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high lactate levels in cfs , aerobic glycolysis

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there was some events intense oxidative stress of long duration . now the cfs patient is stuck in the cycle of high oxidative stress, high antioxidant system upregulation , and aerobic glycolysis . during times of oxidative stress certain antioxidant and glycolytic enzymes are upregulated . Normally muscle express PKM1 . PKM2 expression helps to deal with oxidative stress. PKM2 inhibits the activity of p53 . p53 is important for oxidative phosphorylation . p53 is found to be low in cfs . without adequate oxidative phosphorylation , we depend more on aerobic glycolysis for our energy production , hence the increase in lactate . Normallizing this cycle of high oxidative stress and normalizing the upregulated antioxidant system may result in normalizing p53 activity and normal energy production.
 
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No the antioxidant system is already running high . If they check muscle cells they would actually find high total glutathione levels but at the same time high oxidative stress , its a cycle one keeps the other going .

Whats getting people confused is they're testing mononuclear cells where the cfs mechanism is not happening . Ron Davis found downregulated glycolysis ( because they tested in patient serum which contained high 2,3dpg ). Another group out of Standford found a completely opposite result when they tested cfs mononuclear cells ( upregulated glycolysis and high atp levels ) . They tested without patient serum so did not conatin abnormal levels of 2,3dpg and the glycolytic enzymes adpted to inhibition by 2,3dpg when free of 2,3dpg had a rebound effect. But 2,3dpg is just a downstream metabolite of what is happening in muscle of cfs patents and cleaning up the 2,3dpg is not gona fix cfs .

The antioxidant system and aerobic glycolysis is upregulated and oxidative phosphorylation is downregulated in cfs . There are many enzymes that upregulated and many others are downregulated . To keep it simple i'll mention PKM2 and p53. I believe this mechanism can be normalized (maybe even simply). p53 has already been found low in cfs .p53 is very for oxidative phosphorylation . I'm looking into testing for PKM2 and 2,3dpg if available (the result of these could make me believe or not in this mechanism ). Shikonin and derivatives is what i'm looking at as a possible treatment . Shikonin is from a plant , the plant has other toxic substances so you gotta be careful . I wonder if pure shikonin products still contains these toxic products or have they been removed . The ultimate goal is normalize this mechanism and normalize p53 levels and get oxidative phosphorylation working normally again.
 
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no be careful , shikonin products may contain other compounds that are toxic can can liver damage , i'll look further into this mechanism first , and hopefully some blood testing , hopefully not have to do muscle biopsy and report back . pkm2 and 2,3dpg is what i'm looking to test for , there are many others but I don't have the resources or the time to test for all those other markers .