"The Primary Sources Of Acidity In The Diet Are Sulfur-containing AAs, Salt, And Phosphoric Acid"

[Amazoniac]

- The Continuum of Acid Stress

Acid-related injury from chronic metabolic acidosis is recognized through growing evidence of its deleterious effects, including kidney and other organ injury. Progressive acid accumulation precedes the signature manifestation of chronic metabolic acidosis, decreased plasma bicarbonate concentration. Acid accumulation that is not enough to manifest as metabolic acidosis, known as eubicarbonatemic acidosis, also appears to cause kidney injury, with exacerbated progression of CKD. Chronic engagement of mechanisms to mitigate the acid challenge from Western-type diets also appears to cause kidney injury. Rather than considering chronic metabolic acidosis as the only acid-related condition requiring intervention to reduce kidney injury, this review supports consideration of acid-related injury as a continuum. This “acid stress” continuum has chronic metabolic acidosis at its most extreme end, and high-acid-producing diets at its less extreme, yet detrimental, end.

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- An obsession with CO2

The concept that underlies this paper is that carbon dioxide (CO2) removal is at least as important as the delivery of oxygen for maximum performance during exercise. Increases in CO2 pressure and reductions in the pH of muscle influence muscle contractile properties and muscle metabolism (via effects on rate-limiting enzymes), and contribute to limiting symptoms. The approach of Barcroft exemplified the importance of integrative physiology, in describing the adaptive responses of the circulatory and respiratory systems to the demands of CO2 production during exercise. The extent to which failure in the response of one system may be countered by adaptation in another is also explained by this approach. A key factor in these linked systems is the transport of CO2 in the circulation. CO2 is mainly (90%) transported as bicarbonate ions--as such, transport of CO2 is critically related to acid-base homeostasis. Understanding in this field has been facilitated by the approach of Peter Stewart. Rooted in classical physico-chemical relationships, the approach identifies the independent variables contributing to homeostasis--the strong ion difference ([SID]), ionization of weak acids (buffers, Atot) and CO2 pressure (PCO2). The independent variables may be reliably measured or estimated in muscle, plasma, and whole blood. Equilibrium conditions are calculated to derive the dependent variables--the most important being the concentrations of bicarbonate and hydrogen ions. During heavy exercise, muscle [H+] can exceed 300 nEq.L-1 (pH 6.5), mainly due to a greatly elevated PCO2 and fall in [SID] as a result of increased lactate (La-) production. As blood flows through active muscle, [La-] increase in plasma is reduced by uptake of La- and Cl- by red blood cells, with a resultant increase in plasma [HCO3-]. Inactive muscle contributes to homeostasis through transfer of La- and Cl- into the muscle from both plasma and red blood cells; this results in a large increase in [HCO3-]. In the lungs, oxygenation of hemoglobin increases red blood cell [A-] aiding rapid conversion of HCO3- into CO2 in red cells (containing carbonic anhydrase), with diffusion of CO2 into alveoli, but full equilibration of the CO2 system in plasma may not occur during the short pulmonary capillary circulation time in heavy exercise. The ionization state of imidazole groups on protein histidine may provide integration between acid-base homeostasis, membrane anion transfer proteins, and activation of rate-limiting enzymes.

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[Amazoniac]

- Lipopolysaccharide directly inhibits bicarbonate absorption by the renal outer medullary collecting duct

 

[Amazoniac]

- A Brain Protein–Centered View of H+ Buffering

Spoiler

"In the traditional approach to buffering of H+ during metabolic acidosis, the sole focus is on lowering the H+ concentration, but this overlooks several important points. First, increased binding of H+ to proteins changes their charge, shape, and possibly function. Second, organs in which buffering of H+ occurs is not assessed even though it would be advantageous to spare brain proteins in this process. Third, only the arterial and not the capillary Pco2 of individual organs is considered. This article provides a “brain protein–centered” view, which leads to different conclusions concerning the way H+ are removed physiologically."

