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While this explanation touches on some interesting concepts, there are several points that need clarification and might be oversimplified or speculative: Lets start with neuronal compensation
The interplay between autophagy and ferroptosis exerts a marked yet context-dependent influence on LC progression, functioning as a precise biological rheostat that can be co-opted to either promote tumor progression or trigger tumor suppression
Oral administration of glutathione cannot be assumed to have a physiological effect due to hydrolysis in the gastrointestinal tract, and giving large quantities of glutathione percursors such as cysteine may actually increase neurological concentrations of sulfhydryl-reactive heavy metals
I truly appreciate the intention to explore performance and recovery science more deeply
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