'Adding Pyruvate makes ME cells normal' - What questions does this prompt?

ljimbo423

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It's also a known carcinogen.

If you've eaten any chicken in the US between 1949 and 2016, you have arsenic. Yes, it was added to chicken feed for decades...

More details on the removal of arsenic containing drugs given to chickens. It looks like all of them have been removed in the last few years.

According to this quote, there aren't anymore arsenic containing drugs given to chickens-

On April 1, 2015, Zoetis announced that it would discontinue marketing Histostat (nitarsone), the only remaining arsenic-based animal drug on the market, by Fall 2015, and would request withdrawal of the approval for the drug by the end of 2015.
https://www.fda.gov/AnimalVeterinary/SafetyHealth/ProductSafetyInformation/ucm257540.htm

Lucky for me I just started eating chicken on a regular basis in the last couple of years. Got in just under the wire.:lol:

EDIT- This is really good news to me. I thought they were still using those drugs. Thanks, caledonia for posting this!

Jim
 

caledonia

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Methyl90

Senior Member
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282
I've posted elsewhere about this before. I'm pretty certain that the normalization with pyruvate in Ron Davis’ test device is excellent confirmation that the pyruvate dehydrogenase (PDH) complex is in fact being inhibited by the PDH kinases (PDK1, 2 & 4) as found by Fluge & Mella.

Pyruvate is a potent inhibitor of the PDKs. Under the relatively simple test conditions Ron Davis is using I think it's most likely that the added pyruvate is simply de-inhibiting the PDH complex - by inhibiting the PDKs.

This is because of the following:

1.The activity of the PDH complex is under the complete control of the PDKs and the PDH phosphatases (PDPs). The reaction that the PDH complex performs in converting pyruvate to acetyl-CoA cannot be “driven” by adding additional pyruvate like you'd be able to do with many other enzymatic reactions.

2.No other pathways utilizing pyruvate as an energy source come even close to the amount of ATP produced by injection of the acetyl-CoA made by the PDH complex into the Krebs Cycle.

So the question is, what is causing the increased levels of PDKs? The unknown substance in the blood would presumably somehow be causing this.


Sorry if I recover this thread but in my personal experience with PDK inhibitors I strongly argue that the problem on glycolysis is greater.

ALA It worked very well initially as a 4 PDK inhibitor but it further lowered my pyruvate ... this made me realize the problem started earlier.

I inserted calcium pyruvate which brought enormous positive effects (500mg-1gr) ... now I would like to repeat the analyzes.

Obviously it is ALSO a PDK inhibitor so the use of glucose becomes efficient in all tissues and organs of the body ... as well as the release of insulin by the pancreas.
 
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