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

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Amazoniac

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- All About Progesterone & Estrogen; Strokes; Milk; Sugars; and So Much More (1:40:30) | One Radio Network
Carbonic acid in medicine - Achilles Rose | Internet Archive

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- Bicarbonate in the body fluid compartments | Deranged Physiology

upload_2020-1-21_7-50-54.png
 
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Amazoniac

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- Supercritical carbon dioxide - Wikipedia

'Carbon dioxide phase changes':



'Supercritical carbon dioxide':



That's the principle of the extraction method where temperature and pressure are raised beyond their critical level with no room for oxygen to oxidize compounds:



I think that Jorge's TocoVit is obtained this way. Terma has a private plant (tut) to extract his exocannabinoids.
 
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Amazoniac

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- Cellular acidification as a new approach to cancer treatment and to the understanding and therapeutics of neurodegenerative diseases (!)
- Ketoacidosis – Where Do the Protons Come From? (!)
- Body Fluid pH Balance in Metabolic Health and Possible Benefits of Dietary Alkaline Foods (⚠)


Here's a review on my store for a book titled 'Alkalize or Die':

"[..]the author presents the information in a very humble and open-ended manner, merely passing along his experiences and observations rather than imposing a rigid dogma, as to make for a "gentle" read."​

How do you link to the actual time in Youtube?
By right-clicking on the video.
 

Such_Umami

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Responding to the initial post;

What would be the optimal amount of salt to take? Would it be the minimum amount before the aldosterone pathway is activated?
 

yerrag

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- Cellular acidification as a new approach to cancer treatment and to the understanding and therapeutics of neurodegenerative diseases (!)
- Ketoacidosis – Where Do the Protons Come From? (!)
- Body Fluid pH Balance in Metabolic Health and Possible Benefits of Dietary Alkaline Foods (⚠)


Here's a review on my store for a book titled 'Alkalize or Die':

"[..]the author presents the information in a very humble and open-ended manner, merely passing along his experiences and observations rather than imposing a rigid dogma, as to make for a "gentle" read."​


By right-clicking on the video.
This is a very nice feature. Guys! Please share videos with the time embedded this way so we don't have to watch the whole video just to listen to snippet of it. Nice find Amazoniac!
 
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Amazoniac

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I thought that I had posted this one, but couldn't locate:

- Acidosis Potentiates the Host Proinflammatory Interleukin-1β Response to Pseudomonas aeruginosa Infection

"The microenvironments surrounding inflammatory sites feature acidosis of tissues and fluids to pH levels well below the physiological norm of ∼7.4 (20, 21). Relevant to our studies, this is observed during bacterial infection, where anaerobic glycolysis, lactic acid accumulation, hypoxia, bacterial fatty acids, and hypochlorous acid (HOCl) production by activated neutrophils contribute to local acidosis with measured pH values ranging from 5.9 to 7.0, depending upon the disease process and method of measurement (22,27). In CF, the loss of CF transmembrane conductance regulator (CFTR)-mediated bicarbonate transport has been proposed to contribute to pulmonary acidosis, which is supported by pH measurements of airway surface liquid, submucosal gland fluid, and mucopurulent airway secretions that range from ∼6.1 to 6.9 (28,33). While the importance of homeostatic maintenance of pH has been well studied, reports on how low pH affects inflammation are just now emerging (23, 24). In particular, recent reports have demonstrated that in vitro acidosis can enhance IL-1β release from lipopolysaccharide (LPS)-primed mouse glial cells and human monocytes (34,37). In a study by Rajamaki et al., the IL-1β response was found to be dependent on the activation of the NLRP3 inflammasome by the acidic environment, and it was proposed that acidosis serves as a novel danger signal (37). Therefore, based on the clinical observations of acidosis during bacterial infection and the pivotal role of IL-1β in disease pathogenesis, we investigated how physiologically relevant changes in pH alter the inflammatory response to P. aeruginosa.

In this report we demonstrate that a low-pH microenvironment enhances IL-1β production in vitro and in vivo in response to infection with P. aeruginosa. We demonstrate the specificity of this response and identify two intracellular mechanisms that generate the amplified response observed during P. aeruginosa infection under acidic conditions: there is increased production of pro-IL-1β and increased caspase-1-dependent cleavage to its active form. Additionally, in contrast to previous in vitro studies (34,37), in vivo analyses revealed that bacterial T3SS function is required to trigger acidosis-enhanced IL-1β responses; acidosis, even in the presence of bacterial LPS, is not sufficient to enable robust in vivo IL-1β responses. These studies are the first to show that extracellular pH governs the host response against P. aeruginosa through modulation of cytokine release, and they provide new insights into the role of acidic pH in the regulation of the innate immune response during infections."​
 
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Amazoniac

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- Human stomach

upload_2020-4-2_21-5-15.png

Copyright © 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings.

