Amazoniac
Member
As many of my readers know, mainstream science has been catching up on the malefits of excess lactate but continues to erroneously refer to it as lactic acid believing the terms to be interchangeable. Well, in yet another striking example of synchronicity (Synchronicity - Wikipedia), just a few days after posting again that plain thiamine HCl treats... everything, including cases of "lactic acidosis", the article below appeared on my news feed. It corroborates Peat's claim that mainstream consensus lags behind advances in the medical field and decades are needed for a revised concept to gain acceptance. Not only that, but it adds to the evidence that detrimental effects when there's too much lactate are a concern whether it's the acid (exogenous) or base (endogenous) form, they end up being metabolized similarly. Now, when lactic acid is invoked in the context of what takes place in our cellular respiration, the rescuing principle is ignored. In other words, it fails to acknowledge the very purpose for its generation, which is to put protons to use and prevent local acidification while regenerating NAD+ (see attached table), the molecule of life. When I mentioned it to a few doctors (who have adopted me against my will), the responses were nothing but dismissive, it just shows how dogmatic, idiotic, incapacitating, imbecilizing, indoctrinating, rigidifying, misleading, putrid, disgraceful, immoral, miserable, satanic, son of a b****, and damaging the academic shaping of your common white coat can be.
@aguilaroja @Drareg @Regina @tankasnowgod
Researchers unravel how humans differ from a pot of yogurt
Lactate, not Lactic Acid, is Produced by Cellular Cytosolic Energy Catabolism
"...it is unfortunate that the authors referred to cellular lactate production as lactic acid, repeatedly associated cellular lactic acid production as a cause of acidosis, and used the term lactic acid within their title. Such repeated use, totaling 50 occurrences of “lactic acid” throughout the entirety of the manuscript, severely detracts from the scientitic quality of their work."
"...there is no such entity as lactic acid in any living cell or physiological system. Indeed, it is impossible, based on the fundamental laws of physics that underpin the disciplines of organic chemistry, metabolic biochemistry, acid-base chemistry, and physiology, for lactic acid to be produced or present in living systems where cellular and tissue pH is regulated to be between 6.0 and 7.45."
"Sun et al. (12) explained cellular lactate production as the conversion of pyruvate to lactic acid (not true), that this was a reaction within glycolysis (not true, although there is debate as to what constitutes the true end of glycolysis, pyruvate or lactate), and that because of the low pKa of lactic acid (pK = 3.86) (true) [although the NIST (8) reference resource has this as pK = 3.67], there was an immediate and near-complete dissociation of lactic acid to lactate and a proton (H+) (p. 453) (not true because in living systems there is no lactic acid to begin with)."
"For glycolysis, there are nine reactions, commencing with the 6-carbon substrate glucose-6-phosphate (G6P) and ending with two 3-carbon pyruvate molecules (see Ref. 9, Table 2, p. R506). The first carboxylic functional group intermediate of glycolysis is produced in the sixth reaction where 1,3-bisphosphoglycerate is converted to 3-phosphoglycerate (see Ref. 9, Fig. 5, p. R507). This is a phosphate transfer reaction, adding the phosphate to ADP forming ATP, with the co-production of 3-phosphoglycerate having an ionized (unprotonated) carboxylic functional group at carbon-3. This is key to understanding the H+ load of glycolysis and H+ metabolic buffering from lactate production. Each glycolytic intermediate following this reaction remains in an ionic form. There is never a glycolytic production of a carboxylic acid since they are all carboxylic ions. This remains true for obvious acid-base reasons from 3-phosphoglycerate to 2-phosphoglycerate to pyruvate and then to lactate. There is no metabolic production of lactic acid or any preceding glycolytic carboxylic ion metabolite, and, as previously explained, lactate production consumes, not releases, ~H+ (see Table 1; also see Ref. 9, Fig. 9, p. R509)."
