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

Discussion in 'Acidity vs. Alkalinity' started by Amazoniac, Apr 12, 2018.

  1. Amazoniac

    Amazoniac Member

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    - Acidosis: An Old Idea Validated by New Research

    (the author appears to be credible, you can tell because he's wearing a tie and has his arms crossed)

    "The idea that “being too acid” contributes to disease susceptibility, especially cancer, has been around for a long time in the natural/integrative medicine world. This concept was easily discounted by conventional medicine as measuring blood pH on various types of diets showed no change.

    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."

    "When talking about diet-induced acidosis, please be clear we are not talking about the pH of the food or beverages consumed. Rather, this is about the acid/base changes induced by the food constituents. The preagricultural diets we evolved on are estimated to be base-producing, with a mean NEAP of negative 88 mEq/d. In contrast, according to NHANES III, the average diet in the United States is acid-producing, with an NEAP of positive 48 mEq/d.2 This is the equivalent of 4.9 g HCl being added to our metabolism every day. Although, as discussed below, the kidneys and lungs get rid of almost—but not all—of this excessive acidity, when these systems start to fail, calcium from bone is used instead as the buffer. The mineral content from 3 g of bone is needed to neutralize 1 g of acid. As I will show below, this excessive acidity turns out to be a seriously underrecognized cause of osteoporosis. The obvious question, then, is: What constituents of diet cause acidity, versus those that increase alkalinity? The answer is surprising.

    The primary sources of acidity in the diet are sulfur-containing amino acids, salt [Cl], and phosphoric acid in soft drinks (For a more complete discussion of the adverse effects of phosphates, see Lara Pizzorno’s article in IMCJ 13.6).3 You will likely immediately scoff that salt is neutral in pH and is not metabolized to anything that is acid—and you would be right. Nonetheless, research has clearly shown that—happily reversibly—NaCl accounts for 50% of the net acidity of the average American diet.4 The mechanism is not definitively known, it is currently thought to be impairment of the kidney’s ability to excrete acid compounds. Figure 1 shows the sources of salt in the typical Western diet. If you look closely, you will see that wheat products are the primary source of salt—which may account for the common belief that wheat products are acid forming (wheat itself is only slightly acid forming)."

    "Be clear that the kidneys mitigate but do not eliminate all the excess acidity. After considering all the unnecessary work put on the kidneys to deal with this excess acidity, it occurred to me that perhaps this is a key cause for the loss of kidney function seen with aging. As the kidneys lose function with aging, their ability to excrete acid becomes impaired, which may be another explanation for the loss of bone with aging.8"

    "The major reservoir of base is the skeleton (in the form of alkaline salts of calcium), which provides the buffer needed to maintain blood pH and plasma bicarbonate concentrations when renal and respiratory adaptations are inadequate. Acid-promoting diets are associated with increased urinary excretion of both calcium and bone matrix protein and decreased bone density.9 Neutralizing acid intake with diet or alkalinizing supplements decreases urine Ca and bone matrix protein excretion. Also, to a much smaller degree, skeletal muscle can act as a buffer."

    "A growing body of research has now clearly documented clinical benefit through diet and alkalinizing supplements. A diet rich in fruits and vegetables and low in animal protein and sodium chloride reduces acid load and is consistently associated with greater bone density.16 Alkalinization through supplementation with potassium and magnesium citrates decreases urinary excretion of calcium, increases bone density, and decreases fracture.17 This is especially interesting, as this reversal of osteoporosis is accomplished without increasing either vitamin D or calcium!18

    Equally important is the research on prevention and treatment of kidney stones. Prospective studies have now shown that supplementation with potassium and magnesium citrates prevents recurrence of calcium oxalate stones by a remarkable 85%.19 More exciting, however, is research showing dissolution of kidney stones. One study found that 5 of 8 patients completely dissolved their stones after 6 months supplementation with potassium citrate/bicarbonate.20

    Other areas are showing benefit from alkalinization such as strength training, aerobic exercise, and pain reduction.21,22,23"​

