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

yerrag

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But what happens if these nutrients can't be transported because we are lymphaticlly congested, for example? Congestion that can be seen through lack of sediment in urine, among other things. If the bowel walls, again, made up of a bunch of fluid surrounding the cells, is congested, we get malabsorption because these nutrients can't be transported effectively.

I think of blood as the kitchen and the lymphatic system as the sewer system, with the lymph nodes acting as the septic tanks. When the sewer system backs up, it's not going to matter how much food is in the kitchen so it's not as simple as targeting the blood and everything will correct itself, not that that is what you are implying. I'm just trying to address what it feels like the article/Kopp is sort of doing.

The lymphatic gland is important, and I profess ignorance about it as I don't think it is being given enough attention. It is very much a black box to me. But I also have to narrow my scope given the complexity of our body. Now that you have mentioned it, I have to assume my lymphatics are working within normal bounds, and with that assumption, I could narrow my scope so that I can work with what I understand so far. This may seem like me looking for my contact lenses where there is more light, and not where I dropped it. But that is all I've got now.

If I fail to resolve my issues with this approach, I could always go back and revisit my assumptions. And then proceed. Otherwise, I would not have a system or methodology to finally uncover what ails me. I would be so overwhelmed that I would not know where to begin.
 

Jennifer

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Sorry if I came off judgmental, @yerrag. Pay no mind to what I say. I can understand your position but even so, you don't owe me any explanation or need to justify what you feel is right for you. You go be your biohacker self! I'm rooting for you!
 
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Sorry if I came off judgmental, @yerrag. Pay no mind to what I say. I can understand your position but even so, you don't owe me any explanation or need to justify what you feel is right for you. You go be your biohacker self! I'm rooting for you!
Please note this comment. Maturity at its finest.
 

yerrag

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Sorry if I came off judgmental, @yerrag. Pay no mind to what I say. I can understand your position but even so, you don't owe me any explanation or need to justify what you feel is right for you. You go be your biohacker self! I'm rooting for you!
Thanks Jennifer. No offense taken at all. All your points are well taken and given in the spirit of helping and sharing. Sometimes, we may come across as being pushy with our ideas but that is the cost of breaking roadblocks to better understanding.
 

yerrag

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Regarding details, I have to learn more about it to comment. Ray recommends this guy and his approach to start learning:
acidbase.org
This is nice. I will try to seal myself and read this. There is much to learn.
 

Jennifer

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Thanks Jennifer. No offense taken at all. All your points are well taken and given in the spirit of helping and sharing. Sometimes, we may come across as being pushy with our ideas but that is the cost of breaking roadblocks to better understanding.
Phew, okay! Thanks for your understanding, yerrag. :)

Thank you, @lisaferraro. :)
 

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I've been wondering about digestion, GERD and what this thread has mentioned about acidity. If NaCl helps people digest food, then perhaps it's better to have it in bigger amounts in the diet rather than not? Why would people recommend betaine HCl to help digestion and then go on to talk about acidity as if betaine HCl wasn't a potential major issue (and methyl donor?)? What about thiamine HCl as per haidut's suggestion? If stomach acids are not strong enough to support digestion then why would supplementing apple cider vinegar, lemon juice, NaCl or the other ones that were mentioned not be a good idea? What is the percentage of people who skip posts with too many questions?

Digestion experiment

Not sure about the use of that one:
The effect of NaCl or NaHCO3 on digestion in the stomach of weaned calves | The Journal of Agricultural Science | Cambridge Core

http://www.uwyo.edu/uwe/pubs/b1183/_files/sodium_chloride.pdf
Essentiality
Both Na and Cl are essential elements for practically all forms of life. Sodium (Na+) is the major extracellular cation while Cl- is the major extracellular anion; together, they are responsible for maintaining acid-base balance and regulating the osmotic pressure of bodily fluids.515,516 Excitable cell membranes (e.g. nerve and muscle cells) depend upon tightly regulated Na+ and Cl- concentrations in cells and the extracellular fluid (ECF). Blood, a
specialized form of ECF, consists of approximately 0.9% NaCl.514 Sodium chloride is reportedly the only mineral animals truly crave and will actually seek out. 514,517 The
dietary NaCl requirement of swine is between 0.10 and 0.14%, and 0.18% Na is needed to achieve optimal performance. 518-521 Similarly, the optimal dietary Na concentration in horses is 0.16-0.18% DM 515 and for cattle is 0.08-0.1%. 522 Under extreme conditions, such as high temperatures, lactation, or hard work, these requirements increase due to increased excretion of both Na+ and Cl- . 523,524

...

Metabolism

Once ingested, 85-95% of Na and Cl are absorbed in the GI tract, particularly the small intestine. Large amounts of Na and Cl are recycled into the intestinal tract via salivary, pancreatic, and intestinal epithelial secretions, as well as bile. The high intestinal Na+
concentration is required to transport glucose, amino acids, and other nutrients across the mucosa. Chloride is also secreted into the intestine to aid in creating the low pH environment needed for proteolysis.
...
It has been suggested that elevated dietary NaCl can increase protein digestion. Hemsley 530 discovered that increased NaCl in the diet increased the rate of passage of solid digesta from the rumen, which decreased microbial degradation within the rumen and increased the amount of protein available in the small intestine. Altered ruminal fatty acid concentrations have also been related to dietary NaCl. 531-533 Dietary Na+ and Cl- in excess of physiologic requirements are usually efficiently eliminated from the body via the kidneys. 534 Potassium is the main intracellular cation, Na is the main extracellular cation, and Cl- is the main extracellular anion. The relative concentrations of these three elements creates an electrochemical gradient across cell membranes that is essential for nutrient transport, nerve conduction, muscle contraction, and energy generation, and they indirectly aid in maintaining pH balance. Imbalances of these elements result in a variety of disorders from decreased gains to acute death. 535-537

Toxicity

The toxicity of NaCl is intimately related to the availability of water and is sometimes referred to as “sodium ion toxicity-water deprivation syndrome;” however, if the dose of Na+ is high enough, Na is toxic regardless of water intake. 538 If adequate water is present, most animals can tolerate relatively large doses by increasing Na+ excretion. 534,539-542

etc..
 
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yerrag

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Up until about 10 years ago, no research existed to counter this skepticism. However, since then, a growing body of research has documented not only that “acidosis” is a real phenomenon, but that it is now known to contribute to a wide range of diseases, such as metabolic syndrome, cancer, osteoporosis, kidney stones, and increased susceptibility to environmental toxins—and new research is adding to the list."

"We are talking here about acidosis as a process or a trend toward acidemia, not acidemia, which is an actual change in blood pH. Acidemia is defined as a blood pH of less than 7.35. This is very unlikely to occur, as the body has multiple mechanisms for ensuring a very stable blood pH. Acidosis only becomes acidemia when compensatory measures become overwhelmed. This typically only happens in “advanced disease” like kidney and lung failure. In many ways, we can consider acidosis as the constant pressure on the body’s physiology to compensate for all the acid-inducing challenges."

