Prefacing everything I mention below as "specifically, in our disease model", "this is not medical advice", "YMMV", etc -
"For a moment, hypothetically
forget everything you know about the immune response, or that we've heard the words 'triterpenes' or 'reishi'."
(I think I gave
@Hoosierfans a mild heart-attack earlier, as I ineloquently gave her a preview of this post content and my casual phrasing may have given her the impression I was abandoning my research. lol.. Not a chance!)
Lets carefully look at the disease model again and at the ROOT CAUSE of the cascade.
Per paper 3: All non-autoimmunity issues (AKA lytic phase) are created by the ratio of activity between
GDH and
a-KGDH.
View attachment 42896
The carbohydrate intake profile therefore becomes a sensitive lever (or driving force) for creating ongoing or additional ROS and PEM, primarily because the concomitant hyper-secretion of insulin (caused by high
GDH) is forcing energy into the mitochondrial reactions (think about kids getting "high" on sugar).
1) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3178282/
2) https://diabetes.diabetesjournals.org/content/51/3/712
3) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3136010/
Simultaneously, due to high
GDH:
If the mitochondria have been getting force-fed mostly from "anaplerosis" via
a. glutaminolysis (->),
b. glutamate->a-KG (with high NAD+),
or
c. (once ROS becomes so high that the mitochondria "fragments", being very low /
depleted a-KGDH), transamination at akg->glutamate + aspartate->oxaloacetate
d. excess urea->fumarate
e. excess B12+P5P->succinate (human intervention)
then there is already "sufficient" (or excess, rather) energy inside the mitochondrial reactions.
This means that due to "load sensing" vs "energy availability", glycolysis would be much less used and you'll likely see lactate later becoming higher than pyruvate.
Likewise, fatty acid oxidation will not be triggered as much... (which is probably helpful, considering that once the nitrogen excess has begun ramping up the disposal process via phenylacetylglutamine, acetyl-CoA is being rapidly depleted, impairing beta-oxidation - needed for burning fat, etc.)
Once acetyl-CoA starts being depleted, the cascade of messes start.
(see post #74 for some of the many examples)
So, to CONTROL ALL OF THE METABOLIC ISSUES, it’s all about maintaining GDH vs a-KGDH, at the core of everything.
Once the ROS get too high, this becomes a runaway train and the symptoms snowball, because a-KGDH is ALWAYS going to be lower than GDH. "It's a trap!"
The ROS needs to be "reset" before you can climb out.
Accordingly, we can turn off PEM, burning, high glutamate / low GABA etc., without fixing the immune side, however this is "just" symptomatic remission.
The Balancing Act:
After we've cleared out -
1) The ammonia->urea issues, via eg. consuming additional water + (BCAAs, benzoate, B5, glycine, cysteine)
2) The energy overload crisis, high ROS has been arrested / reset (via induced carbohydrate, energy deficit)
The protocol aims to decrease and maintain all of the ROS-dysregulating factors to the barest minimum and normalise
GDH.
The ROS is .. very highly catered for in the protocol (Vitamin C, E, R-ALA, liposomal glutathione, carb management and additional factors like eating broccoli / sulforaphane, etc.).
This therefore normalises
a-KGDH.
The
GDH elevation is treated by a combination of the triterpenes and EGCG. The dosing is based on a “natural model”, which includes one-or-more HHV infection(s) and no other drug interactions / pathogens / variables.
In many people (who don’t have any extra "unnatural" GDH altering factors), the suggested 25mg EGCG dose, every 4.5 hours is now quite balanced, when combined with the GDH "normalising" effect of the tripterpenes from reishi.
In others people, assuming the ROS/low
a-KGDH issues are now resolved (no salicylates, arsenic, heavy metals, etc),
GDH may still be too high, due to extra variables in play, or "bad reishi".
GDH / glutamate increasing factors:
Androgens (Endogenous: 5-AR metabolites, such as DHT. Exogenous: synthetic androgens that are either suitable DHT-derivatives or have an affinity for 5-AR and act as a suitable ligand to programatically alter GDH.)
Various drugs (we need to make a list of these), such as gabapentin, pregabalin (?)
Leucine (when above a serum threshold)
Sodium (when above a serum threshold)
Other infections:
C.diff
GDH / glutamate decreasing factors:
EGCG
Caffeine (however increases beta-oxidation efficiency and can create more ROS / increased energy availability)
.. others(?)
ROS increasing / a-KGDH decreasing factors:
Low E
Low C
Low glutathione (depleted glycine, P5P, cysteine, B5), etc
Lots of mTOR (viral activity, tissues adaptations - resistance training, immune response)
Some radiant energy sources
Excess serum glucose (+ excess insulin)
Excess Succinate (or B12 + P5P)
Excess Fumarate (urea, etc)
..
So, if someone is still seeing PEM, etc and their
a-KGDH / ROS management is being correctly handled, this only leaves the
GDH variable.
The simple answer is that after being absolutely sure that a-KGDH isn't impaired (feeling hypoxic, or the succinate challenge may help here), we can keep increasing the EGCG dose amount until PEM / burning stops, while temporarily dosing extra water, BCAAs, benzoate, B5, glycine, cysteine. (If this dose gets too high, we may see elevated ALT in pathology markers, showing alanine is being used to make glutamate.)
However with drugs like gabapentin, BCAAs may not work well, because gabapentin disables one of the key cycles that the BCAAs influence here.
View attachment 42895
Normalising serum hormones, by increasing estrogen and/or decreasing DHT by increasing anti-androgens (DHEA / spironolactone) may also be helpful here.