    - Influence of nutrition on acid-base balance – metabolic aspects

    "There is a necessity to excrete acid (hydrogen ions, H+) when the sum of major non-metabolizable anions eliminated in urine exceeds the sum of the mineral cations sodium (Na), potassium (K), calcium (Ca), and magnesium (Mg) (Fig.1). Major urinary anions encompass chloride (Cl), phosphate (P), sulfate (SO4) and a mixture of different organic acids (OA) of which the majority cannot be metabolized (e.g., aliphatic or aromatic acids). The difference between these non-bicarbonate anions (sum acid-forming inorganic anions + OA) and the mineral cations (sum base-forming cations) is net acid excretion (NAE indirect). NAE is analytically quantified as the sum of NH4 + TA – bicarbonate (Fig.1). The urine ionogram shows that NAE may also be estimated from the dietary intakes of Cl, P, SO4 (originating mainly from metabolism of sulfur-containing amino acids), on the one hand, and Na, K, Ca, Mg, on the other hand, provided the respective intestinal absorption rates of these nutrients are known and no quantitatively important nutrient retention or catabolic tissue degradation occurs. In fact, we were able to show that it is possible to reliably estimate the renal NAE of healthy subjects from the composition of their diets."

    "When nutrient data from current food composition tables were used, the calculation model yielded negative PRAL [potential renal acid load] values for fruits and vegetables, meaning they reduce acid excretion; milk and yogurt yielded about 1 mEq, whereas meats, fish, poultry, cheeses and even some grain products potentially had 7 mEq or more per 100g serving."

    "A schematic representation of how the different organs interact in managing acid-base balance is given in Fig.2. The initial organ with an important impact on acid-base metabolism after the ingestion of food is the intestine. The intestine itself does not specifically generate acid or base equivalents, but depending on diet composition it modulates the blood bicarbonate level by increasing or decreasing the amount of alkali (from pancreatic secretion) that is continuously reabsorbed (for more details see below,Fig.3). In addition, the gut determines the absorbed amounts of sulfur-containing amino acids (AA-S) and alkali salts of metabolizable OA, which then are available in the liver or other metabolically active tissues as substrates for the generation of either acids or alkalis. After oxidation of AA-S and OA the released protons or alkali ions add to the total acid-base pool in blood and are finally excreted by the kidney (Fig.2). On the other hand, the lung regulates the carbonic acid-bicarbonate buffer system and herewith the blood pH is maintained within a narrow range (respiratory compensation)."

    "The intestine does indeed not directly generate acids or alkalis, but it generates “so-called” acid or alkali loads. The reason for this is the specific absorption rate of each electrolyte. For example, from a given amount of Mg only about one third is absorbed (Fig.3), whereas the average bioavailability of Cl is 95%. If MgCl2 is ingested a clear excess of Cl over Mg enters the blood (Fig.3). Due to the principle of electroneutrality it is clear that other cations need to compensate. The primary cation that is abundantly available to be absorbed along with an excess of anions (such as Cl) is Na stemming from pancreatic secretion of large amounts of sodium bicarbonate. The bicarbonate anion forms carbonate salts with the unabsorbed portion of Mg. As a result the circulating bicarbonate pool is not appropriately replenished (Fig.3). This lack of sodium bicarbonate in blood, which means a loss of buffer capacity, can be called acid load. Comparable consequences for the intestinal bicarbonate reabsorption are seen when Ca salts of unmetabolizable acids are ingested. Thus, in metabolism CaCl2 also has acidic properties [13]."*

    "A similar mechanism operates when high amounts of phosphorus are ingested in the form of phosphoproteins (Fig.4). These proteins are hydrolyzed into the respective amino acids and phosphoric acid. Both components are absorbed to a comparable degree. The phosphate anion enters the cells of the gut along with sodium, again reducing the systemic bicarbonate pool. In this case, the intestine has not generated an acid load due to different absorption rates for anions and cations, but due to the release of an acid after digestion."

    "In contrast, a real production of “true” acid or alkali occurs in the liver or other metabolic active tissues (Fig.5). For example, the oxidation of sulfur-containing amino acids to urea and carbon dioxide also yields sulfuric acid. On the other hand, the alkali salts of organic acids, for example sodium citrate, ingested with the diet are metabolized to carbon dioxide and water and yield the respective cation along with bicarbonate, thus, increasing the circulating alkali reserve or blood base pool (Fig. 5)."

    "In blood, the acid (sulfuric acid) is buffered by bicarbonate. Thereby neutral sodium sulfate and carbonic acid are formed. The latter is eliminated as carbon dioxide by the lung. The neutral salt, sodium sulfate, is transported to the kidney and the sodium is reabsorbed for the restoration of the circulating bicarbonate pool. An active renal hydrogen ion secretion, for example through a H+/Na+ antiporter transport protein in the distal renal tubular duct, drives this process. Since the kidney can not elaborate urine more acid than pH 4.4, only negligible quantities of strong acids, such as sulfuric acid, can be eliminated in free titratable form. Consequently, appropriate hydrogen ion acceptors must buffer most of the secreted hydrogen ions. The most important proton acceptor is NH3."

