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@Travis stated "Without enzymes such as fatty acid synthase the body is incapable of creating excessive lipids even if it could, having lowered plasma glucose, and thus has no need to uncouple the mitochondria to commandeer its acetyl-CoA. In such a situation, with the cell operating under a more respirational suite of enzymes: the Warburg Effect evaporates, lactic acid decreases, and methylglyoxal in increased"
ACV/BS turns to acetate and is used as acetyl-CoA to couple mitochondria and evaporate the Warburg Effect. Aspirin would stop FAS, COX 1 & 2. Ubiquniol would aid in ECT. Thoughts?
slightly off topic but how do you recommend we take pau d'arco @Travis ? tea, extract, raw powder etc..? thanks
Personally, I'd would add the bark to coffee grounds in a French press—medium roast ground course. I have actually done this and it tastes good, just as pleasant had cinnamon bark been used instead. Yet baicalein is certainly no kitten and this can be purchased in purified form. Baicalein is indisputably the most powerful natural glyoxylase inhibitor among flavanoids, an observation demonstrated repeatedly through direct binding and inferred by its effect on cells. Baicalein has been shown to inhibit the translocation of both the androgen and the estrogen receptor in multiple studies, despite not binding them directly, and it has been confirmed repeatedly to catalyze the rate of carbonic anhydrase. These functions can be achieved by methylglyoxal acting through arginine ➝ hydroimidizalone signalling. I have confirmed that both the androgen and estrogen receptors have key arginine residues, the loss of which corresponds to loss of activity (i.e. androgen insensitivity). A key arginine binds the 3-keto group of DHT in the androgen receptor, in a manner completely analogous to how the ERα binds the 3-hydroxy group of estradiol. Carbonic anhydrase has many arginines, and the substitution* of one of them in particular translates into a 250-fold reduction in enzyme activity. The transformation of this arginine into a hydroimidizalone, by methylglyoxal, would be expected to enhance the transmission of the 'proton wire' leading out of the catalytic domain. Carbonic anhydrase has free access to its substrates carbon dioxide and water, and it's rate is limited only by the removal of its two products: the bicarbonate ion (HCO₃⁻) and protons (H⁺). It has been proven by enzyme kineticists that proton transfer is indeed the rate limiting step, perhaps the reason why adding pyrroles to solution always increases the enzyme's rate: A small planar dibasic molecule having a pKa ≈ 15.7 would be an ideal catalyst of rapid proton transmission in aqueous solution. Pyrrole has a pKa = 16.5 and has been shown to increase the rate of carbonic anhydrase. The pKa of imidazole is 14.9.
Four years before it's ability to inhibit glyoxylase had been discovered, baicalein had been shown to inhibit 12-lipoxygenase. This is still what the molecule is best known for, and you will in fact often see it listed as 12-lipoxygenase inhibitor. The arginine leading into 12-lipoxygenase is so important that it's called the 'Hornung determinant' and is responsible for binding the carboxy-end of fatty acids, swinging them into it's oxidizing catalytic domain. The arginine ➝ hydroimidizalone transformation of Hornung determinant—induced by methylgyoxal—would be expected to abrogate lipid binding.
[*] I think arginine had been replaced by valine, yet would expect a histidine substitution to effect a lesser change in kinetic rate. Since the carbonic anhydrase enzyme had been expressed and purified from yeast cells normally have high intracellular methylglyoxal concentrations, it could be presumed that particular carbonic anhydrase enzymes used in the abovementioned kinetic study did in fact had their exposed arginines pre-converted into hydroimidizalone..