This is interesting. The range of allowable blood pH is 7.35 - 7.45. Is 7.4 the ideal blood pH? Is anything between 7.35 and 7.4 pH considered acidosis? And anything between 7.4 and 7.45 pH considered to be alkalosis? All the while I have been thinking of pH below 7.35 as acidosis, but it should be called acidemia.

Yet pH between 7.35 and 7.45 is considered acceptable and within range.

By the way, how do we get our blood pH? Why isn't it a standard lab test?
 
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Amazoniac

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This is interesting. The range of allowable blood pH is 7.35 - 7.45. Is 7.4 the ideal blood pH? Is anything between 7.35 and 7.4 pH considered acidosis? And anything between 7.4 and 7.45 pH considered to be alkalosis? All the while I have been thinking of pH below 7.35 as acidosis, but it should be called acidemia.

Yet pH between 7.35 and 7.45 is considered acceptable and within range.

By the way, how do we get our blood pH? Why isn't it a standard lab test?
I guess just as important as those questions is what the body is doing to keep those levels within the reasonable range.
 
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Amazoniac

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- Electrolyte and Acid–Base Disorders in Malignancy (potassium, sodium and magnesium deficiency along with calcium excess)

- Mechanism of Hypokalemia in Magnesium Deficiency

"Hypokalemia associated with magnesium deficiency is often refractory to treatment with K+. Co-administration of magnesium is essential for correcting the hypokalemia."

"The cytosol is the largest intracellular compartment for Mg 2+. The cellular Mg2+ concentration is estimated between 10 to 20 mM. In the cytosol, Mg2+ ions mainly form complexes with ATP and, to a smaller extent, with other nucleotides and enzymes. Only approximately 5% of Mg2+ (0.5 to 1.0 mM) in the cytosol is free (unbound).14 The degree of exchange of Mg2+ between tissues and plasma varies greatly. It was shown in kidney and heart that 100% of intracellular Mg2+ can exchange with plasma within 3 to 4 h.15 In contrast, only approximately 10% of magnesium in brain and 25% in skeletal muscle can exchange with plasma, and the equilibrium occurs after >= 16 h. The basis for the differences is not known. The intracellular concentration of free Mg2+ in renal tubules in magnesium-deficiency states has not been measured. Nevertheless, these results support the idea that intracellular Mg2+ in renal tubules falls readily during magnesium deficiency. Consistent with the rapid exchange between heart and plasma, Mg2+ depletion causes profound adverse effects on myocardium.16"

It's no wonder people feel heart of the palpitations with vit D supplementation:
Calcirol - Liquid Vitamin D3

"Magnesium deficiency will not only exacerbate K+ wasting but also aggravate the adverse effects of hypokalemia on target tissues.16 Recognition of concomitant magnesium deficiency and early treatment with magnesium are imperative for effective treatment and prevention of complications of hypokalemia."​
 

yerrag

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I guess just as important as those questions is what the body is doing to keep those levels within the reasonable range.

It is as important as a matter of survival. But not as important in terms of optimizing the health of the organism. The body could adapt to different sub-optimal situations presented to it, but that adaptation always requires more energy (wasted energy actually) and it slowly takes away the life force of the organism.
 

SOMO

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NAC (N-Acetyl-L-Cysteine), but not L-Cysteine was used in the early 90s to keep those infected with "AIDS" from decreasing CD4 cells. NAC is a Sulfur-containing AA. The rationale is that it increased Glutathione.
Is there any reason why raising Glutathione would be bad?
Also whey protein was used for the same purpose of treating AIDS patients back in the 90s: Whey proteins as a food supplement in HIV-seropositive individuals. - PubMed - NCBI
The mechanism was also raising Glutathione.

But I see Peat views Cysteine as one of those slightly inflammatory amino acids? Does NAC preferentially convert to Glutathione? NAC is used over L-Cysteine is used in Acetaminophen overdose in hospital settings and it's likely because L-Cysteine doesn't convert to Glutathione as well as NAC.
 

yerrag

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NAC (N-Acetyl-L-Cysteine), but not L-Cysteine was used in the early 90s to keep those infected with "AIDS" from decreasing CD4 cells. NAC is a Sulfur-containing AA. The rationale is that it increased Glutathione.
Is there any reason why raising Glutathione would be bad?
Also whey protein was used for the same purpose of treating AIDS patients back in the 90s: Whey proteins as a food supplement in HIV-seropositive individuals. - PubMed - NCBI
The mechanism was also raising Glutathione.

But I see Peat views Cysteine as one of those slightly inflammatory amino acids? Does NAC preferentially convert to Glutathione? NAC is used over L-Cysteine is used in Acetaminophen overdose in hospital settings and it's likely because L-Cysteine doesn't convert to Glutathione as well as NAC.
I don't see why raising Glutathione would be bad since it is an antioxidant. If I remember correctly, and not sure if it was Ray Peat who said it, is that it's useless taking Glutathione supplements because these end up external of the cell. It's the internal gluathione that really works. I suppose that NAC is better because it is a precursor and when it converts to glutathione it is glutathione internal of the cell, and thus it can work its magic.
 
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Amazoniac

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Contribution of Various Dietary Constituents to the Acid Base Status: Interest of Animal Models of Latent Metabolic Acidosis

"In contrast to humans westernized diets, resulting in a majority of the population with a permanent status of an at least modest H+ retention [5], rodent diets are generally well-balanced and even overprotective against the risk of LMA since they rich in potassium (partly as citrate) as well as in calcium and magnesium and limited in sodium. Therefore, even if they are relatively rich in proteins (around 20%), chow diets and most of the semi-purified diets are poor models of modern human nutrition but are rather reminiscent of the features of hunter-gatherers food habits [6]."

"Sulfur amino acids catabolism is the major source of sulfate anions, which essentially circulate as Na salts in plasma but, following ultrafiltration and Na reabsorption by kidneys, sulfate anions have to be buffered in urine by endogenous cationic species (Ca, Mg and/or NH4+) or metabolically generated alcalinizing compounds (KHCO3 from dietary organic K salts). In principle, excreted SO4 anions are proportional to dietary protein level (other sulfur derivatives such as taurine represent a minor part of sulfur excretion, [11]), even if there are some differences in the sulfur AA content of the dietary proteins, animal protein being generally higher in sulfur AA."