    "In response to an acid load, for example induced by an elevated protein intake, the kidney increases NAE. As has been explained previously, this means that the urinary output of bicarbonate falls and that of NH4 and TA rises (compare Fig.1). Since the major constituent of TA in the urine is phosphate, an increase in “nonphosphorus” renal acid load (e.g., due to elevated oxidation of sulfur-containing amino acids) must be primarily managed by an elevated NH4 output. Consequently, NH4 excretion is generally increased after an elevation of protein intake when no simultaneous rise in food-derived alkali load is present."

    "[..]in healthy subjects, the final degree of the renal capacity to excrete NH4 (and thus to excrete net acid) is modulated by the amount of protein ingested. This mechanism would allow the kidney to meet acid-base demands more efficiently and thus leaves a renal surplus capacity for the elimination of additional acid loads."

    "As the urine pH is regarded to reflect the primary stimulus for renal ammoniagenesis, urinary NH4 output was also plotted against the urine pH (Fig.10). For this, data from another diet study with high and low protein intake [4] were also included. As can be seen, renal NH4 output is also elevated for any given urine pH range, whether it is high, medium or low. Furthermore, this clearly increased capacity for net acid excretion is associated with a small but significantly (P < 0.05) elevated urine pH – even under conditions of an already alkaline urine. This has practical implications: as under our living conditions (common Western diets) the protein intake is at least moderately high [16], special care should be taken if higher amounts of alkalizing supplements are ingested. In that case, the additional ingestion of higher amounts of calcium supplements should be avoided since the alkalizing agent together with a relatively high protein intake would result in the highest possible urine pH levels, thus, increasing the risk of urolithiasis because calcium phosphate is poorly soluble at higher urine pH values."​

    - Dietary, Metabolic, Physiologic, and Disease-Related Aspects of Acid-Base Balance: Foreword to the Contributions of the Second International Acid-Base Symposium | The Journal of Nutrition | Oxford Academic

    "An aggravating factor with regard to acidosis induction is the intake of high amounts of sodium chloride. As argued by Lynda Frassetto et al. (9), the high salt together with low potassium intake in the typical American diet substantially contributes to acid-base imbalance.

    Aside from strong catabolic effects on bone architecture and bone strength, an acute metabolic acidosis also affects important endocrine functions including functional glucocorticoid activity. Remer et al. (10) examined whether normal variation in net endogenous acid production may already show an association with potentially bioactive free glucocorticoids in healthy adults. In their study, the authors focused on a new noninvasive marker of functional glucocorticoid activity (11) and took into account additional endocrine-metabolic determinants such as circulating leptin levels and overall daily cortisol secretion (12).

    Acid-base metabolism is influenced not only by intakes of protein, alkalizing food constituents, or metabolically noncombustible dietary organic acid; drinking water must also be taken into consideration. The probable impact of differences in drinking water acidity is reviewed in the article from Ragnar Rylander (13). Not only the usual drinking water but also the choice of mineral water influences acid-base balance. Peter Burkhardt et al. (14) actually showed that in several studies in humans, alkali mineral waters decreased bone resorption markers.

    Using an animal model, namely the dietary alkali-depleted herbivore rabbit, Heidrun Kiwull-Schöne et al. (15) provided evidence that the exhausted renal base-saving function is one cause for an increased susceptibility to develop chronic metabolic acidosis."​

    - Adverse Effects of Sodium Chloride on Bone in the Aging Human Population Resulting from Habitual Consumption of Typical American Diets | The Journal of Nutrition | Oxford Academic

    "Because previous investigations have shown that, under ordinary physiological conditions, the diet's sodium chloride load independently of net acid load determines systemic acid-base status, that discovery provides perhaps the most solid support to date for the hypothesis that the low-grade metabolic acidosis of the American diet contributes to the pathogenesis of age-related osteoporosis.