Acetate is a very common cellular product, yet less often found in the extracellular space. There's some reason to believe that a larger percentage of extracellular acetate would affiliate with potassium over sodium, entering the cell as potassium acetate while displacing the latter. An increased intracellular K⁺/Na⁺ ratio translates into a greater absolute membrane potential, perhaps the single macroscopic parameter most highly correlated with mitotic rate. Alpha-tocopherol acetate does something similar yet chaperones calcium, an intracellular ion having other functions besides. Although osmotic balance is certainly a prime factor in cellular proliferation, this is no less a determinant than polyamine and glyoxylase systems. So from time to time, a brief mention of other natural ancillaries is still called-for—lest the should be forgotten: baicalein, lapachol, and selenomethionine have all been shown highly effective in slowing and preventing the proliferation of carcinogenic cells.
The idea of focusing on oxidative stress to recover seems to me just a milder version of the barbaric conventional approach. The goal must be to restore oxidation in the least stressful way.The studies talk about immune response so lets look at ROS some more
More on ROS:
Pathogen response[edit]
When a plant recognizes an attacking pathogen, one of the first induced reactions is to rapidly produce superoxide (O−2) or hydrogen peroxide (H
2O2) to strengthen the cell wall. This prevents the spread of the pathogen to other parts of the plant, essentially forming a net around the pathogen to restrict movement and reproduction.
In the mammalian host, ROS is induced as an antimicrobial defense. To highlight the importance of this defense, individuals with chronic granulomatous disease who have deficiencies in generating ROS, are highly susceptible to infection by a broad range of microbes including Salmonella enterica, Staphylococcus aureus, Serratia marcescens, and Aspergillus spp.
The exact manner in which ROS defends the host from invading microbe is not fully understood. One of the more likely modes of defense is damage to microbial DNA. Studies using Salmonella demonstrated that DNA repair mechanisms were required to resist killing by ROS. More recently, a role for ROS in antiviral defense mechanisms has been demonstrated via Rig-like helicase-1 and mitochondrial antiviral signaling protein. Increased levels of ROS potentiate signaling through this mitochondria-associated antiviral receptor to activate interferon regulatory factor (IRF)-3, IRF-7, and nuclear factor kappa B (NF-κB), resulting in an antiviral state.[15] Respiratory epithelial cells were recently demonstrated to induce mitrochondrial ROS in response to influenza infection. This induction of ROS led to the induction of type III interferon and the induction of an antiviral state, limiting viral replication.[16] In host defense against mycobacteria, ROS play a role, although direct killing is likely not the key mechanism; rather, ROS likely affect ROS-dependent signalling controls, such as cytokine production, autophagy, and granuloma formation.[17] -Wikipedia
ROS are produced as a normal product of cellular metabolism. In particular, one major contributor to oxidative damage is hydrogen peroxide (H2O2),
I found this interesting- Hydrogen peroxide is also used for tooth whitening. It can be found in most whitening toothpastes. Hydrogen peroxide has shown positive results involving teeth lightness and chroma shade parameters. It works by oxidizing colored pigments onto the enamel where the shade of the tooth can indeed become lighter. Hydrogen peroxide can be mixed with baking soda and salt to make a home-made toothpaste.[68]
So now I brush with 3% Hydrogen peroxide and BS 2x per day. My teeth are definitely whiter...but since this is done orally I wonder if I increase cellular ROS...
The idea of focusing on oxidative stress to recover seems to me just a milder version of the barbaric conventional approach. The goal must be to restore oxidation in the least stressful way.
But one can get caught up in the trees instead of looking at the forest. When the body has what it needs and is stimulated, it will control the amount of oxidative stress needed to take care of the problem. But when the focus is on stress, you tend to disturb more than needed and compromise other parts. Just an opinion.But " On the other hand, normal cells appear to have, under lower basal stress and reserve, a higher capacity to cope with additional ROS-generating insults than cancer cells do.[52][54] Therefore, the elevation of ROS in all cells can be used to achieve the selective killing of cancer cells." -Wikipedia
But one can get caught up in the trees instead of looking at the forest. When the body has what it needs and is stimulated, it will control the amount of oxidative stress needed to take care of the problem. But when the focus is on stress, you tend to disturb more than needed and compromise other parts. Just an opinion.