"From the data of Table 1, it is clear that lactate production consumes a H+ load that is essentially stoichiometric to lactate production, regardless of pH across the cellular pH range. Conversely, as cellular pH declines, pertinent reactions of glycolysis sum to be more net ~H+ releasing. Glycolysis is independently ~H+ releasing, and the ~H+ consumption of lactate production opposes this, and it is unlikely that perfect matching of H+ exchange ever occurs, as is commonly represented in summary metabolic equations of glycolysis [−2 H+ (release)] and lactate production [+2 H+ (consumption)]. Indeed, as a cell becomes more acididic, there is an increasing ~H+ release from glycolysis, whereas that for lactate remains essentially unchanged."
"We understand that the term “lactic acidosis” has been used in clinical research and practice for more than 100 years. With the duration of this use comes considerable engrained misunderstanding and misapplication, and to expect a rapid change from any engrained convention may be unrealistic. However, given that the terminology is wrong based on incorrect understanding of metabolic biochemistry and acid-base chemistry, that clinical practice involves treating illnesses and saving lives from premature mortality, and that correct treatment most often requires a correct understanding of the true mechanisms of disease and symptomology, one would hope that clinical professionals would prefer to base their practice on empirical truths rather than engrained convention."
"It has been encouraging to see many physicians altering their view of a lactic acidosis based on revised explanations consisting of expressions of elevated blood lactate (hyperlactatemia) and an associated (or not) systemic acidosis (3, 5, 7). For example, considerable research of hyperlactatemia occurs for the condition of sepsis (3, 5, 7) and also metformin toxicity (1). For sepsis, hyperlactatemia is predictive of disease severity and premature mortality, with more than a threefold increase in mortality when hyperlactatemia is accompanied by tissue hypo-perfusion (5). The prior conventional interpretation of sepsis-associated hyperlactatemia accompanied by acidosis is framed on belief in a causal connection between the disease state, altered perfusion causing a localized hypoxia, stimulation of glycolysis, and lactic acid-induced metabolic acidosis. This is false knowledge, since there is no such condition as lactic acid-induced metabolic acidosis. The increased lactate presumably occurs due to increased stimulation of energy catabolism, causing increased substrate flux through glycolysis, which will therefore also increase lactate production and/or compromise blood lactate removal. For many patients, there is no accompanied acidosis (3, 5, 7), which is consistent with the metabolic biochemistry of the combined production of lactate and the retained function of mitochondrial respiration, since a continual H+ supply is needed as a substrate for each aspect of energy catabolism. For patients with a systemic acidosis, there could be a localized or systemic inflammatory response that triggers altered mitochondrial function and a metabolic milieu now consistent with metabolic acidosis (3, 7). Such a scenario is more aligned with altered mitochondrial respiration (normally a H+ sink) accompanied by increased glycolytic stimulation, the consequence of the two conditions causing increased net H+ release and an eventual acidosis."
@aguilaroja @Drareg @Regina @tankasnowgod
Researchers unravel how humans differ from a pot of yogurt
Lactate, not Lactic Acid, is Produced by Cellular Cytosolic Energy Catabolism
"...it is unfortunate that the authors referred to cellular lactate production as lactic acid, repeatedly associated cellular lactic acid production as a cause of acidosis, and used the term lactic acid within their title. Such repeated use, totaling 50 occurrences of “lactic acid” throughout the entirety of the manuscript, severely detracts from the scientitic quality of their work."
"...there is no such entity as lactic acid in any living cell or physiological system. Indeed, it is impossible, based on the fundamental laws of physics that underpin the disciplines of organic chemistry, metabolic biochemistry, acid-base chemistry, and physiology, for lactic acid to be produced or present in living systems where cellular and tissue pH is regulated to be between 6.0 and 7.45."
"Sun et al. (12) explained cellular lactate production as the conversion of pyruvate to lactic acid (not true), that this was a reaction within glycolysis (not true, although there is debate as to what constitutes the true end of glycolysis, pyruvate or lactate), and that because of the low pKa of lactic acid (pK = 3.86) (true) [although the NIST (8) reference resource has this as pK = 3.67], there was an immediate and near-complete dissociation of lactic acid to lactate and a proton (H+) (p. 453) (not true because in living systems there is no lactic acid to begin with)."
