I have communicated with Rich concerning chelating and will post
that next week. Among other things we discussed magnesium which is needed to
increase and make both Glutathione and ATP - but magnesium levels are exceeding
difficult to increase ,unless one does it transdermally with as pure a product
as possible.
Blessings
Shan


From: Rich Van Konynenburg
Subject: RES, MED: How might the Blasi protocol work in CFS?

http://listserv.nodak.edu/cgi-bin/wa.exe?A2=ind0509c&L=co-cure&P=1585

There have been enough positive results reported from taking the salts of the
Blasi protocol that I have started to think about how it might be working at
the biochemical and physiological levels, in the context of what I already
believe to be true. I will confine my remarks to CFS, since I don't have a
working hypothesis for FM.

I would like to suggest three possibilities:

First, the protocol is highest in sodium. It is known that continually taking
more sodium has the effect of raising the blood volume. We know that many
PWCs test low in total blood volume, and we also know that increasing the blood
volume raises the venous return to the heart, and its preload. In view of the
work of Dr. Arnold Peckerman et al., confirmed by the more recent measurements
reported by Dr. Paul Cheney in Texas last June, we know that diastolic
cardiomyopathy is a problem in many PWCs, especially those with more severe
symptoms.
While increasing the preload does not correct the cardiomyopathy, it will
help to increase the cardiac output somewhat in the presence of the
cardiomyopathy. Increased cardiac output would have salutory effects on many
aspects of the
pathophysiology of CFS. This may be one mechanism by which the Blasi protocol
could benefit PWCs.

A second suggestion I would make is as follows:
there is good evidence for mitochondrial dysfunction in the skeletal muscle
cells in CFS (and in the later stage of CFS, it now appears that the heart
muscle is similarly affected), and I suspect that in many cases this is due to
glutathione depletion, which allows peroxynitrite to rise and to partially block
the Krebs cycle and probably also the respiratory chain. This decreases the
rate of production of ATP in these cells. It's true that ATP is used directly on
the muscle fiber proteins to enable them to extend, in preparation for a new
contraction (sort of like arming a mousetrap; you put the energy in
when you set the trap, and it is utilized when the trap is triggered
by the mouse.) The lack of a rapid enough supply of ATP is what is proposed
to limit the relaxation of the left ventricle of the heart in the diastolic
cardiomyopathy observed in CFS by Dr. Cheney. But ATP is also utilized in a big
way in cells to power the ion pumps. The system of ion pumps maintains the
proper concentrations of sodium, potassium, calcium and magnesium
inside the cells, relative to the outside. In muscle and nerve cells,
particularly, these concentration gradients are continually being degraded by
the
nerve impulses that are powered by them, and in cells in general, the sodium
gradient is used to power transport of needed substances into the cells, so the
pumps have to continue to operate to restore the concentration gradients and the
electrical potential across the cell membrane. When there is a decrease in
the rate of production of ATP, it can be expected that these pumps will not be
able to operate as rapidly as normal. The concentration
gradients of the ions can then be expected to decrease from their
normal operating values. I suspect that supplying potassium and magnesium in
the Blasi protocol may assist the underpowered ion pumps in their job of
maintaining proper concentrations of these ions inside the cells.

The third suggestion I would make is that we know that many PWCs
have mild diabetes insipidus (not the same as the more common diabetes
mellitus, which involves blood sugar). In diabetes insipidus, the person
produces
excessive amounts of urine. In the process, there is a tendency to waste more
electrolytes in the urine. The Blasi protocol may be helping to restore the
electrolytes that are wasted.

None of these actions would produce a cure of the underlying causes
of CFS, as far as I can tell, but they would be supportive of the overall
physiology and would contribute to better quality of life.

In my view, the more fundamental issues that also need to be
addressed are

(1) getting the glutathione levels and rate of production back up to normal,

(2) addressing the reasons why the glutathione went down originally (possible
genetic variations, which can perhaps be compensated using certain
supplements, and various physical, chemical, biological and/or psycholical or
emotional
stressors that probably combined with a genetic predisposition to
lower the glutathione) and

(3) correcting the problems that have subsequently arisen as a result of the
glutathione going down, which now produce positive feedback or vicious circle
mechanisms, making it difficult to restore the glutathione level. These latter
problems include infections of various sorts (viral, bacterial and fungal)
and buildup of toxins (especially mercury).

Rich Van Konynenburg, Ph.D.

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