Spoiler

Source: the internet.

 

[Amazoniac]

- Amino acid | Wiktionary
- The acid-base properties of amino acids | Revision Science

 

[Sani]

How chloride from salt can be bad when it's the only thing that cured my acid reflux? My acid reflux started when I stopped adding salt to my food and it lasted almost a year. I even started to plan suicide, the pain was so bad every single day every second. When I started to add salt to my food a little ovet 1 tsp per day, the acid reflux was gone in less than two weeks.

 

[yerrag]

How chloride from salt can be bad when it's the only thing that cured my acid reflux? My acid reflux started when I stopped adding salt to my food and it lasted almost a year. I even started to plan suicide, the pain was so bad every single day every second. When I started to add salt to my food a little ovet 1 tsp per day, the acid reflux was gone in less than two weeks.

Yeah. Good you learned your lesson.

An uncle of mine he was salt-free for so long. No surprise he died young.

Stupid doctor of his. He lived a short life of eating bland food. Probably better outcome though. Why live long when you can't even enjoy what you eat right?

 

[Sani]

Yeah. Good you learned your lesson.

An uncle of mine he was salt-free for so long. No surprise he died young.

Stupid doctor of his. He lived a short life of eating bland food. Probably better outcome though. Why live long when you can't even enjoy what you eat right?

I really don't care how my food tastes, I just want to live pain free. It is truly horrible to experience a pain that feels like someone is burning your throat with a lighter 24/7 for a year. I really was ready to die at that point, I didn't enjoy doing anything, just wanted the pain to stop. Then I found naturopathic doctor Peter Glidden's video on acid reflux and he said that acid reflux is caused by a lack of chloride and calcium. Now I can eat my belly completely full and go to sleep right after with full stomach and I still won't get any burning.

 

[yerrag]

I really don't care how my food tastes, I just want to live pain free. It is truly horrible to experience a pain that feels like someone is burning your throat with a lighter 24/7 for a year. I really was ready to die at that point, I didn't enjoy doing anything, just wanted the pain to stop. Then I found naturopathic doctor Peter Glidden's video on acid reflux and he said that acid reflux is caused by a lack of chloride and calcium. Now I can eat my belly completely full and go to sleep right after with full stomach and I still won't get any burning.

I was talking about my uncle. But certainly pain is more painful than blandness in food.

Do you have a link to that video? There's a member who's experiencing that pain now, of acid reflux. I'll tag her so she knows you came out of that. Can you help her?

@Healing 2021

 

[Sani]

Here's the video.

 

[yerrag]

Thank you!

 

[Healing 2021]

Thank you!

Thank you both!

 

[yerrag]

The adequate level of those metabolites can be a proxy for good metabolism (protein synthesis and enzyme function). But I would indeed be skeptical about it because the reaction of ingested bases with stomach acid affects those in circulation, and I don't think that it's from diffusion, so it's suspicious.

Replying to a year-old reply from you to my question, which I should have asked a year ago. You've read so many studies, and you have developed a writing style that mimics that of the heavily ambiguous language of these studies (written mostly by people of which English is not the first language, and by people who purposely make use of language to confuse than to elucidate-big pharma ghost writers), unfortunately. I'll try to interpret your answer, and please let me know if I interpret you correctly:

The adequate level of carbon dioxide and carbonic acid (which you refer as a metabolite) can be a proxy for good metabolism. But I would indeed be skeptical about serum carbon dioxide and serum carbonic acid mainly accounting for HCl production (this is the meaning of "it") because the reaction of bicarbonates (which you refer to as ingested bases) with stomach acid affects the amount of carbon dioxide and carbonic acid (which you refer to as "those") in circulation, and I don't think it's from diffusion (of carbonic acid - a substrate need to produce HCl : H2CO3 + NaCl = HCl + NaHCO3), so it's suspicious.

