but it seems like there's real concern about DCA toxicity.
I detail my particular experience with DCA here, in which I also address toxicity:
From brain fog to clarity in 30 minutes. That particular thread is actually misnamed now given that at my current dosage of DCA (1.5g/day) there is zero brain fog: I wake up from sleep fully energized. And there might even be an explanation for that, here:
Sleep and Brain Energy Levels: ATP changes during sleep.
Doesn't it basically inhibit aerobic and anaerobic glycolysis?
DCA makes sure pyruvate is converted to acetyl-CoA instead of lactate. Acetyl-CoA is subsequently fed into the Krebs cycle leading to the production of ATP in the mitochondrial electron transport chain. With DCA, you get less lactate and more ATP. Note that DCA doesn't inhibit the production of lactate, it simply prevents most of the pyruvate from ending up converted to it. This is due to the fact that pyruvate dehydrogenase is subject to product inhibition: too much acetyl-CoA will inhibit pyruvate dehydrogenase. This works as negative feedback to prevent over-production of acetyl-CoA.
My initial objection was toward making a definitive statement that DCA is the only thing that is likely to help.
Understood, although you keep forgetting that what I said was "anything without dichloroacetate will
probably won't help
a great deal." (I'm even keeping the broken English!) Note my use of "
probably" and "
a great deal." This assertion of mine is based on
Fluge et al conclusion that:
"The amino acid pattern suggested functional impairment of pyruvate dehydrogenase (PDH), supported by
increased mRNA expression of the inhibitory PDH kinases 1, 2, and 4"
Increased expression of the various PDKs is not the same as PDH deficiency. As such, what might work for a genetic PDH deficiency won't necessarily work for increased PDK expression.