What I read on the video was the following:
MMS changes the "mitochondrial membrane electrical potential" --- Leading to increased power in every cell in the body including immune system cells.
Could this be the reason I've experienced increased energy from my years-long experiences with MMS? I don't know the chemistry of the above claims, but on the surface, it would seem like a more plausible explanation for my almost immediate increased energy than the killing of pathogens, etc. --- I've long felt a core part of ME/CFS was somehow "electrical". The above description (mitochondrial membrane electrical potential) seems to fit in with my long held belief (bias?).
Hi
@Wayne I was looking at thiamine cures (as you most probably know I am on high thiamine with very good results) when I came across this case study in Germany:
Non-Hodkins Lymphoma Reversal with Dichloroacetate which gives a good explanation on how it works on the mitochondria. It is interesting that the good results occurred when this was paired with a lot of thiamine, which is also working on the mitochondria.
"DCA is a by-product of water chlorination [
6,
7] that inhibits aerobic glycolysis. It has been used in medicine for over 30 years [
8] as an investigational drug to treat severe metabolic disorders such as diabetes and hypercholesterolemia [
5,
9] as well as the treatment of congenital lactic acidosis in North American children [
10]. The bioavailability [
11] and pharmacokinetics [
12] of DCA have been well researched over several decades in adults [
6], children [
13,
14], and animals [
15]. As a medicinal, DCA is generally well tolerated from dosages between 10 mg/Kg and 50 mg/Kg, although prolonged exposure is associated with peripheral neuropathy [
16]. Its activation of the pyruvate dehydrogenase enzyme (PDH) of the mitochondria decreases glycolysis and reactivates glucose oxidation, a favorable approach to ameliorate lactic acidosis [
9].
Cancer cells predominantly utilize a system of glycolysis for energy instead of the glucose oxidation used by healthy cells. Cancer appears to be a form of intracellular lactic acidosis caused by a block in the oxidation of glucose at the level of PDH (pyruvate dehydrogenase). The glycolysis metabolism of glucose increases cancer cells’ lactic acid and reduces the intracellular pH [
7] resulting major shifts in the intracellular biochemistry. Aerobic glycolysis, known as the “Warburg Effect” [
17], inactivates mitochondrial respiration which allows cancer cell growth [
18]. DCA reverses this glycolysis causing several major detrimental changes in the cancer tumor cells.
First and foremost DCA inhibits pyruvate dehydrogenase kinase (PDK). PDK blocks pyruvate dehydrogenase (PDH) through its phosphorylation activity. When this kinase is inhibited by DCA, the PDH is reactivated causing the mitochondria to no longer be hyperpolarized, instead the membrane and the mitochondria are depolarized, reactivating the mitochondrial K+ channels which then decreases cytosolic K+. When PDH is inhibited in cancer cells by PDK, an excess cytosolic K+ occurs that inactivates the caspases 3 and 9, important factors in apoptosis. DCA reactivates these caspases along with an increase in H2O2 intracellularly, allowing the release of cytochrome c from the mitochondria. The release of cytochrome c is a major activating step for cell apoptosis as it triggers the caspase cascade [
19]. The results of DCA on cancers are seen both in vitro and in vivo. These effects are not seen in normal cells.
Dichloroacetate’s other major effect on cancer cells is the release of mitochondrial calcium (Ca++). The increase of Ca++ in cancer cells is associated with the increase and proliferation of transcription factors. Calcium also activates ornithine decarboxylase, the rate limiting enzyme in DNA synthesis [
20], and the antiapoptosis factor NFAT (nuclear factor of activated T lymphocytes) [
21]. When the calcium decreases with the introduction of DCA, the cell is further directed toward apoptosis and a decrease in cell replication. In addition to DCA causing a major shift in the mitochondria, cytoplasm, and cellular membrane [
19], the end effect of DCA is a cell cycle arrest in the Gap 1 phase (G1), which also increases apoptosis [
22]."
Be well!

Asklipia