- Parental cell of the stomach

upload_2020-4-2_21-5-27.png

Source: the internet.

- Agmatine - Wikipedia

- The Source of Carbon Dioxide for Gastric Acid Production

"The hydration of carbon dioxide resulting in the production of gastric acid requires a significant supply of carbon dioxide. Although the source of carbon dioxide is unknown, textbooks suggest interstitial fluid as the source. However, the possibility that this carbon dioxide comes from the gastric vascular system is untenable. The gastric vascular system does not have any specific modifications which would enable the stomach to be supplied with carbon dioxide enriched blood."

"The theoretical background to the conclusion that the decarboxylation of amino acids is one of the principle sources of carbon dioxide for gastric acid production has been outlined (Steer, 2005). Biochemically, basic amino acids are ideally suited to act as a source of carbon dioxide in the stomach and the most basic amino acid is arginine (isoelectric point 11.15). A significant source of arginine is present in the stomach."

"Pepsinogens are the major proteins produced by the chief cells of the stomach. These pepsinogens are converted into pepsins with the release of activation segment. Activation segment of human pepsinogen I is made up of forty seven amino acids. Six of these amino acids are arginine (Kageyama and Takahashi, 1980). This is a significant amount of arginine in a small protein molecule. The decarboxylation of the arginine derived from a single molecule of activation segment would result in the release of six molecules of carbon dioxide."

"The decarboxylation product of arginine is agmatine. Agmatine has been recognized because the work of Professor Albrecht Kossel (Kossel, 1910). Agmatine had originally been extracted from herring roe (Kossel, 1910), and for many years agmatine had been considered to be absent from mammalian tissues. This misapprehension was corrected in 1994 with the identification of agmatine in mammalian tissue (Li et al., 1994). An examination of various mammalian organs has revealed that the greatest concentration of agmatine is found in the stomach (Raasch et al., 1995)."

"The process of decarboxylation of arginine in the stomach has been confirmed in the present study by finding the end product of this reaction, namely agmatine, in the parietal cell canaliculi. The decarboxylation of arginine provides a source of carbon dioxide. The hydration of this carbon dioxide results in the release of hydrogen ions. The decarboxylation of another basic amino acid, lysine, may also provide carbon dioxide for this process but the possible role of lysine has not been studied. In human pepsinogen I, the activation segment has fifteen basic amino acids out of a total of forty seven amino acids. As previously stated, six of these basic amino acids are arginine but of the remaining nine basic amino acids eight are lysine (Kageyama and Takahashi, 1980) which has an isoelectric point of 9.59. Thus, if both arginine and lysine are involved in this process of decarboxylation, one molecule of activation segment would produce fourteen molecules of carbon dioxide."

"For almost two centuries ever since acid has been identified in the stomach (William Prout 1785–1850), it has been a dilemma explaining why the acid does not destroy the stomach? The finding that the greatest concentration of agmatine in the body is in the stomach (Raasch et al., 1995), the fact that agmatine is such a strong base and the cellular localization of the agmatine in the gastric mucosa (present work) makes agmatine a strong candidate for that protective role. This mucosal defence role of agmatine is best illustrated by the gastric mucus secreting cells. When considering the source of the agmatine in the mucus secreting cells of the stomach, it is interesting to note that radiolabeled agmatine is taken up from the gastric lumen by the gastric mucosa (Molderings et al., 2002). The agmatine present in the mucus secreting gastric cells could have been taken up by these cells from the lumen and this agmatine derived from the decarboxylation of arginine from the activation segment of pepsinogen."

"Helicobacter pylori infection of the stomach is associated with a decrease in the amount of mucus in the mucus secreting cells of the stomach (Steer, 2005). This change is associated with a decrease in the amount of agmatine in these mucus secreting cells (Steer, 2005). Such a decrease in the amount of agmatine in the epithelium of the helicobacter pylori infected stomach would make this epithelium more vulnerable to damage by gastric acid."

"The extracellular production of gastric acid by the hydration of carbon dioxide which has been derived from the decarboxylation of arginine is shown in Fig. 4. This extracellular, rather than intracellular, hydration of carbon dioxide and the formation of agmatine would explain why the parietal cells are not destroyed by the production of the strong acid. The current observations and their interpretations concur with the principle expounded by Hoerr and Bensley (1936) that “gastric juice (including gastric acid) ……… is a result of the interaction of the various products on one another modified by the living membrane over which the secretion flows.” The “reaction space” described by Hoerr and Bensley (1936) for gastric acid production is in the parietal cell canaliculi."

upload_2020-4-2_21-5-40.png
 

yerrag

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- Human stomach

View attachment 17303
Copyright © 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings.