So in short, you are saying you don't think that HCl production in the stomach is mainly from the use of serum carbonic acid (and implied is that it is from arginine, and a metabolite of it, agmatine, which can be broken up into carbon dioxide to form carbonic acid, to which this reaction occurs, from which HCl is produced: H2CO3 + NaCl = HCl + NaHCO3).

 

[Amazoniac]

Replying to a year-old reply from you to my question, which I should have asked a year ago. You've read so many studies, and you have developed a writing style that mimics that of the heavily ambiguous language of these studies (written mostly by people of which English is not the first language, and by people who purposely make use of language to confuse than to elucidate-big pharma ghost writers), unfortunately. I'll try to interpret your answer, and please let me know if I interpret you correctly:

The adequate level of carbon dioxide and carbonic acid (which you refer as a metabolite) can be a proxy for good metabolism. But I would indeed be skeptical about serum carbon dioxide and serum carbonic acid mainly accounting for HCl production (this is the meaning of "it") because the reaction of bicarbonates (which you refer to as ingested bases) with stomach acid affects the amount of carbon dioxide and carbonic acid (which you refer to as "those") in circulation, and I don't think it's from diffusion (of carbonic acid - a substrate need to produce HCl : H2CO3 + NaCl = HCl + NaHCO3), so it's suspicious.

So in short, you are saying you don't think that HCl production in the stomach is mainly from the use of serum carbonic acid (and implied is that it is from arginine, and a metabolite of it, agmatine, which can be broken up into carbon dioxide to form carbonic acid, to which this reaction occurs, from which HCl is produced: H2CO3 + NaCl = HCl + NaHCO3).

I was skeptical about arginine being the source because changing the craponate species in circulation can affect stomach acid production, which makes the idea that the process is heavily dependent on the amino acid questionable.

 

[yerrag]

I was skeptical about arginine being the source because changing the craponate species in circulation can affect stomach acid production, which makes the idea that the process is heavily dependent on the amino acid questionable.

But it's a nice backup mechanism in case the circulation system is low on carbonic acid, isn't it? This would allow CO2 to be produced and converted to carbonic acid in the gut walls, without affecting the systemic pH, and regardless of the systemic pH.

So in a case of low stomach acid condition causing acid reflux, taking arginine may help with increasing gastric acid production, wouldn't it?

 

[Amazoniac]

But it's a nice backup mechanism in case the circulation system is low on carbonic acid, isn't it? This would allow CO2 to be produced and converted to carbonic acid in the gut walls, without affecting the systemic pH, and regardless of the systemic pH.

So in a case of low stomach acid condition causing acid reflux, taking arginine may help with increasing gastric acid production, wouldn't it?

I'm confused after reading parts of it again, but it doesn't seem like it would work.

They claim that it's sourced from pepsinogen, yet for its activation hydrogen ions are necessary. Without sufficient acidity we won't even obtain those arginines. If taken isolated, I'm not aware of we being able to decrapoxylate it; microorganisms can, but relying on them in the stomach can't be good. Also, if it's possible to obtain it from outside, I don't think that we would have adequate control of it, as opposed to deriving crapon dioxide from cells.

 

[yerrag]

I'm confused after reading parts of it again, but it doesn't seem like it would work.

They claim that it's sourced from pepsinogen, yet for its activation hydrogen ions are necessary. Without sufficient acidity we won't even obtain those arginines. If taken isolated, I'm not aware of we being able to decrapoxylate it; microorganisms can, but relying on them in the stomach can't be good. Also, if it's possible to obtain it from outside, I don't think that we would have adequate control of it, as opposed to deriving crapon dioxide from cells.

Thanks.

Aren't there enzymes that can enable conversion of arginine to agmatine and CO2 without the need for bacteria? And if arginine can be a source of CO2 for production of stomach acid, can't arginine be diverted to making CO2 for the stomach instead of become urea in the urea cycle, as part of the body's ability to conserve instead of waste resources, as urea will just be excreted as urine?

 

[Amazoniac]

Thanks.

