It was mentioned that often Lactate will be higher than Pyruvate and Succinate would be likely low to non-existent in the model.

I've re-interpreted some of my older tests, and really only see this pattern in a most recent one (which is after a lot of gut related interventions)

Could this be confounded by SIBO / gut microbes as GPL proposes?

Quote from: shanman75 on June 27, 2021, 09:30:18 AM

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Yes - microbiome has potentially a huge part to play here (see paper 2).

Funnily enough, further research has shown that the "high lactate, low pyruvate, low succinate" levels would also be drive when high ROS / low a-KGDH exists, and simultaneously, low [B12/folate/riboflavin] + P5P, and low [GABA] + P5P exists. At this stage, you'd expect to see HIF-1a issues (low PDH - high lactate) and downstream connective tissue issues from prolyl hydroxylase deficiencies.

I only included the GABA->succinate pathway, via SSAL in the figure for the 3rd paper (which is the main method of GABA metabolism), however there are a number of others. B12 is the other one I'd finger the most here. (see bottom left quadrant, below)

Quite interesting. Yes, an overall reduced cofactor availability would also create malformations of the cycles.

That doesn't leave one a good option for confirming the situation of Glutamine shunting is occurring.

My last Genova OAT (From the end of March, below) is the one that shows the most characteristic (after much "gut cleaning" interventions, but I still had pretty high Arabinose / Arabinitol ... indicating yeast still present).

Prior to learning of your research, I was very puzzled by the high lactate given I know I have enough Thiamine to drive the Pyruvate into the Kreb cycle and was definitely not doing any heave anaerobic work. The model of Glutamine shunting sub-driving the Kreb is a reasonable explanation for much of the Kreb lumpiness in this sample.

If the Urea cycle turns more to process Ammonia, that might make sense! I was definitely having mild headaches during the period which I thought were mainly caused by the elevated Lactate.

My diet was under-caloric the day before and low carb (18g) according to Cronometer. I took .2g of Tryptophan the night before to test the Kynurenic pathway and get a read on B6 status (alongside a plasma test). Plasma B6 was low quartile 5.5ng/mL (2.1-21.7 ng/mL range). 

Both XA and KA were reasonably high (barely within normal, but I had only taken .2g instead of the 2g test). So, I am reasonable positive I had lowered B6 function. A possible confounder in the "quantification" of EBV impact given it likely limited pathways the hypothesized EBV modification puts pressure on. (I also have HSV-1, but believe that it's far more limited in activity than EBV)

Hippurate is the only blip, and it could easily be confounded by SIBO, which I definitely had at the time (and, may still have now...though I've gone thru two rounds of anti-microbials since).

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All aside, I'm beginning to think that OAT is a very poor way to quantify one's current HHV state.

It would be nice to have a way to evaluate Ammonia and Lactate levels. Lactate in the blood is possible, but pricey. And, the Ammonia tools available seem to be more calibrated to monitoring fish tanks...probably too inaccurate.