- Parental cell of the stomach

View attachment 17304
Source: the internet.

- Agmatine - Wikipedia

- The Source of Carbon Dioxide for Gastric Acid Production

"The hydration of carbon dioxide resulting in the production of gastric acid requires a significant supply of carbon dioxide. Although the source of carbon dioxide is unknown, textbooks suggest interstitial fluid as the source. However, the possibility that this carbon dioxide comes from the gastric vascular system is untenable. The gastric vascular system does not have any specific modifications which would enable the stomach to be supplied with carbon dioxide enriched blood."

"The theoretical background to the conclusion that the decarboxylation of amino acids is one of the principle sources of carbon dioxide for gastric acid production has been outlined (Steer, 2005). Biochemically, basic amino acids are ideally suited to act as a source of carbon dioxide in the stomach and the most basic amino acid is arginine (isoelectric point 11.15). A significant source of arginine is present in the stomach."

"Pepsinogens are the major proteins produced by the chief cells of the stomach. These pepsinogens are converted into pepsins with the release of activation segment. Activation segment of human pepsinogen I is made up of forty seven amino acids. Six of these amino acids are arginine (Kageyama and Takahashi, 1980). This is a significant amount of arginine in a small protein molecule. The decarboxylation of the arginine derived from a single molecule of activation segment would result in the release of six molecules of carbon dioxide."

"The decarboxylation product of arginine is agmatine. Agmatine has been recognized because the work of Professor Albrecht Kossel (Kossel, 1910). Agmatine had originally been extracted from herring roe (Kossel, 1910), and for many years agmatine had been considered to be absent from mammalian tissues. This misapprehension was corrected in 1994 with the identification of agmatine in mammalian tissue (Li et al., 1994). An examination of various mammalian organs has revealed that the greatest concentration of agmatine is found in the stomach (Raasch et al., 1995)."

"The process of decarboxylation of arginine in the stomach has been confirmed in the present study by finding the end product of this reaction, namely agmatine, in the parietal cell canaliculi. The decarboxylation of arginine provides a source of carbon dioxide. The hydration of this carbon dioxide results in the release of hydrogen ions. The decarboxylation of another basic amino acid, lysine, may also provide carbon dioxide for this process but the possible role of lysine has not been studied. In human pepsinogen I, the activation segment has fifteen basic amino acids out of a total of forty seven amino acids. As previously stated, six of these basic amino acids are arginine but of the remaining nine basic amino acids eight are lysine (Kageyama and Takahashi, 1980) which has an isoelectric point of 9.59. Thus, if both arginine and lysine are involved in this process of decarboxylation, one molecule of activation segment would produce fourteen molecules of carbon dioxide."

"For almost two centuries ever since acid has been identified in the stomach (William Prout 1785–1850), it has been a dilemma explaining why the acid does not destroy the stomach? The finding that the greatest concentration of agmatine in the body is in the stomach (Raasch et al., 1995), the fact that agmatine is such a strong base and the cellular localization of the agmatine in the gastric mucosa (present work) makes agmatine a strong candidate for that protective role. This mucosal defence role of agmatine is best illustrated by the gastric mucus secreting cells. When considering the source of the agmatine in the mucus secreting cells of the stomach, it is interesting to note that radiolabeled agmatine is taken up from the gastric lumen by the gastric mucosa (Molderings et al., 2002). The agmatine present in the mucus secreting gastric cells could have been taken up by these cells from the lumen and this agmatine derived from the decarboxylation of arginine from the activation segment of pepsinogen."

"Helicobacter pylori infection of the stomach is associated with a decrease in the amount of mucus in the mucus secreting cells of the stomach (Steer, 2005). This change is associated with a decrease in the amount of agmatine in these mucus secreting cells (Steer, 2005). Such a decrease in the amount of agmatine in the epithelium of the helicobacter pylori infected stomach would make this epithelium more vulnerable to damage by gastric acid."

"The extracellular production of gastric acid by the hydration of carbon dioxide which has been derived from the decarboxylation of arginine is shown in Fig. 4. This extracellular, rather than intracellular, hydration of carbon dioxide and the formation of agmatine would explain why the parietal cells are not destroyed by the production of the strong acid. The current observations and their interpretations concur with the principle expounded by Hoerr and Bensley (1936) that “gastric juice (including gastric acid) ……… is a result of the interaction of the various products on one another modified by the living membrane over which the secretion flows.” The “reaction space” described by Hoerr and Bensley (1936) for gastric acid production is in the parietal cell canaliculi."