"Minimizing SO4 production and excretion could be achieved through a reduction of protein intake, but with a risk to disturb growth or protein renewal, and bone/muscle protein matrix are altered by protein deficiency [12]. In fact [?], the dietary protein intake in western countries (around 1 g/d/kg bw) is higher than the maintenance requirements, and the question arises as to whether this level will frequently promote LMA or whether other diet constituents will modulate this effect. In fact, data in the literature have frequently ascribed a favourable effect of protein consumption on bone health [12,13] but this point has been qualified in other investigations, especially as regards the balance between plant and animal proteins [14-16]. In rats, it has been observed that LMA takes place in animals adapted to high (26%) but also in those adapted to a moderate (13%) casein diet, if the mineral moiety of the diet is poorly alkalinizing. On the other hand, the high protein diet acidifying effect was blunted if the diet also contained a sufficient amount of K citrate [9]. This indicates that intake of relatively high levels of protein would not lead to acid-base desequilibrium if accompanied by sufficient amounts of K organic salts, as observed with well-balanced omnivorous diets."​

Effect of potassium salts in rats adapted to an acidogenic high-sulfur amino acid diet

"A substantial part of KHCO3 used by the kidneys to neutralise fixed acidity arises from oxidation in tissues, especially in the splanchnic area, of K organic anions found in substantial amounts in fruits and vegetables. Citrate and malate anions are present in relatively similar amounts in portions of usually consumed fruits and vegetables, where they are partly neutralised by K and Mg; typically less than 50% in fruits (down to 5% in citrus) but 70-90% in vegetables (Demigne et al. 2004a). Relatively few studies have addressed the respective importance of K and organic anions (such as citrate or malate) in the effects of plant foods on acid–base status and metabolism, especially mineral homeostasis, whereas there are reports supporting the interest of K itself as a protective element (He & McGregor, 2001; Demigne et al. 2004b)."

"The characteristics of the present acidogenic diet are typical of the so-called Western diet and probably provide a more physiological model of latent acidosis than, for example, addition of NH4 Cl in drinking water, which is effective in providing an overload of hydrogen ions but also profoundly disturbs N metabolism (Cheema-Dhadli et al. 1987). Dietary protein intake in excess of maintenance requirements generates a substantial fixed acidity, namely SO4 2-, as a result of sulfur amino acid catabolism (Remer, 2000). Methionine supplementation itself is an effective mean to increase urinary net acid excretion as SO4 2- (Remer & Manz, 1994). The present results suggest that increasing dietary K is not effective against acidosis in the form of the Cl salt, as previously reported (Morris et al. 1999). In fact, acidosis may even be more pronounced with KCl in the diet, as reflected by the very high rate of Mg, Ca or H+ excretion. This point is noteworthy since KCl is frequently proposed as a substitute of NaCl in dietetic interventions aiming at lowering blood pressure and the risk of stroke (Gilleran et al. 1996). Some previous studies support the view that KCl loading could decrease acid excretion, but to a lesser extent than KHCO3, and an indirect effect of K on H+ excretion has been postulated (van Buren et al. 1992). Nevertheless, it must be kept in mind that investigations in this domain have seldom been carried out in acidotic models. In contrast to KCl, KHCO3 or potassium malate were effective in alkalinising urine and counteracting various adverse effects of low-grade acidosis such as excessive Ca and Mg elimination, or hypocitraturia."

"In control or KCl-fed rats, the percentage of ingested Mg excreted by the kidneys was high (about 50 %). Considering that the percentage of Mg absorption in normal rats is about 70 (Coudray et al. 2002), there was certainly a very poor Mg retention in acidotic rats in contrast to rats fed alkalinising K diets. It is well established that metabolic acidosis is associated with urinary Mg wasting, possibly due to a direct effect of H on distal Mg transport (Dai et al. 1997; Quamme, 1997). In spite of the large fluctuations of renal Mg excretion, plasma Mg concentration was extremely constant. However, since extracellular Mg represents less than 1 % of the total Mg pool, it remains to be assessed if the changes observed in the present study had any significant influence on the intracellular Mg activity (Ryan, 1993). Ca excretion represents a minute percentage of Ca supplied by the diets (presently 1 –2 %) except in rats fed the KCl diet (about 6 %). Rat diets are frequently rich in Ca (4 g/kg in the present experiment), and since Ca absorption is subjected to a tight regulation, the observed excretion of Ca could represent a relatively substantial part of absorbed Ca. In this view, calcaemia was significantly lower in rats fed the control or KCl diets than in rats fed the alkalinising diets. Conceivably, rats fed these last diets had a normal calcaemia whereas acidotic rats were relatively hypocalcaemic. The comparison between Ca and Mg excretion in the present experiment suggests that Mg may play a substantial role, besides Ca, in the compensation of low-grade metabolic acidosis (in the short term at least)."

"In conclusion, the present study proposes a model of low-grade metabolic acidosis of dietary origin in the rat. This model is responsive to dietary K manipulations and it establishes that, for example, potassium malate is practically as potent as potassium bicarbonate in exerting alkalinising effects. The present experiment raises questions about the actual effects of K organic salts on protein metabolism, since effects of potassium malate on blood urea are in line with a role of hepatic urea synthesis as a pathway for the removal of metabolically generated bicarbonate (Haussinger, 1997) but are less consistent with the purported inhibition of proteolysis by alkalinising agents [balance))](Greiber & Mitch, 1992). Another noticeable observation is the fact that Mg shows the same responsiveness to urine acidification or alkalinisation as Ca and it would be interesting to assess whether Mg, abundant in plant foods together with K, is liable to spare Ca in case of metabolic acidosis."​

There was someone suggesting lime juice with sodium bicarbonate and wasser on ther rheumatitis of the arthritis thread, but potassium bicarbonate with a sour citrus and a sweet one can be just as good if not better for some. And when you add magnesium malate you'll have the citrate-malate combination that they mentioned here.

I was reading this the other day:
Absorbability of calcium sources: The limited role of solubility (calcium citrate malate)

A very interesting of the reads:
Factors governing correction of the alkalosis associated with potassium deficiency; The critical role of chloride in the recovery process
I'm sure gbolduever would approve.
 
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Amazoniac

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Other than "latent metabolic acidosis", there's also "eubicarbonatemic metabolic acidosis" . al dere

Chronic acidosis: An insidious cause of significant morbidity

"In this review, we will emphasize that the term metabolic acidosis should be applied to the process of generating excess acid, and not be reserved for patients with abnormal serum HCO3- concentrations." "the existence of a normal serum HCO3- concentration does not invalidate the diagnosis of metabolic acidosis. It should also be appreciated that in a patient with a mild metabolic acidotic process, that homeostatic mechanisms may bring the serum HCO3- concentration back to within the normal range. Nevertheless, an abnormal acidotic process is still present, which is likely of significant clinical importance."

"significant changes in net acid production lead to undetectable changes in the serum HCO3- concentration."

"The normal physiologic response to prevent acidosis activates homeostatic mechanisms which return blood pH to normal, but have a number of negative consequences or trade of the offs."

"aging can cause a clinically significant metabolic acidosis"

"when considered as a pathologic process rather than as an abnormal serum HCO3- concentration, chronic metabolic acidosis is a common clinical problem. Indeed, it may be ubiquitous in elderly patients."

"The cortical collecting duct contains two H+/HCO3- transporting cells, referred to as intercalated cells. The type A intercalated cell secretes H+ into the luminal fluid, while the type B intercalated cell secretes HCO3- into the luminal fluid. Cortical collecting ducts dissected from rats or rabbits fed an acid diet, mediate net luminal W secretion, while cortical collecting ducts from animals fed an alkaline diet secrete HCO3- (9,10)."

"A related acidosis-induced adaptation occurs in citrate transport and metabolism. Citrate is a molecule of intermediary metabolism that at pHs 7-7.4 possesses three negatively charged carboxyl groups. Its metabolism generates three HCO3- ions, and thus from the acid-base perspective it is equivalent to HCO3-. In response to chronic metabolic acidosis, urinary citrate levels markedly decrease. This is of significant clinical importance because citrate is also responsible in the urine for complexation of Ca2+, inhibition of renal stone formation, and prevention of nephrocalcinosis (18). Any condition which decreases urinary citrate levels increases the risk of nephrolithiasis and nephrocalcinosis."