    Not surprisingly, then, the adverse effects of increased dietary sodium chloride on urine calcium excretion and bone turnover markers in postmenopausal women might be preventable by coadministration of potassium alkali (citrate). Sellmeyer et al. (43) adapted 60 postmenopausal women to a low-salt (87 mmol sodium/d) diet for 3 wk, then randomized them to a high-salt (225 mmol sodium/d) diet plus potassium (90 mmol/d) or to a high-salt diet plus placebo for 4 wk. Urine calcium increased 42 ± 12 mg/d (11 ± 3 mmol/d, mean ± SEM) on the high-salt-plus-placebo diet but decreased 8 ± 14 mg/d (2 ± 4 mmol/d) in the high-salt-plus-potassium-citrate group (P < 0.008, potassium citrate vs. placebo, unpaired t-test). N-Telopeptide increased 6.4 ± 1.4 nmol bone collagen equivalents/mmol creatinine in the high-salt-plus-placebo group and 2.0 ± 1.7 nmol bone collagen equivalents/mmol creatinine in the high-salt-plus-potassium citrate group (P < 0.05, potassium citrate vs. placebo, unpaired t-test). Thus, the addition of oral potassium citrate to a high-salt diet prevented the increased excretion of urine calcium and the bone resorption marker caused by a high salt intake.

    From the above considerations, it would behoove us to consider both the inordinate dietary sodium chloride load and the habitual dietary net acid load of contemporary American diets among the many factors contributing to the pathogenesis of osteopenia and osteoporosis in the aging population. To what extent Americans realistically will restrict sodium chloride intake remains uncertain, and to what extent such restriction is necessary if Americans will substantially increase potassium intake and its associated bicarbonate precursors remains uncertain. However, both decreasing sodium chloride intake and increasing potassium- and bicarbonate-rich precursors may likely not just help the aging skeleton but provide other potential health benefits as well."​

    - Increased protein intake and corresponding renal acid load under a concurrent alkalizing diet regime

    "All in all, the findings of Teunissen‐Beekman et al. (2016) underline the importance of increasing dietary alkali equivalents, that is, low‐PRAL foods, particularly if protein intake is raised, so that the protein‐related dietary acidity can be effectively neutralized. Also, the conclusions of Teunissen‐Beekman et al. that no postprandial changes in blood pH or bicarbonate are to be expected with increase of around 60 g/day in daily protein intake, cannot be generalized to more typical subjects eating more typical Western diets with a higher PRAL or having a more typical age‐specific GFR."​

    - Examining the relationship between diet-induced acidosis and cancer

    "Most fruits and vegetables are net-base producing foods since the metabolized products are organic anion precursors such as citrate, succinate, and conjugate bases of carboxylic acids [16-18]. The final metabolite of these precursors is bicarbonate anion. Sulfur containing amino acids, methionine and cysteine, typically found in meats, eggs and dairy products, are oxidized into sulfuric acid which is ultimately net-acid producing [16]. Cationic amino acids such as lysine and arginine can be acid producing if their anionic counterpart is chloride, sulfate, or phosphate. However, if the anionic component is a metabolizable organic acid (glutamate or aspartate), there is almost no impact on systemic acidity [17,18]. Other dietary factors are known to influence acid-base status as well. Sodium chloride is reported to be an independent and causal factor for inducing metabolic acidosis in a dose-dependent manner [19,20]. Conversely, potassium salts, and to a lesser degree magnesium, serve as a countervailing effect on net acid excretion and help to promote alkaline balance [21,22]."

    "Acidogenic dietary intake such as high protein consumption can have an immediate effect on increasing net acid production while low protein lacto-vegetarian consumption can result in significantly reduced net acid excretion [23,24]. Short-term dietetic acid loading may cause temporary acid-base disequilibrium, but is quickly compensated and has no measureable clinical effect. A persistent acidogenic diet, however, raises the likelihood of an increased [H+ surplus and chronically lower levels of serum bicarbonate if compensatory processes become less efficient and are unresolved by dietary adjustments. Potential long-term effects of acidogenic diets are further compounded by the reduction of renal function typically from ageing [16,25-28]."

    "Blood pH from prolonged or chronic acidogenic diets is reported to be near the lower physiological range (7.36-7.38) rather than the higher end (7.42-7.44). Specifically, persistent acidogenic diets have the potential to cause small decreases in blood pH and plasma bicarbonate, but not beyond the normal physiological range. This condition is described as ‘diet-induced’, ‘low-grade’, or ‘chronic metabolic acidosis’ [28-30] or sometimes ‘latent acidosis’ [31]. Diet-induced acidosis is distinct from clinical metabolic acidosis in that clinical metabolic acidosis occurs when factors other than just acidogenic diet contribute a system’s inability to compensate for blood [H+ perturbations, typically resulting in blood pH below 7.35 [32]. The patho-physiological effects of clinical metabolic acidosis are well known [33], while the true pathophysiological impact of long-term, diet-induced acidosis is not well understood. For example, it is unknown if [H+ accumulation from chronic diet-induced acidosis can be stored at the cellular level if it does not play a role in lowering blood pH or is compensated by competent renal or respiratory function."