Aren't there enzymes that can enable conversion of arginine to agmatine and CO2 without the need for bacteria? And if arginine can be a source of CO2 for production of stomach acid, can't arginine be diverted to making CO2 for the stomach instead of become urea in the urea cycle, as part of the body's ability to conserve instead of waste resources, as urea will just be excreted as urine?

The 'canaliculi' (small channels) in stomach cells (where they think that the reaction occurs) is already outside the body, I'm not sure how it would work or how controlled the reaction can be. Pepsinogen (pepsin precursor that's not active) is their claimed source for arginine, but activation would require an acidic medium in the first place, yet the ideal pH for such decrapoxylase is fairly high. I find it confusing and it's why I thought that detecting agmatine in the stomach could be derived from microbes.

They also argue that this mechanism protects against erosion, but they didn't found pepsinogen to be widely distributed.

 

[yerrag]

The 'canaliculi' (small channels) in stomach cells (where they think that the reaction occurs) is already outside the body, I'm not sure how it would work or how controlled the reaction can be

The canaliculi is outside the body, that is true. But it does not have to be the case that pepsinogen has to be secreted (to be outside the body) for the pepsinogen to be activated, so that its activation segment, which contains arginine and lysine, can be decarboxylated in the extracellular space. In the process, carbon dioxide can be made available to be converted to carbonic acid, which is used as a substrate for producing HCl, which the canaliculi would release together with pepsin (the product of the conversion of pepsinogen). And agmatine would also be there to counter the harsh acidic environment due to HCl. Furthemore, if a more alkaline environment is needed to effect the conversion of CO2 to carbonic acid, agmatine would be effecting the alkaline environment.

 

[Amazoniac]

The canaliculi is outside the body, that is true. But it does not have to be the case that pepsinogen has to be secreted (to be outside the body) for the pepsinogen to be activated, so that its activation segment, which contains arginine and lysine, can be decarboxylated in the extracellular space. In the process, carbon dioxide can be made available to be converted to carbonic acid, which is used as a substrate for producing HCl, which the canaliculi would release together with pepsin (the product of the conversion of pepsinogen). And agmatine would also be there to counter the harsh acidic environment due to HCl. Furthemore, if a more alkaline environment is needed to effect the conversion of CO2 to carbonic acid, agmatine would be effecting the alkaline environment.

Its activation depends on HCl, which is what we're after: there has to be a starting source or else we won't even be able to release the amino acids for decrapoxylation. Since the ideal operating pH range for (in this case) arginine decrapoxylase is higher than the stomach acid, there's a mismatch between that of the medium for pepsinogen to be activated [↓] and the sites where decrapoxylation is occurring [↑]. If the pH is raised too much, pepsinogen can't be activated; if the pH drops greatly, it might impair the activity of decrapoxylases. Maybe the decrapoxylases are located on cells in a way that the extreme acidity of the canaliculi doesn't get to them.

They argue that this mechanism protects cells from acidity, but what about the patchy distribution where pepsinogen doesn't occur?
And how 'protod pump inhibitors' relate?

 

[yerrag]

Its activation depends on HCl, which is what we're after: there has to be a starting source or else we won't even be able to release the amino acids for decrapoxylation.

Can't the starting source be the usual suspect - not from pepsinogen, but from vascular carbonic acid? That would act like the spark that initiates a chain reaction in the gut walls where the activation segment is activated , and this perpetuates the acidity needed to enable a chain reaction of producing carbon dioxide and agmatine, and the agmatine would provide the alkaline environment for carbon dioxide to turn into carbonic acid for use as substrate for making HCl?

Since the ideal operating pH range for (in this case) arginine decrapoxylase is higher than the stomach acid, there's a mismatch between that of the medium for pepsinogen to be activated [↓] and the sites where decrapoxylation is occurring [↑]. If the pH is raised too much, pepsinogen can't be activated; if the pH drops greatly, it might impair the activity of decrapoxylases. Maybe the decrapoxylases are located on cells in a way that the extreme acidity of the canaliculi doesn't get to them.

Yes!