Re: ~*Online WACOC News*~

Co-Cure Archives - August 2005 Week 4
http://listserv.nodak.edu/cgi-bin/wa.exe?A1=ind0508d&L=co-cure

MED: Coxsackie B3, selenium and chronic fatigue syndrome

[Resent for proper distribution.]

>>From Rich Van Konynenburg <richvank@xxxxxxx>:

It is well-known that people with chronic fatigue syndrome (PWCs) often
test positively for various viral infections. In the U.S., these
commonly include the herpes family viruses Epstein--Barr,
cytomegalovirus and HHV-6A. There are reports in the literature of
Coxsackie B3 viral infections being found in PWCs as well, but these
reports appear to originate primarily from the U.K. and from other
European countries, not from North America. I have been puzzling over
this apparent difference for some years.

Recently I learned of the work of Prof. Harold D. Foster of the
University of Victoria in Canada (http://www.hdfoster.com). Among
other things, Prof. Foster has advanced a recommendation for the
treatment of AIDS that is based on supplementing selenium and three of
the amino acids (tryptophan, cysteine and glutamine). The basis for
this treatment is his theory that the HIV virus produces full-blown
AIDS by depleting the body of these nutrients. In his view, the virus
does this by expressing the enzyme glutathione peroxidase, which is
encoded in its genome. This enzyme requires these nutrients for its
synthesis. I think this is a very promising approach to the treatment
of AIDS, as his initial testing has shown (Journal of Orthomolecular
Medicine 20(2), pp. 67-69 (2005)).

Prof. Foster notes, based on the work of E.W. Taylor (Journal of
Orthomolecular Medicine 12(4), pp. 227-239 (1997)) that not only the
HIV virus, but also several other viruses are known to encode for
selenoproteins in their genomes, and he suggests that these viruses may
produce infections by depleting their hosts of selenium, also. These
viruses include Coxsackie B3, Ebola Zaire, Molloscum contagiosum, and
hepatitis C.

It is known that the intake of selenium by the populations of the U.K.
and other European countries has been dropping in recent years since
the formation of the European Union and the consequent greater
proportion of the wheat consumed in these countries coming from Europe
rather than North America. Wheat from Europe is known to be
significantly lower in selenium content than that from Canada and the
U.S., because of differences in the soil contents in these areas
(Rayman, M.P., British Medical Journal 314, p. 387 (1997)).

Putting these propositions together, it occurs to me that perhaps the
reason for the occurrence of Coxsackie B3 infections in PWCs in the
U.K. and other European countries, but for the most part not in the
PWCs in North America, may be a result of greater selenium deficiency
in the populations of the former countries as a result of differences
in food sources. Coxsackie B3 may be more prevalent in general in
these populations because of the generally lower levels of selenium in
them.

This is not to say that selenium deficiencies are not also present in
PWCs in North America. In fact, it is known that mercury forms stable
complexes with selenium in the body, taking it out of bioavailability.
When glutathione depletion occurs, as it does in many PWCs, the body is
not able to rid itself of mercury with normal efficiency. PWCs who are
exposed to mercury from dental fillings, fish consumption, or nearby
environmental sources such as coal-fired power plants, therefore
experience a buildup of mercury in their bodies, and this can deplete
the bioavailable selenium, impacting not only the activity of the
glutathione peroxidase enzymes, but also those that convert the thyroid
hormone T4 to the more active hormone T3, as well as the other
selenoenzymes.

Nevertheless, Coxsackie B3 appears to be much less prevalent among PWCs
in North America. Again, perhaps this is a result of a smaller general
prevalence of this virus in this population because of its generally
higher selenium levels.

As I noted in my poster paper at the most recent AACFS meeting last
October
http://www.cfsresearch.org/cfs/research/treatment/15.htm
the herpes family viruses that are found to be producing infections in
PWCs are highly prevalent in their latent state in the general U.S.
population, and they are reactivated at the onset of CFS. It appears,
based on work at the University of Rome which I cited in that paper
(Palamara, A.T. et al., Antiviral Research 27, pp. 237-253 (1995)),
that the reactivation of these viruses in PWCs is a direct result of
glutathione depletion.

I would appreciate receiving comments on these hypotheses.

Rich Van Konynenburg. Ph.D.

~

:-)


Enjoy the sunsets and sunrises,

Diana Saba
Retired Nurse
FM ME/CFIDS
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