    "Acid-base balance in the body influences adrenal hormone production of cortisol. When bicarbonate [HCO3- levels are low, the kidneys upregulate glutaminase activity and trigger cortisol production [35-37]." "Dietary induction of acidosis increases serum cortisol concentrations [38]."

    "Cortisol activates the tryptophan metabolism pathway which is carried out by rate-limiting enzymes of tryptophan catabolism, 2,3-dioxygenase (TDO) and indoleamine 2,3-dioxygenase (IDO). Cortisol directly stimulates TDO activation and may augment IDO activity indirectly through inflammatory cytokine signaling such as interferon gamma [49,50]. Excessive or chronic cortisol production acquired from a ‘Western’ dietary lifestyle could play a role in augmenting the tryptophan metabolism pathway and drive downstream molecular events that promote carcinogenesis."

    "Upregulated cortisol bioactivity driven by diet-induced acidosis may be a factor in metabolic syndrome by promoting insulin resistance. Chronic hyperglucocorticoidism upregulates visceral obesity while reducing insulin sensitivity mainly in visceral adipocytes which appear to be more responsive to cortisol than subcutaneous adipocytes due to higher expression levels of glucocorticoid receptors [58,59]."

    "Acidosis associated insulin resistance through cortisol activity may result in compensatory pancreatic insulin secretion and higher levels of circulating insulin in the serum, a condition known as hyperinsulinemia." As Travisord would say: [sick]

    "A very recent discussion about the role of diet-induced acidosis and pathophysiology introduces the hypothesis that persistent acidogenic or ‘Western’ diets lead to latent or low-grade metabolic acidosis, subsequent acid-base balance disequilibrium, and production of lactic acid at the cellular level. These events appear to be critical upstream precursors to a host of ill-conditions, diseases, and ageing. The premise further explains that increased [H+ accumulates persistently in the mitochondrial matrix without contributing to ATP production. This dynamic is theorized to inhibit mitochondrial energy production (MEP) through inhibition of the TCA cycle. MEP inhibition results in the diversion of electrons away from completion of the electron transport chain and toward the reduction of oxygen (O2) into reactive oxygen species (ROS) such as free radical oxygen species or peroxides [34,157]. As this cycle continues, vulnerable cells develop a reduced capacity to restore homeostatic balance and are subject to increased intracellular oxidative stress.

    The oxidative stress generated by ROS has multiple effects causing damage to cellular and organelle membranes, sulphydryl groups in proteins, and cross-linking or fragmenting ribonucleoproteins and DNA. DNA mutagenesis through persistent oxidative stress is generally accepted as a major mechanism behind carcinogenesis and cancer progression [158]. Oxidative DNA damage has been associated with breast cancer [159,160], hepatocellular carcinoma and liver cancer [161,162], and prostate cancer [163-165]. Oxidative stress in correlation with obesity can manifest and have significant pathogenic effects within the first two decades of life [166]. Although oxidative stress can be measured directly and indirectly through various methods, it is far more difficult to differentiate between acidogenic diet-induced and endogenous ROS production coupled with antioxidant status and other molecular factors that may impact oxidative steady state [167]."

    "Although not fully understood, the long-term effect of diet-induced acidosis is considered to have an impact on bone osteoclasts [28]. Serum [HCO3- concentrations may only partially account for neutralization of acidity, and may be supplemented further by alkaline stores from the soft tissue and bone [168]. Osteoclastic resorption of minerals is a proposed mechanism in buffering systemic acidosis [169,170]." "Bicarbonate [HCO3- deficiency may be sufficient to acidify media and promote net [H+ influx into bone [176], and appears to be necessary (not just reduced pH conditions which could be induced by respiratory acidosis) to stimulate calcium [Ca2+ efflux from bone [177]."

