

Hi, all.

I want to point out that glutathione depletion looks like a very

good candidate to explain the cardiomyopathy that Dr. Cheney

discussed in the recent write-up by Carol Sieverling:

http://www.virtualhometown.com/dfwcfids/medical/cheney/heart04.htm

Dr. Cheney noted under " Etiology (Cause) " that " The short version is

that cardiac muscles have lost power because their mitochondria are

dysfunctional. They're not functioning well because of a redox-

state problem. But, what causes the redox-state problem? I don't

know... "

I would just point out that the redox potential in cells is normally

controlled by glutathione. A depletion of glutathione in the heart

muscle cells would very definitely lead to a " redox-state " problem

and dysfunction of the mitochondria.

Dr. Cheney also discussed viruses, heavy metals and toxins as

possible causes of the cardiomyopathy. I would just point out that

some of the other well-known roles of glutathione in the body are to

suppress the activation of viruses and to remove heavy metals and

other toxins from the body.

Dr. Cheney further discussed the increase in concentration of

peroxynitrite, as is the basis of Prof. Pall's theory, as a

causative mechanism. He noted that the rise in superoxide is what

causes the increase in peroxynitrite concentration. I would point

out that glutathione depletion can be responsible for the rise in

superoxide concentration as well, since it will promote a rise in

the concentration of hydrogen peroxide, and this in turn will

exert " product inhibition " on the superoxide dismutase reaction.

This backlog will cause superoxide to rise.

In summary, I think that all the mechanisms that Dr. Cheney cited as

possibly being responsible for cardiomyopathy in CFS can in turn be

caused by glutathione depletion. I think this offers the

possibility of putting together a comprehensive hypothesis for the

pathogenesis of CFS. I suggest that genetic predisposition,

combined with the mechanisms I presented in my recent AACFS poster

paper, may very well serve as the " front end " of a comprehensive

hypothesis for the etiology and pathogenesis of CFS, which can be

combined with Dr. Cheney's new thinking about the cardiomyopathy to

explain a major part of what goes on in CFS.

I would also note that this approach can also explain the milder

cases of CFS, in which cardiomyopathy is not observed. The reason

for this would be that it is known that the heart has a higher

concentration of the rate-limiting enzyme needed for synthesizing

glutathione than do most of the other organs of the body.

Therefore, in the early stages of CFS, the heart is able to maintain

its concentration of glutathione sufficiently high to avoid the

mitochondrial dysfunction, which may result from a redox shift,

toxin buildup, or reactivation of endogenous viruses.

My glutathione depletion paper can be found at any of the following

three websites:

http://www.personalconsult.com/articles/glutathioneandchronicfatigue.

html

http://www.cfsresearch.org/cfs/research/treatment/26nf.htm

or

http://phoenix-cfs.org/GluAACFS04.htm

Rich