View attachment 17305
Interesting.

Does this then mean that having a high amount of CO2 in the blood, and thereby having good acid-base balance, has very little to do with having good gastric acid production? Maybe it still does, but the smaller role may still be significant in tipping the availability of gastric juice towards optimality in the part played by the stomach in digestion.
 

tfcjesse

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Admittedly not having read the several textbooks and biology courses worth of info in this thread, has any consensus been reached with regards to dietary recommendations? Or is it just baking soda before acidic meals?
 
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Amazoniac

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Interesting.

Does this then mean that having a high amount of CO2 in the blood, and thereby having good acid-base balance, has very little to do with having good gastric acid production? Maybe it still does, but the smaller role may still be significant in tipping the availability of gastric juice towards optimality in the part played by the stomach in digestion.
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.

A salty collagen broth?
Admittedly not having read the several textbooks and biology courses worth of info in this thread, has any consensus been reached with regards to dietary recommendations? Or is it just baking soda before acidic meals?
:lol:

If you're dealing with issues in this regard, it's likely not of dietary origin.

Prolactinese grossary:
  • K ↔ Cardiarrestium (Ca)
  • Na ↔ Edemium (Ed)
  • Ca ↔ Killcium (Ki) or Atherostiffium
  • Mg ↔ Laxarium (La)
  • P ↔ Nephrosium (Ne) (nephros-osis-ium, sounding like necrosium was a bonus)
- Potassium - Wikipedia

"The symbol "K" stems from kali, itself from the root word alkali, which in turn comes from Arabic: القَلْيَه‎ al-qalyah "plant ashes". In 1797, the German chemist Martin Klaproth discovered "potash" in the minerals leucite and lepidolite, and realized that "potash" was not a product of plant growth but actually contained a new element, which he proposed to call kali. In 1807, Humphry Davy produced the element via electrolysis: in 1809, Ludwig Wilhelm Gilbert proposed the name Kalium for Davy's "potassium". In 1814, the Swedish chemist Berzelius advocated the name kalium for potassium, with the chemical symbol "K".

The English and French speaking countries adopted Davy and Gay-Lussac/Thénard's name Potassium, while the Germanic countries adopted Gilbert/Klaproth's name Kalium. The "Gold Book" of the International Union of Pure and Applied Chemistry has designated the official chemical symbol as K."​

Focusing on a potassium-rich diet is a good start, only stopping the consumption before your heart does. Just kidding. But getting plenty of it from foods should provide you the alkalinizing factors, and you can add baking soda for management.
 
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"In our study, despite relatively low citrate content (2.1 mmol/L), coconut water therapy revealed a significant increase in urinary citrate excretion from baseline (mean increase of 161mg/d). This citraturic effect is likely due to the very high total alkali load (13.8 mEq/L), which is higher than in any of the other juices or nonjuice fluids discussed [20]. The high total alkali load is mainly a function of the high pH of coconut water and the malate content. Of note is that this increase in citrate occurred in nonstone forming individuals with a normal citrate at baseline; whether there would be a similar or greater impact on citrate levels in hypocitraturic stone-formers has yet to be tested. Interestingly, we did not record a significant change in urinary pH. Our findings also revealed significant increase in urinary potassium and chloride, which may be explained by the high potassium and chloride content of coconut water. The coconut water studied contains approximately 1456 mg/L (37.3 mEq) of potassium, which is 31% of the Food and Drug administration daily recommended value for adults [21]. Of note, potassium depletion has been associated with hypocitraturia [11].

Of interest, coconut water contains a significant amount of chloride, which is unusual for a fruit beverage. Potassium content of a beverage is often used as a gauge of alkali content on the assumption that most potassium is accompanied by organic anions. In coconut water, this assumption is not correct as most potassium is actually potassium chloride. This point highlights the need for direct measurement of organic anions and pH to assess the alkali content of a beverage."​
 
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✗ Spanner.
✓ Capsule.




 

Ableton

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how did hunter gatherers get their salt?
their intake must have been really low, right?
 

yerrag

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how did hunter gatherers get their salt?
their intake must have been really low, right?
I guess they are able to find salt licks like wild animals would?
 

GAF

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Same way as carnivores like lions. Eating meat/blood of animals, such as deer that find the salt licks.

I just read Salt, A History. Great Book.
 
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Amazoniac

Amazoniac

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mmHg:


(The distance is from exposed surface.)

- Millimetre of mercury - Wikipedia


On distribution:



Hemoglobid:



And its function depending on conditions:

 
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