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IROM

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Feb 25, 2020
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148
Anyone have any clue about the musuclar dystrophy? My girlfriend's sister has the disease and I just want to know if Ray Peat has ever said anything about it. Is distrophin just a red herring? Most of what I see as symptomology is large amounts of pyruvate and lactate in the bloodstream which indicates a breakdown in the Krebs and Randall cycle.

@haidut had mentioned Acetoacetate cures MD in mice and that makes sense because Acetate =(acetyl-CoA) it is a direct precursor to ATP and it processes pyruvate which otherwise in excess would turn into lactate. I am coming from the Peatarian assumption that it is a metabolic disease and if sufficient ATP was produced the body would not catabolize muscle. Pyruvate-and-Ac-CoA-metabolism-Pi-inorganic-phosphate-CO2-carbon-dioxide-Enzyme (1).png.

Acetate is also required for proper fatty acid metabolism... and people with muscular dystrophy have abnormal fat tissue.

I think I am onto something but do not want to reinvent the wheel if this has already been discussed.
 

mostlylurking

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Most of what I see as symptomology is large amounts of pyruvate and lactate in the bloodstream which indicates a breakdown in the Krebs and Randall cycle.

also:

"Thiamine participates as a cofactor in oxidative phosphorylation, and its absence is sorely missed.

Historically, this is a cause of lactic acidosis in the malnourished patient in who there is no other apparent cause of lactic acidosis.

diagram of lactic acidosis in thiamine deficiency


Among its many uses, thiamine acts as a coenzyme with pyruvate dehydrogenase to form acetyl-CoA. So of course, if you completely abolish thiamine, there will be no entry for pyruvate into Krebs cycle. And even if it could enter, alpha-ketoglutarate dehydrogenase would also need thiamine as a coenzyme to convert alpha-ketoglutarate into succynyl coenzyme A. Thus, a deficiency of thiamine produces an excess of lactate by preventing pyruvate from becoming a substrate for oxidative metabolism."
 
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mostlylurking

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@IROM : I found an article by Ray Peat that addresses lactate: Lactate vs. CO2 in wounds, sickness, and aging; the other approach to cancer Vitamin B1 = thiamine.

"The features of the stress metabolism include increases of stress hormones, lactate, ammonia, free fatty acids, and fat synthesis, and a decrease in carbon dioxide. Factors that lower the stress hormones, increase carbon dioxide, and help to lower the circulating free fatty acids, lactate, and ammonia, include vitamin B1 (to increase CO2 and reduce lactate), niacinamide (to reduce free fatty acids), sugar (to reduce cortisol, adrenaline, and free fatty acids), salt (to lower adrenaline), thyroid hormone (to increase CO2). Vitamins D, K, B6 and biotin are also closely involved with carbon dioxide metabolism. Biotin deficiency can cause aerobic glycolysis with increased fat synthesis (Marshall, et al., 1976)."
 

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