Re: Will Lugol's kill MRSA?

All this stuff depends on GSH deficiency, iodinated people are less GSH deficient...

http://www.doewatch.com/
(Censored)
The GSH damage process then allowed toxic metals to build up in the body as the phase I and phase II glutathione clearance was impaired. The loss of the liver bile pathway placed more clearance of metals demand on the kidneys, which set the stage to metabolic acidosis and shift of the blood pH toward acid, which further impaired toxic metal clearance. The rise of the toxic metals caused the cell mitochondria to produce increased rates of free radicals, which required the up regulation of the superoxide dimutase enzymes (Mn-SOD). These enzymes employed all the trace metal manganese, which upset the production of the cytokine interferon (IFN) and the production of effective 2-5A RNase L enzymes.

The high oxidative stress in the cells caused the mutation of the 2-5A RNase L enzyme from its normal 83 kDa MW to an ineffectual 37 kDa MW. This is the prime enzyme within cells that kills viral RNA by cleaving it, sets up cell apoptosis, and calls in the NK and macrophage cells. The mutation of this enzyme is the prime effect that allows cancer viruses to grow, HIV to grow, and Chronic-Fatigue-Syndrome problems with EBV, CMV, and mycoplasma to affect long-term health.

When this principle cellular enzyme that controls cell viral and mycoplasma mutates due to the manganese loss, the immune system goes into a Th-2 mode due the interferon cytokine system failing. As the varied viruses and mycoplasma effects proliferate within the cells of organs, they generate their own cytokine factors that cause the growth of blood supplies and uncontrolled cell growth for cancers. In other cases, depending on the genetic pre-dispositions, these viruses just cause increasing rates of cell damage leading to slow and eventual death.