"Cytoplasmic citrate is then metabolized to HCO3- and either C02 and water or glucose. The specific site of metabolism has generally been considered to be the mitochondria (22). According to this scheme, citrate is transported into mitochondria on a citrate/malate exchanger (referred to as the tricarboxylic acid transporter) and is then metabolized within the tricarboxylic acid cycle, leaving the mitochondria as malate. Malate is then converted within the cytoplasm to oxaloacetate, then to phosphoenolpyruvate and finally can be converted to glucose."

"The importance of hypocitraturia in nephrolithiasis has been best demonstrated by Pak and his colleagues. These investigators have shown low levels of urinary citrate in a high proportion of patients with kidney stone disease (24)."

"One of the most important adaptations to chronic metabolic acidosis is an increase in renal NH4+ excretion. Quantitatively NH4+; provides the greatest component of the increase in renal net acid excretion. An increase in renal NH4+; excretion requires regulation of two separate processes. First, as discussed above, there must be an increase in net tubular H+ secretion. This leads to a lower luminal pH in the medullary collecting duct and enhanced trapping of NH4+ by nonionic diffusion. A second, equally important, component of this response is enhanced synthesis of NH3/NH4+; in the kidney. NH3/NH4+: is synthesized in the renal proximal tubule by a sequence of events which includes glutamine transport into the cell on a Na/glutamine coupled transporter, glutamine transport into mitochondria, and then metabolism of glutamine (27)."
"Increases in proximal tubule NH3/NH4+; synthesis require increased availability of glutamine. In addition, other amino acids can be utilized for ammonia synthesis to a lesser extent (32). This may provide a teleologic reason for the enhanced breakdown of proteins observed in metabolic acidosis. Human subjects administered oral NH4Cl develop a significantly negative nitrogen balance (33). The majority of this effect is due to enhanced protein degradation."

"Evidence also suggests that the protein wasting seen with aging may be attributable to acidosis. As noted earlier, aging is associated with a decrease in glomerular filtration rate which may be associated with a subtle degree of metabolic acidosis. Sebastian and coworkers examined nitrogen balance in 14 postmenopausal women maintained on a constant diet in a clinical research center. Their studies demonstrated that provision of KHC03 to these women improved nitrogen balance (3,7)."

"Studies have suggested that acidosis can enhance the rate of progression of renal disease (39,40)."
"The ability of acidosis to promote renal growth may be most important in polycystic renal disease. The first suggestion that intracellular acidosis may contribute to cyst formation was made by Torres and coworkers who noted that patients with hyperaldosteronism and potassium deficiency (associated with intracellular acidosis) have renal cysts (41)."

"The last component of the homeostatic response to acidosis is bone alkali release. This homeostatic mechanism has two interrelated components. First, metabolic acidosis directly regulates bone function by mobilizing Ca2+ and alkali. Second, metabolic acidosis directly inhibits renal Ca2+ absorption leading to Ca2+ removal from the body. These two effects are likely synergistic."

"Chronic metabolic acidosis increases alkali mobilization from bone by two mechanisms. First, acidosis leads to the physicochemical dissolution of bone, causing release of HCO3- together with Na+ and K+ and a small amount of Ca2+ (43,44). Second, chronic metabolic acidosis leads to increases in the activity of osteoclasts and decreases in the activity of osteoblasts (45-48). This leads to net bone dissolution with mobilization of Ca2+ and alkali. The net result in chronic metabolic acidosis is protection of blood pH and HCO3- concentration at the expense of bone mineral content."

"Thus, in summary, chronic metabolic acidosis leads to mobilization of alkali from bone which helps to defend blood pH. In the steady state, this likely explains a significant amount of the discrepancy between net acid production and renal net acid excretion. Unfortunately, this process is accompanied by mobilization of Ca2+ from bone and hypercalciuria. These processes occur secondary to the ability of acidosis to physicochemically dissolve bone, to increase osteoclast activity, to inhibit osteoblast activity, and to directly impair renal distal nephron Ca2+ absorption."

"The significance of this effect has been suggested in a number of studies. Sebastian and coworkers examined Ca2+ balance in 18 postmenopausal women. These women were found to be in negative Ca2+ balance. Administration of KHC03 decreased urinary Ca2+ excretion and improved net Ca2+ balance (51). Increases in protein intake increase urinary Ca2+ excretion, an effect which is reversed by administration of HCO3- (52). This effect of protein is likely mediated by the increased endogenous acid production associated with ingestion of protein."

"In addition, metabolic acidosis directly inhibits renal tubular Ca2+ reabsorption leading further to hypercalciuria and negative Ca2+ balance."

"[..]Changes in extracellular and cell pH are likely too small to elicit such effects. It is far more likely that a number of pH sensitive proteins exist that are designed to alter their function in response to small changes in cellular and/or extracellular pH. These proteins would thus function as pH sensors." "A second mechanism for regulating cellular function, is to activate an acid signaling system whereby multiple proteins could be regulated. Given the large number of effects elicited by small changes in cell pH, this mechanism seems more likely."

"Thus, chronic metabolic acidosis causes a number of complications in patients. These include bone demineralization, nephrolithiasis, nephrocalcinosis, and muscle wasting. Acidosis-induced enhanced renal growth may be a problem in certain patients, particularly patients with polycystic kidney disease. In order to avoid these complications, it becomes important to correct metabolic acidosis."

"The treatment of metabolic acidosis is relatively simple. One can utilize either HCO3- or citrate as oral alkali supplements. HCO3- can cause a feeling of bloating due to the reaction of gastric acid with HCO3- to form C02. Therefore, citrate may be the preferred source of alkali. Citrate, however, can enhance aluminum absorption (62,63). Aluminum absorption is a major problem in patients with renal insufficiency. However, this is not a problem in patients with normal renal function (64)."

"A second choice is whether to give the alkali as a Na+ or K+ salt. The problem with the Na+ salt is that Na+ is more likely to expand extracellular fluid and intravascular volume. This will result in worsening hypertension in patients with renal insufficiency. In addition, volume expansion increases urinary Ca2+ excretion which can further contribute to bone demineralization, nephrocalcinosis, and nephrolithiasis. Thus, in most patients KHCO3 or K citrate is preferred. In patients with renal insufficiency, one generally administers NaHC03 to avoid the K+ load and enhanced aluminum absorption."

"Patients with eubicarbonatemic metabolic acidosis may be difficult to detect. A history of diarrhea, excess meat ingestion, nephrolithiasis, or renal insufficiency would be suggestive of an excessive acid load. Increased urinary NH4+; excretion and decreased urinary citrate excretion would also be indicators of excessive acid. Increased urinary sulfate excretion would be an indicator of excessive protein loads."

"the combination of Ca2+ with excessive alkali could lead to milk-alkali syndrome"
 

benaoao

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So... a whole foods plant diet plus the lowest mEq low fat dairy plus bone broth, BCAA and taurine comes to mind. At least for a few weeks. There’s a lot of muscle meat related damage to undo in the West.

I’d always start a meal with a few ounces of leafy greens and a MCT oil+Bragg’s ACV+honey dressing. “Prepares” the stomach for the main course.
 
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- https://www.kidney-international.org/article/S0085-2538(15)51228-3/fulltext

"In the summaries, there is a wealth of data to show that metabolic acidosis has deleterious effects, particularly in patients with chronic kidney disease. A variety of hormonal abnormalities can occur, including insulin resistance, suppression of the growth hormone/IGF-1 axis, and increased circulating levels of glucocorticoids. Vitamin D production is suppressed and parathyroid hormone's sensitivity to calcium is reduced. In the absence of appropriate therapy, skeletal growth is impaired, muscle protein is subject to increased catabolism, and amino acids undergo increased oxidation: negative nitrogen balance results, and muscle wasting occurs. Ultimately, appropriate correction of metabolic acidosis with alkali can do much to ameliorate and correct this condition."


"not only kidney disease patients, but all individuals, have to be concerned about metabolic acidosis"

"Besides its direct effect on bone metabolism, metabolic acidosis can alter parathyroid hormone's sensitivity to ionized calcium. Graham and colleagues9 studied 8 hemodialysis patients with secondary hyperparathyroidism. They found that correction of metabolic acidosis increased the sensitivity of the parathyroid gland to ionized calcium, resulting in its suppression. Calcitriol did not have the same effect; however, rapid correction of metabolic acidosis in patients with renal failure resulted in a 2-fold response: circulating intact parathyroid hormone levels were suppressed, and vitamin D3 levels increased significantly10."

"Insulin resistance has been reported in patients with moderate to severe uremia. Fasting glucose levels tend to be elevated despite higher circulating levels of insulin, and there is an abnormal response to a glucose load. As a result, these patients have reduced sensitivity to the hypoglycemic action of insulin; defects in insulin secretion have also been reported11. As a complication of uremia, metabolic acidosis has been reported to contribute to insulin resistance. In rat studies, correction of metabolic acidosis partially corrects insulin resistance12. In patients not yet on dialysis, correction of metabolic acidosis with sodium bicarbonate has been shown to increase insulin sensitivity13. Mak14 studied 8 patients on chronic hemodialysis before and after 2 weeks of oral sodium bicarbonate therapy to correct the metabolic acidosis, and measured insulin sensitivity using the hyperinsulinemic euglycemic clamp technique. He also measured insulin secretion by the hyperglycemic clamp technique. Seven healthy volunteers served as control subjects. To control for the effect of the additional sodium, the patients and controls were also studied after 2 weeks of sodium chloride. Mak found that sodium bicarbonate therapy led to significant increases in venous pH and serum bicarbonate levels. There was no significant change in parathyroid hormone concentrations; however, circulating 1,25 dihydroxyvitamin D3 levels, which had been low prior to treatment with sodium bicarbonate, increased significantly following treatment. Insulin sensitivity and secretion increased as well following sodium bicarbonate therapy. Sodium chloride had no effect."

"Still other hormones are affected by metabolic acidosis. In normal adults, metabolic acidosis lowers serum levels of free triiodothyronine (T3) and thyroxine (T4), and thyroid-stimulating hormone (TSH) levels are mildly increased. The concentration of reverse T3 is unchanged. The clinical significance of this mild hypothyroid state is unknown, but it could affect both calcium and protein metabolism."

"It has long been noted that patients with chronic kidney disease appear malnourished. In the early 17th century, physicians from France and England who visited St. Petersburg to attend Peter the Great noted how emaciated he appeared. They concluded that his appearance was due largely to the sequella of his disease. About 300 years later, Lyon, Dunlop, and Stewart17 advocated the use of alkali for the treatment of patients with kidney disease. They noted a connection between renal failure and metabolic acidosis, and attributed the latter as a cause of malnutrition in this disease. As did others, they noted that a low protein diet was beneficial for treatment of patients with kidney disease. Giordano18 would later verify through detailed dietary records that there was a relationship between a reduction in protein intake and relief of uremic symptoms. Today we know that protein, particularly animal protein, is rich in sulfur-containing amino acids and is a major source of acid in the diet. It is this acidosis that has a negative impact on the body's protein stores. Coles19, who performed careful measurements of various muscle groups in patients with chronic kidney disease, demonstrated that a decrease in muscle mass was often masked by fluid retention. He concluded that patients with kidney disease were malnourished."

"How does metabolic acidosis cause protein wasting? It would seem intuitively obvious that metabolic acidosis would act directly on cells and lower intracellular pH, but the available evidence suggests that this is not the case. When metabolic acidosis is induced in rats by feeding them ammonium chloride in the diet or by infusing them with hydrochloric acid, or by induction of chronic renal failure, intracellular pH as measured by 31 PNMR (phosphorus nuclear magnetic resonance) is maintained despite the severity of the low extracellular pH21. [!!] This work suggests that other signal transduction pathways must be involved when metabolic acidosis stimulates muscle proteolysis. A prime mediator of this process appears to be glucocorticoids. When May and colleagues22 induced chronic renal failure in rats, they noted that urinary corticosterone levels increased in proportion to the degree of metabolic acidosis. Moreover, they found that only the acidotic rats had accelerated rates of muscle protein degradation. When sufficient sodium bicarbonate was added to the diet to correct the acidosis, urinary corticosterone levels remained elevated but rates of protein degradation were no different from those in control rats. The authors concluded that both acidosis and a high glucocorticoid level were required to stimulate muscle proteolysis. Garibatto and colleagues23 extended these results to patients with chronic kidney disease. They also found an inverse correlation between serum cortisol and bicarbonate levels—ie, the lower the serum bicarbonate levels, the higher the serum cortisol levels. They also measured rates of protein degradation in these patients and found that higher rates of protein degradation correlated directly with serum cortisol levels and indirectly with serum bicarbonate levels. Although a correlation between serum cortisol levels and serum bicarbonate levels exists in the setting of metabolic acidosis, it does not prove causality. More definitive evidence for this cause-and-effect relationship comes from both cell culture work and animal studies."

"Glucocorticoids alone did not stimulate protein degradation. Only in the presence of both glucocorticoids and acidosis could protein degradation occur."
It's almost a sign of things going down of the hills.

"Besides an increase in protein degradation, metabolic acidosis is accompanied by an acceleration of amino acid oxidation. Because they play an important role in protein metabolism, the branched-chain amino acids have served as markers of malnutrition in various disease states, including chronic kidney disease. The branched-chain amino acids include valine, leucine, and isoleucine and constitute 18% of the amino acids in muscle. Altered cellular and serum levels of the branched-chain amino acids are regularly found in patients with chronic kidney disease31, and the relative abundance reflects disease severity."

"even short-term correction of metabolic acidosis has implications for patients with chronic kidney disease. Even patients with fairly advanced chronic kidney disease can potentially benefit from correction of metabolic acidosis."​

- Diet-Induced Low-Grade Metabolic Acidosis and Clinical Outcomes: A Review

"Diet-induced low-grade metabolic acidosis is a condition that has been investigated since the early 1980s, when Kurtz et al. (1983) [4] showed that an increased dietary acid load led to small changes in the acid-base balance (increase in [H+] and reduction in [HCO3−]). From time to time, other studies have been published focusing on these minimal alterations in the acid-base balance [5,6,7,8], and several terminologies have been used, such as "eubicarbonatemic metabolic acidosis" [9] and "acid retention" [10]."

"The nutrients that release acid precursors into the bloodstream are phosphorus and proteins (mostly containing sulfur amino acids, such as cysteine, methionine, and taurine, and cationic amino acids such as lysine and arginine). In addition, sodium chloride (NaCl) intake is reported to be an independent predictor of plasma bicarbonate concentration. Assuming a causal relationship, NaCl may exert approximately 50–100% of the acidosis-producing effect of the dietary acidic load, and is therefore considered a predictor of diet-induced low-grade metabolic acidosis [14]. On the other hand, the nutrients that are precursors of bases are potassium, magnesium, and calcium. Thus, in general, the main foods that release precursors of acids into the bloodstream are mostly of animal origin (except for beans and nuts), and foods that are precursors of bases are mainly those of plant origin [2,3]."

"the foods that contribute most to the release of acids into the bloodstream are meats (beef, pork, or poultry), eggs, beans, and oilseeds, and the foods that contribute most to the release of bases are fruits and vegetables. If there is an excessive consumption of acid precursor foods, to the detriment of those precursors of bases, volubility of the acid-base balance occurs [2,3,17]. If this acid-base balance disorder occurs in a prolonged and chronic way, low-grade metabolic acidosis may become significant and predispose to diseases [18,19,20,21]."

"Some mechanisms have been proposed to explain the influence of an increased dietary acid load on bone metabolism (Figure 2). The slight reduction of the extracellular fluid pH suppresses the activity of osteoblasts and decreases the gene expression of specific matrix proteins and alkaline phosphatase activity. In addition, low-grade metabolic acidosis has been associated with osteoclast activity and increased urinary calcium excretion without increased intestinal calcium absorption, resulting in the depletion of bone calcium [22,23]. Net acid excretion (NAE), a predictor of the acidifying potential of the diet, is shown to be associated with increased serum levels of parathyroid hormone (PTH) and the urinary excretion of calcium and N-telopeptide, an important marker of bone resorption [20]. In the study conducted by Buclin et al. (2001) [11], the ingestion of an acidogenic diet for four days caused an increase in the urinary excretion of calcium and C-telopeptide of 74% and 19%, respectively, compared to the intake of an alkalizing diet for the same period. Moreover, the consumption of this dietary pattern was associated with a discrete, but significant, reduction in blood and urinary pH."

"Studies have shown that the deleterious effects of low-grade metabolic acidosis on bone tissue are independent of calcium intake [11,27]."
"Recently, Kong et al. (2017) [28] showed in their study with 7187 participants from the Korean National Health and Nutrition Examination Survey (KNHANES) that the dietary intake of potassium was positively associated with a higher mineral density in the lumbar spine, femur, and hip, even in participants with a low dietary calcium intake—a fact that can be attributed to the lower acidifying potential of diets rich in food sources of potassium [28]."

"[..]dietary proteins (mainly animal sources) may exert an anabolic effect on bone turnover by increasing levels of insulin-like growth factor (IGF-1), stimulating intestinal calcium absorption, suppressing PTH action, and improving shape and muscle mass [32,33,34]. Furthermore, bones are formed by the protein matrix, and dietary proteins appear to exert an osteotrophic effect [33,35]. Considering these facts together, it is raised that in the presence of an adequate dietary intake of base-forming nutrients, proteins may exert benefits on the bones [32]."

"The effects of an acidogenic diet on the formation of kidney stones are the clinical outcome with the highest number of published studies. In response to diet-induced low-grade metabolic acidosis, the kidneys perform adaptive responses in an attempt to restore the acid-base balance, and these responses include an increased excretion of calcium and oxalate salts, and reduced citrate excretion. Citrate inhibits the formation and agglomeration of calcium oxalate crystals and, thus, the reduction of its excretion is associated with the formation of a less soluble complex of calcium oxalate [2,36]."

"Two mechanisms have been proposed to elucidate the associations between dietary acid load and chronic kidney disease (CKD). As the demand for acid elimination rises, there is an increase in endothelin-1, angiotensin II, and aldosterone production. These substances are associated with the reduction of the glomerular filtration rate (GFR) and the stimulation of pro-fibrotic factors, which are associated with renal fibrosis. In addition, in an attempt to neutralize the H+ load, an increase in ammonia production occurs in the proximal tubule, which can cause tubular toxicity and renal damage. These processes, when constantly stimulated, are associated with the increased risk and progression of CKD [39,40,41]."

"In this context, it has been shown that the serum bicarbonate level is an independent predictor of CKD progression. Raphael et al. (2011) [42] showed that higher serum bicarbonate levels within the normal range (20 to 30 mEq/L) are associated with a reduced risk of negative outcomes in patients with CKD, as dialysis, worsening renal function, and death [42]."

"In the summaries, based on available data, the dietary acid load seems to be an important predictor of CKD and interventions taking into account the frequent consumption of base-producing foods, such fruit and vegetables, should be considered."

"The mechanism involving the association between dietary acid load and the risk of diabetes mellitus has not yet been fully elucidated, but it is believed that the maintenance of blood pH close to the lower limit of the normal range may lead to a decrease in the uptake of glucose by the muscle, the disruption of insulin binding to its receptor, and the inhibition of the insulin signaling pathway. This may lead to peripheral insulin resistance, the main risk factor for the development of type 2 diabetes mellitus [22]."

"Some mechanisms are suggested to justify the association between a high acid diet load and the risk of hypertension. In the presence of low-grade metabolic acidosis, there is an increase in the pituitary stimulus for ACTH synthesis and a consequent production of cortisol and aldosterone [56], which in excess, may induce an increase in blood pressure [57,58]. In addition, the acid-base balance influences mineral homeostasis by regulating the calcium absorption in the kidneys, and it is reported that the increased urinary excretion of this mineral may be associated with an increased blood pressure [59,60]. In addition, NaCl intake, the most known risk factor associated with the etiology of hypertension, is an independent predictor of diet-induced low-grade metabolic acidosis [14]."

"Recently, Chan et al. (2015) [61] evidenced a positive association between the acidogenic diet and the risk of non-alcoholic hepatic steatosis (NASH) in 793 Chinese individuals aged 19–72 years. An increase of 1.32 in the odds of developing NASH, independently of the intake of fiber, saturated fatty acids, carbohydrates, and proteins—dietary constituents known to influence the risk of NASH–was observed for each 20 mEq/day of NEAP [61]. Although this is the only available study evaluating this association, it can be suggested that the influence of diet on the acid-base balance is a factor that contributes to the development of this disease.

The mechanisms by which an acidogenic diet may influence the pathogenesis of NASH are not fully understood. Taking into account that the slight reduction in plasma pH caused by an acidifying diet is associated with insulin resistance, the consequent hyperglycemia and increased inflammation could contribute to hepatic insulin resistance, which is related to the increase in the availability of free fatty acids, and is a risk factor for the development of the disease [62]."

"The mechanism that surrounds the association between a high dietary acid load and the loss of muscle mass involves the effect of low-grade metabolic acidosis on the stimulation of the proteolysis pathways. This stimulus can be triggered by an increased production of glucocorticoids, such as cortisol, which stimulates the degradation of amino acids for release into the bloodstream. Glutamine is essential for the process of tubular ammoniagenesis, important for the elimination of the body’s hydrogen ions [66,67]."

"Studies have shown that diets with high values of NEAP and PRAL may predispose to several metabolic damages, such as the stimulation of bone resorption associated with a decrease in bone mineral density and bone mass, leading to a higher risk of fractures. There are some interventional and observational studies showing that increasing fruit and vegetable consumption is associated with better bone outcomes, such as reduced reabsorption markers excretion, an increased bone mineral content, and lower fractures and osteoporosis risk [27,71,72,73]. Furthermore, other studies have reported that alkalinizing supplementation (including potassium citrate or potassium bicarbonate) can attenuate the deleteriuous effects of low-grade metabolic acidosis on bone tissue, as demonstrated by Dawson-Hughes et al. (2009 and 2015) [74,75] and Moseley et al. (2013) [76]. However, the effects promoted by alkalinizing supplementation are acute and there must be a dietary pattern change to reduce the risk of negative bone outcomes, and the frequent consumption of base-producing foods should be considered."

"Some studies have shown that a slight reduction in extracellular pH decreases the beta cell response and leads to a disruption of insulin binding to its receptor. This may lead to peripheral insulin resistance, the main risk factor for the development of type 2 diabetes mellitus [78,79,80]. In addition to high PRAL and NEAP values, other markers of metabolic acidosis have been associated with insulin resistance, such as plasma bicarbonate reduction, an increased anion gap, elevated levels of plasma lactate, and low urinary pH values [12,51,52,80]."

"[..]it has been suggested that intracellular potassium reduction is compensated for by elevated sodium levels and, as a consequence, blood pressure elevation [87]. In this context, studies have showed that a higher intake of fruit, vegetables [88,89,90], and some specific nutrients (i.e., potassium and magnesium) [91,92,93] are associated with a lower hypertension risk. However, there are no studies evaluating the effect of specific dietary interventions correcting low-grade metabolic acidosis on the hypertension risk."​

- Chronic Metabolic Acidosis Destroys Pancreas((

Travisord would probably add [sick!] after destroys.

I was quoting it but gave up halfvvay through because it's a painful text, quite confusing. On the hands of the others, the references are good and it's worth checking them out.

Ps.: found this version which had an intervention from a voice of reason.​

- Diet-induced acidosis: is it real and clinically relevant?

"The normalisation of a low-grade chronic metabolic acidosis has been accomplished by two methods: change in dietary patterns and alkaline supplementation."

"Reducing protein consumption down to the US dietary recommended intake in a trial of thirty-nine healthy premenopausal women has also been shown to reduce Ca excretion and raise urinary pH, as well as reduce markers of bone resorption (48). It should be emphasised that this trial did not evaluate a low-protein diet, but rather lowered what could be considered a high protein intake to a level of 0·8 g/kg for this population. Because renal NH4+ formation is dependent upon adequate protein intake, an extremely protein-deficient diet may also increase acidosis (49). In fact, in a recent study of 161 postmenopausal women, protein intake had a positive association with lumbar bone mineral density, but only after adjusting for the negative effect of the sulfur content of the proteid (sulfate), perhaps ‘reconciling reports of positive impacts of dietary protein on bone health with reports of a negative impact of the acid load from sulfur-containing amino acids’ (50). In children, a greater protein intake has been associated with greater bone strength, though this effect is negated if alkalinising nutrients are lacking. It should be noted, however, that clearly bone may be influenced by these minerals in ways unrelated to acid–base chemistry (51)."

"Finallies, increasing sodium chloride intake dose-dependently decreases blood pH and plasma bicarbonate levels (52), independent of the partial pressure of carbon dioxide (PCO2), creatinine clearance and dietary acid load (6). This effect may be due to a decrease in the strong ion difference, as total chloride concentration increases relative to total N and a concentration, an effect that may increase H+ concentration (53). Subjects who are particularly sensitive to salt, generally defined as an increase of 3 to 5 mmHg for a given salt load, have more of a metabolic acidosis than those subjects who are salt resistant (54). So, while everyone’s net acid load would improve by lowering their dietary salt intake, some individuals should benefit more than others from this dietary intervention."

"A number of supplemental interventions have also been used. Salts of carbonic acid are available in a variety of formats. These include sodium or potassium bicarbonate and calcium carbonate. Alkali salts are also available as citrate, acetate or hydroxides. As suggested above, giving Na salts may be partly counterproductive, given their other effects, and so most studies use K or Ca alkali salts. These salts dose-dependently decrease NAE (55,56).
Caution using alkali therapy without careful consideration and expertise in subjects with heart, lung or kidney disease is needed. In congestive heart failure, sodium bicarbonate impairs arterial oxygenation and reduces systemic and myocardial oxygen consumption in these patients, which may lead to transient myocardial ischaemia (57). Additionally there may be several simultaneous processes affecting acid–base status among patients with congestive heart failure (58). Similarly, bicarbonate loading may worsen exercise response in chronic obstructive pulmonary disease patients (59). Finally, subjects with kidney failure may develop elevated blood K levels and potentially fatal cardiac arrhythmias if given K alkali salts, or volume overload and breathing problems if given Na alkali salts."​
 
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Amazoniac

Amazoniac

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- Diet, evolution and aging--the pathophysiologic effects of the post-agricultural inversion of the potassium-to-sodium and base-to-chloride ratios in the human diet

"Although much work has been done on the adverse effects of dietary sodium chloride on blood pressure, very little has been done to explore the specific role of excessive dietary chloride. And yet, the chloride content of the modern diet is at least as high as the sodium content [32]. Does the exchange of the bicarbonate we used to eat for the chloride that we presently eat have any adverse effects?

Morris and colleagues first demonstrated in uninephrectomized rats given deoxycorticosterone that while treatment with sodium as a combination of the bicarbonate and acetate salt raised blood pressure, treatment with sodium as the chloride salt raised blood pressure to a significantly higher level [33]. Luft et al. demonstrated that sodium as the chloride salt raised blood pressure in stroke-prone spontaneously hypertensive rats [34] and sodium as the bicarbonate salt lowered blood pressure in mildly hypertensive humans [35]. More recently, Morris et al. have done studies investigating the effects of KCl and KBC (potassium bicarbonate) on blood pressure, frequency of stroke and severity of the renal lesions in the SHRSP [stroke-prone (spontaneously) hypertensive rat] [36]. Rats treated with KCl had significantly higher PRA than rats treated with KBC. In each group and in all combined, the severity of hypertension was highly correlated with the levels of PRA (log transformed). KCl loading induced greater increases in BP than in control or KBC rats (Fig. 3).

The incidence of strokes was significantly higher with KCl than with KBC (Table 1). In the KCl/KBC rates, strokes occurred only in animals with SBP > 248mmHg and with PRA > 26.5 ng/ml/h (log PRA=1.42).

Light microscopic examination of the kidneys revealed glomerular, tubular, interstitial, and vascular lesions (histologically ranked in combination) similar in quality but significantly more frequent and more severe with KCl supplementation than either KBC or CTL [36]. Irrespective of dietary supplements, renal lesions were rare in rats with SBP [systolic blood pressure] < 200 mmHg. The overall severity of renal lesions was highly correlated with the level of PRA (log transformed) (R2= 0.67, p < 0.0001). Proteinuria was significantly greater with KCl than either KBC or CTL (Table 1). Creatinine clearance was significantly greater in KBC than in KCl or CTL (Table 1). Morris and colleagues concluded that the extent of renal damage and likelihood of stroke are determined by the severity of hypertension."​

- Relationship and Interaction between Sodium and Potassium (same authors as above)

- Dietary sodium chloride intake independently predicts the degree of hyperchloremic metabolic acidosis in healthy humans consuming a net acid-producing diet (same authors as above, which happen to be the same authors as above them)

- Acid-Base Disturbances in Gastrointestinal Disease

"Long-term laxative ingestion with the intent to increase stool volume causes increased and unregulated losses of K+ (44,45). If this excess loss is not counterbalanced by a concomitant increase in dietary K+ intake, then body K+ stores will become depleted, a change that causes hypokalemia and some H+ shift into cells, raising extracellular fluid [HCO3−] (18). The increase in [HCO3−] may be sustained by the effect of K+ depletion to increase renal NH4+ production and excretion. The major clinical feature of laxative abuse is hypokalemia; clinically significant metabolic alkalosis, if present, is usually mild in the absence of concomitant bulimia (44,45). If laxative abuse induces excessive diarrheal losses, then metabolic acidosis can of course occur, as with any severe diarrhea (45)."​

[44] Metabolic and renal studies in chronic potassium depletion resulting from overuse of laxatives

"It is well known that diarrhea caused by a variety of gastrointestinal disorders may lead to potassium depletion (1). This paper presents observations on two otherwise healthy women who, prior to this study, had gradually developed severe potassium depletion and hypokalemia as the result of chronic diarrhea induced by owause of laxatives. Although in each instance there had been a loss of approximately one-third of total normal body potassium, there were no other significant disturbances of water and electrolyte balance and no overt signs of malnutrition."

"The extraordinarily severe potassium deficits in these two women apparently developed gradually over a period of months or years without producing any striking symptoms or signs. This suggests that the rate at which potassium depletion develops is of importance in determining symptomatology. Although rapid loss of potassium from isolated perfused muscle will reduce contractility (22), it has been shown that the gradual production of potassium depletion in rats does not impair the muscular response to a tetanic stimulus (23) or reduce the animals' swimming ability (24). Further evidence that tissue may become acclimatized to potassium deficiency is provided by the "potassium paradox" of Libbrecht (25)."

"Restoration of tissue potassium was also accompanied by a large but transient retention of sodium, an observation similar to that made by Elkinton, Squires, and Crosley (30). Sodium retention may have been related to the reversible disturbances in renal function observed in the present patients."

"potassium depletion may depress renal function"

"Renal dysfunction of the type reported here could account for certain phenomena associated with severe potassium depletion. Sodium retention (30,40,41), elevated blood nitrogen concentration (40), and reduced urea clearance (41) may be in part due to the reduction in glomerular filtration. Renal tubular damage could explain the isosthenuria in these and other cases of potassium depletion (38,39,42) as well as the polyuria in potassium-deficient dogs (43) and rats (44). The failure of the kidney in potassium depletion to adjust extracellular bicarbonate concentration (32) may also be related to the functional disorders reported here. Another interesting implication of these data is that potassium depletion may be responsible at least in part for the renal dysfunction found in many cases of alkalosis (30,45)."

Out of curiosity, in one case the person took a laxative that had Cascara as one of the components. It appears to be irrelevant because the problems appeared from chronic potash depletion.​

- Excess Casein in the Diet Is Not the Unique Cause of Low-Grade Metabolic Acidosis: Role of a Deficit in Potassium Citrate in a Rat Model
 

yerrag

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This is one instance of taking too much baking soda where a perfect storm of low potassium and low chloride comes together to create a metabolic alkalosis condition. A person could also be on a low salt diet, with low chlorides already to begin with, and when he takes in enough baking soda, he could be setting himself up for this alkalotic condition. The high bicarbonate and highly alkaline condition of blood could very well result in increased urination, and if the increased urination rate continues, enough potassium could be lost through the continual increased urination rate. This would result eventually in low potassium, at which point the bicarbonate does not get urinated, but just gets resorbed in the kidney and goes back into the bloodstream. This is one gotcha, probably of many, that one has to be aware of in supplementing with baking soda in large quantities.

In this instance, probably eating enough bananas, like one with each meal, would probably maintain potassium levels, so that excess bicarbonates in the blood could be excreted in the urine, rather than be recirculated back in the blood. This would keep in check a metabolic alkalotic condition from developing.

But why bother with taking baking soda in large quantities? This is a matter of choosing the easy way by supplementation instead of making needed food lifestyle changes, which is more difficult, not as much as implementing it, as much as getting started on. Eating less meat (lessening acid load), drinking fruit and vegetable juices, eating more cooked leafy greens (increasing alkaline input) eating more sugar or carbohydrates (for sugar metabolism instead of fat or protein metabolism) would be a food lifestyle one could live with, with a minimum of supplementation.

If people make the time to get set up, it really isn't so hard to make your own fruit and vegetables juices. You're not even cooking. You're just buying, washing, chopping, and juicing. And cleaning afterwards. And if you're eating less meat, you're cooking less as well. And if you're making casserole dishes, which is the case for collagenous cuts of meat and skin, you can make a larger batch each weekend, and reheat easily the rest of the week. Casserole dishes taste even better when you reheat leftovers. And if you're eating rice, it's just so easy with a rice cooker, especially the programmable ones like from Zojirushi, Panasonic, and Tiger.

Thanks Amazoniac for all the links you've shared. Really setting aside time to read your links. I don't know where you get them, but keep them coming!
 

tara

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@Amazoniac , thanks for mining such interesting sources for us yet again.

By the way, you've all probably read that bicarbonate is needed for magnesium metabolism/absorption. It must be why Ray recommends it in this form as a supplement.
I've read threads here about magnesium bicarbonate, and I've followed a recipe to make and drink it etc. But I wasn't aware that Peat had directly recommended it? I thought I'd seen him recommend magnesium carbonate?

A diet based on starch and meat/fish should be pretty terrible.
Not that I'm recommending a diet of solely meat/fish and super starchy foods, but unless you actually meant pure starch (which isn't really food, and few people eat as a staple), I think to be fair one could distinguish different starchy foods - I'd expect at least some tubers to be more alkalinising than many grains, for instance.
 

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