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dvjorge
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Self-test monitoring of the Th1/Th2 balance in health
and disease with special emphasis on chronic fatigue
syndrome/myalgic encephalomyelitis

Chris Roelant1
* and Kenny De Meirleir2

1Protea Biopharma N.V., De Tyraslaan 111, 1120 Neder-Over-Heembeek, Belgium.
2Department of Human Physiology, Free University of Brussels (VUB), Brussels, Belgium.

Accepted 18 October, 2011

A simple “self-test” principle is described which allows patients to evaluate their Th1/Th2 balance
repeatedly over short periods of time to follow-up the effects of taking pre- and probiotics,
neutraceuticals, drugs or any other therapeutic strategy to balance Th1/Th2 status. By analysing a large
number of first morning urine samples obtained from individuals with medical conditions associated
with an overactive Th2 arm (ulcerative colitis, autism, blastocystis, mercury poisoning and viral
infection), a reaction principle was discovered that uses a redox-active colorimetric substrate changing
color upon reaction with metabolites present at high concentration in the urine samples of Th2-shifted
individuals. The development of color is time-dependent and quantitative. Moreover, 75% of urine
samples obtained from chronic fatigue/myalgic encephalomyelitis patients produced a time-dependent
and quantitative change of color compared to only 4% of the controls (perfectly healthy population),
providing evidence that chronic fatigue syndrome/myalgic encephalomyelitis is a condition associated
with an overactive Th2 arm.

See this fragment :

Solidification of the vicious circle: After the vicious circle has developed involving the methylation cycle block and the depletion of glutathione, another factor must come into play to lock in this situation chronically. It seems likely that buildup of toxins is the factor responsible for this, by blocking the formation of methylcobalamin and thus the activity of methionine synthase. It has been shown that one of the important roles of glutathione normally is to protect the very much smaller (by six orders of magnitude) concentrations of cobalamins from reaction with toxins by forming glutathionylcobalamin (134). Without this protection, cobalamins are vulnerable to reaction with a variety of toxins. An example is mercury. It has been found that very small concentrations of mercury are required to block the methionine synthase reaction (135). Because of this additional factor, attempts simply to correct the glutathione depletion and the oxidative stress after the cobalamins have reacted with toxins in most cases will not restore normal function of the methylation cycle (1).