"For glycolysis, there are nine reactions, commencing with the 6-carbon substrate glucose-6-phosphate (G6P) and ending with two 3-carbon pyruvate molecules (see Ref. 9, Table 2, p. R506). The first carboxylic functional group intermediate of glycolysis is produced in the sixth reaction where 1,3-bisphosphoglycerate is converted to 3-phosphoglycerate (see Ref. 9, Fig. 5, p. R507). This is a phosphate transfer reaction, adding the phosphate to ADP forming ATP, with the co-production of 3-phosphoglycerate having an ionized (unprotonated) carboxylic functional group at carbon-3. This is key to understanding the H+ load of glycolysis and H+ metabolic buffering from lactate production. Each glycolytic intermediate following this reaction remains in an ionic form. There is never a glycolytic production of a carboxylic acid since they are all carboxylic ions. This remains true for obvious acid-base reasons from 3-phosphoglycerate to 2-phosphoglycerate to pyruvate and then to lactate. There is no metabolic production of lactic acid or any preceding glycolytic carboxylic ion metabolite, and, as previously explained, lactate production consumes, not releases, ~H+ (see Table 1; also see Ref. 9, Fig. 9, p. R509)."
"From the data of Table 1, it is clear that lactate production consumes a H+ load that is essentially stoichiometric to lactate production, regardless of pH across the cellular pH range. Conversely, as cellular pH declines, pertinent reactions of glycolysis sum to be more net ~H+ releasing. Glycolysis is independently ~H+ releasing, and the ~H+ consumption of lactate production opposes this, and it is unlikely that perfect matching of H+ exchange ever occurs, as is commonly represented in summary metabolic equations of glycolysis [−2 H+ (release)] and lactate production [+2 H+ (consumption)]. Indeed, as a cell becomes more acididic, there is an increasing ~H+ release from glycolysis, whereas that for lactate remains essentially unchanged."
"We understand that the term “lactic acidosis” has been used in clinical research and practice for more than 100 years. With the duration of this use comes considerable engrained misunderstanding and misapplication, and to expect a rapid change from any engrained convention may be unrealistic. However, given that the terminology is wrong based on incorrect understanding of metabolic biochemistry and acid-base chemistry, that clinical practice involves treating illnesses and saving lives from premature mortality, and that correct treatment most often requires a correct understanding of the true mechanisms of disease and symptomology, one would hope that clinical professionals would prefer to base their practice on empirical truths rather than engrained convention."
"It has been encouraging to see many physicians altering their view of a lactic acidosis based on revised explanations consisting of expressions of elevated blood lactate (hyperlactatemia) and an associated (or not) systemic acidosis (3, 5, 7). For example, considerable research of hyperlactatemia occurs for the condition of sepsis (3, 5, 7) and also metformin toxicity (1). For sepsis, hyperlactatemia is predictive of disease severity and premature mortality, with more than a threefold increase in mortality when hyperlactatemia is accompanied by tissue hypo-perfusion (5). The prior conventional interpretation of sepsis-associated hyperlactatemia accompanied by acidosis is framed on belief in a causal connection between the disease state, altered perfusion causing a localized hypoxia, stimulation of glycolysis, and lactic acid-induced metabolic acidosis. This is false knowledge, since there is no such condition as lactic acid-induced metabolic acidosis. The increased lactate presumably occurs due to increased stimulation of energy catabolism, causing increased substrate flux through glycolysis, which will therefore also increase lactate production and/or compromise blood lactate removal. For many patients, there is no accompanied acidosis (3, 5, 7), which is consistent with the metabolic biochemistry of the combined production of lactate and the retained function of mitochondrial respiration, since a continual H+ supply is needed as a substrate for each aspect of energy catabolism. For patients with a systemic acidosis, there could be a localized or systemic inflammatory response that triggers altered mitochondrial function and a metabolic milieu now consistent with metabolic acidosis (3, 7). Such a scenario is more aligned with altered mitochondrial respiration (normally a H+ sink) accompanied by increased glycolytic stimulation, the consequence of the two conditions causing increased net H+ release and an eventual acidosis."
Attachments
Last edited: