Metabolite analysis in Covid cases.
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In the Upper Right, the light colour shows high concentrations in severe cases.
In the Lower Left, the light colour shows high concentrations of different chemicals in mild cases.
So what does this tell us?
In mild cases, Glucose is low, and Glutamine is high. Humans are not making glucose out of glutamine.
In mild cases, Amino acids(pale green names) are high. Protein isn't being broken down.
In mild cases, there are also almost no ketones in the plasma. Fat mass is being left alone.
In the hospitalized cases, different story. Glucose is sky high. Where is it coming from? Protein breakdown, as the amino acids go almost to zero. Why is the body obsessed with making so much glucose? Because remember, the mitochondria are switched off as there's little oxygen, and HIF-1alpha gets made. So enormous amounts of glucose are being used for very little energy output. It's virtual starvation going on, with protein breakdown to amino acids almost depleted for energy, and fats going to make b-hydroxybutyrate.
This situation is akin to running a starship without its main power supply. Just as we use aux sources of energy to keep going there, we can do the same here.
If we accelerate the fats breakdown to acyl co-A , we can get power from beta-oxidation pathway. That would slow down all the destruction going on to make more glucose.
From general knowledge:
Fibrates also enhance fatty acid oxidation via acyl CoA synthetase and other enzymes, which further reduce the synthesis of triglycerides.
Logically Fibrates should fix this. Do they?
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Lipid-lowering drug TriCor dramatically cuts treatment time for severe COVID-19 patients
The SARS-CoV-2 virus has infected over 165 million people worldwide causing nearly 3.5 million deaths. Recent vaccination efforts have been hindered by multiple coronavirus variants that challenge current vaccines.
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...the patients were given 145 mg/day of TriCor (fenofibrate) for 10 days and continuously monitored for disease progression and outcomes. "The results were astounding", shared Nahmias. "Progressive inflammation markers, that are the hallmark of deteriorative COVID-19, dropped within 48 hours of treatment. Moreover, 14 of the 15 severe patients didn't require oxygen support within a week of treatment,
The theory is foundationally rock solid.
Instead of buying Ivermectin, this is what people ought to be looking at. FENOFIBRATE.
Also, supplementing the mitochondria directly with l-Carnitine to move the fats in, plus alpha-ketoglutarate to kickstart Krebs cycle( it will be short, as it's shunted to make glutamate for energy), and supplementing glutamine IV. These are normal metabolites, which pose no hazard, as our bodies generate them all the time. I still feel that the use of Apigenin is logical since it blocks HIF-1 alpha, and will conserve NAD via inhibiting CD 38, an important energy cofactor.
There's a minor pathway to breakdown fats in peroxisomes, which uses acyl-CoA too, but it makes a lot of peroxide. It would probably be a good idea to supply NAC and glycine to make glutathione to mop up that excess oxidation. Chances are the peroxisome pathway might be accelerated if mitochondria are stalled out.
Instead of buying Ivermectin, this is what people ought to be looking at. FENOFIBRATE.
Also, supplementing the mitochondria directly with l-Carnitine to move the fats in, plus alpha-ketoglutarate to kickstart Krebs cycle( it will be short, as it's shunted to make glutamate for energy), and supplementing glutamine IV. These are normal metabolites, which pose no hazard, as our bodies generate them all the time. I still feel that the use of Apigenin is logical since it blocks HIF-1 alpha, and will conserve NAD via inhibiting CD 38, an important energy cofactor.
There's a minor pathway to breakdown fats in peroxisomes, which uses acyl-CoA too, but it makes a lot of peroxide. It would probably be a good idea to supply NAC and glycine to make glutathione to mop up that excess oxidation. Chances are the peroxisome pathway might be accelerated if mitochondria are stalled out.
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