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Positive or negative?
I've always spelled out "baking soda" for that reason. But you ought to try BS. Works sometimes.
. I also have felt the metabolism boosting effect. Digestion feels cleaner, although I also started at the same time increasing my fiber so I can maybe increase my elimination, I know I was very against it, but..... I am open minded to trying new things when old things are not working so well.
Interesting.
That study is IV sodium acetate, but I just asked him about taking it as a supplement period. I assume he thought I meant oral, because how many people out there are gonna run sodium acetate IVs on themselves?
Interesting. I've mentioned to him using magnesium acetate (Mg carbonate reacted with apple cider vinegar) and he didn't say anything about it. I wonder if the issue is acid salts of sodium or acid salts in general.
i'm pretty sure that study had magnesium acetate too but it yielded a diff. respiratory ratio/less dramatic effects? gotta look at it again
Thanks. Do you have the full text? I only see the abstract.
I see the thermogenesis as a direct consequence of metabolism, and cannot realistically imagine any way to produce heat besides. I feel the confusion had started with the very discoverer of the uncoupling protein, D.G. Nicholls, who had noted an increase of heat independent of cellular changes in adenosine nucleotides. This observation of course would imply no change in metabolic rate had occurred, leading Nicholls and others since to hypothesize a perpetual and rapid 'electron cycling' between either side of the mitochondrial membrane. However: Nicholls had not measured guanosine nucleotides, and it has been since demonstrated that uncoupling protein has a GDP-binding domain. What uncoupling protein actually appears to accomplish is to switch oxidative respiration from adenosine to guanosine nucleotides. This could be expected to increase metabolism on account of a greater GDP substrate availability because most mitochondrial surface area would still be converting ADP into ATP. So if something should increase body heat without effecting vascular tone—i.e. facilitating environmental heat exchange—I feel it could only be doing so by affecting the metabolic rate. But since acetate regenerates the citric acid cycle via acetyl–coenzyme A, you might expect that it would liberate just as much CO₂ as hexose metabolism. Yet once it's noted that pyruvate decarboxylase—together with thiamine and α-lipoic acid—is the enzyme responsible for synthesizing acetyl–coenzyme A during normal hexose metabolism, then acetate's effect on the respiratory exchange ratio can perhaps be understood by its annulment of the made-superfluous CO₂ liberated through the pyruvate pathway.
I tried pretty hard to parse this, but struggling.
I certainly think uncoupling protein would increase oxygen flux, glycolytic rate, NADH formation, heat output, carbon dioxide production, and CO₂ flux—yet not necessarily its concentration. Carbonic anhydrase, which has multiple isoforms, can be expressed in many locations in diverse concentrations. Such things as γ-aminobutyric acid, methylglyoxal, and histamine have all been shown to influence the catalytic rate. Since methylglyoxal is formed from sugar metabolism and increases the enzyme's rate (Biswas, 2012), then concentration of carbon dioxide resulting from increased glycolysis could be partially-offset in some people more than others.
I believe this is because it is metabolized into primary amines—e.g. 5-amino-3-methylcatechol (Lenke, 1992)—all of which take a positive charge at physiological pH. Positively-charged ions and small molecules are attracted to the negative mitochondrial membrane potential (ψ ≈ −180 mV), and mitochondrial histology stains and assay reagents are always cationic by necessity. Ammonia (NH₃) largely becomes ammonium (NH₄⁺) at physiological pH, and I believe the toxicity from this derives from its displacement of intracellular potassium (K⁺) and mitochondrial affinity. Yet there could of course be a different means in which dinitrophenol 'uncouples' mitochondria besides a physical 'smothering effect,' and I have yet to read an article that had proposed a mechanism of action.
I suppose higher-than-average carbon dioxide could be better in many ways, and perhaps a better word than 'superfluous' would have been 'excessive.' I think perhaps I even had the word 'extraneous' in mind, yet had somewhat confounded that with 'superfluous' at some point. Besides that: I still think it's easy to see why acetate should produce less carbon dioxide than pyruvate, and also why Ray Peat was fair in likening acetate to fat metabolism. Beta-oxidation of course produces acetate without liberating any carbon dioxide in the process, yet glucose and fructose metabolism ultimately leads to pyruvate which releases CO₂ in forming coenzyme A-bound acetate. Taking acetate effectively bypasses pyruvate's carbon dioxide emitted when forming acetate. So sucrose should lead to a greater carbon dioxide flux than an isocaloric amount of fat.
That is fair, and some people could certainly do better with more carbon dioxide. I sleep with my head under my blankets so I do get a slightly hypercapnic at night, and thus far haven't experienced many side-effects. I had actually found an older article out of curiosity that had studied this, and the doctor–writer had concluded that the slight hypercapnia induced from this would be harmless. Yet with increased carbon dioxide flux comes more acidity, as carbonic acid is generated by carbonic anhydrase by using this as substrate.
Yes, and since problems with pyruvate dehydrogenase, or pyruvate oxidation have been demonstrated in CFS, this was originally why i was interested in this substance, sodium acetate, to "bypass" that step and make acetylcoa via a different route. But I would imagine ray would rather one use either something to activate PDH more, or directly impair PDK, like thiamine or DCA respectively. May have to revisit thiamine.