    "This work examines the potential for cancer risk or tumor promoting consequences of diet-induced acidosis. Although protein is a major factor involved in promoting endogenous acid production, it should be made clear that attenuation of protein consumption is not a recommended dietary strategy for attaining improved acid-base balance. There is scientific evidence supporting the concept that appropriate alkali supplementation in the form of fruits and vegetables serves aptly to neutralize excess [H+ produced from protein metabolism [34,194]. The analysis provided discusses how diet-induced acidosis is a potential upstream and indirect trigger in a multifactorial cascade of molecular events associated with carcinogenesis. There is limited evidence to suggest that dietary acidosis alone is sufficient in increasing cancer risk, but it may function in concert with other factors associated with cancer risk. Obesity or metabolic syndrome, which effect glucocorticoid and adipokine profiles and are often linked to insulin resistance and the pro-inflammatory state, could also serve as significant factors as they are associated with both acidogenic or ‘Western’ diet [34] and cancer risk [3]."​

    -----
    Sodium chlorid is 60% chloride (pure, not table of the salts)
    Magnesium chlorid is 75% chloride disconsidering the hydration
    However! The absorption of magnesium is only 35% on average, while chloride is 95% (as mentioned on the second link). To get enough magnesium you'll need to deal with a buttload of chloride. It's the problem of using a mineral combined with other: you either have too much of what you don't need to get what's needed, or too little to avoid the excess of the unwanted. All and in and all, it's insane to use this form in chronic degenerative of the conditions due to the reasons discussed above, especially without the aid of sodium bicarbonate.

    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. Check this out:
    Acid-Base Status Affects Renal Magnesium Losses in Healthy, Elderly Persons | The Journal of Nutrition | Oxford Academic

    --
    A note on cheeses:

    http://jandonline.org/article/S0002-8223(95)00219-7/fulltext
    “The purpose of this study was to calculate the potential renal acid load (PRAL) of selected, frequently consumed foods. A physiologically based calculation model was recently validated to yield an appropriate estimate of renal net acid excretion (NAE); the model depends primarily on nutrient intake data. When nutrient data from actual food composition tables were used, the calculation model yielded PRAL values that ranged from an average maximum of 23.6mEq/100 g for certain hard cheeses over 0mEq/100 g for fats and oils to an average minimum of approximately −3mEq/100 g for fruits and fruit juices and vegetables.”

    --
    A review of the role of acid-base balance in amino acid nutrition
    Calcium balance and acid-base status of women as affected by increased protein intake and by sodium bicarbonate ingestion. - PubMed - NCBI

    --
    Calcium-Phosphorous Ratio Of Cheeses
     
  2. Wagner83

    Wagner83 Member

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    Aren't the chlorides helpful for digestion? It could be interesting to try use sodium bicarbonate to replace some of the NaCl, or just use less NaCL, as an experiment. What you posted goes pretty well with this and the idea that sodium bicarbonate could be interesting, maybe potassium carbonate too. However sodium bicarbonate is used to neutralize stomach acids, that sounds like a stupid idea when it comes to digestion (even more so if one believes GERD are not caused by a ph of stomach acids that is too low). Slowing down digestion on purpose is suicide.
    I had reported reflux, among the things I had started eating regularly and have ditched the past few days is onion (sulfur?). It has gotten a lot better but to be fair apple juice and pineapples have also been discarded.
    A diet based on starch and meat/fish should be pretty terrible.
     
  3. OP
    Amazoniac

    Amazoniac Member

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    Since we have a more discernible craving for sodium, and table salt is easily available to everyone, perhaps (based on Ray's idea) there's a tendency to compensate for the lack of other nutrients through its consumption. At least some times, chloride might be taking a ride. Like it was mentioned, the problems don't show up right away and it's an unnecessary form of taxing the System owa time.

    Glycine and taurine are involved in chloride regulation:
    - Glycine Is An Endotoxin (TLR4) Antagonist ("chloride")
    - TAURINE The Key To Restoring Metabolic Function?
    - Taurine-induced Diuresis And Natriuresis In Cirrhotic Patients With Ascites
    - Restoring Levels Of Magnesium

    There might be negative consequences in constantly increasing the p and H of the stomach with bicarbonates, which is why (in my opinion) it's better and safer to balance through the other end: by having an abundance of bases in the diet, with an especial attention to potassium.

    Those values for cheese are probably for hard et salty varieties. Cottage cheese or other similars should be milder (but still contribute to the acid of the loads).

    - Magnesium Chloride Oral Use
    - Chloride: The Forgotten Essential Mineral (direct link for a brief intro)​
     
  4. Jennifer

    Jennifer Member

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    Are you finally coming over to the dark side, @Amazoniac? :D

    Kidding aside, I always enjoy your threads, and I'm especially enjoying your most recent ones because even though I find Dr. Morse does a good job at explaining the chemistry and role of acids and bases in the body, it's really nice to have you guys here to discuss it with since you're my health family. :)

    The medical community could easily discount acids' contribution to disease when only looking at blood pH and ignoring that it isn't the only system in the body that affects or is affected by acids. Systems/tissues such as the two noted, the kidneys and lungs, have their own buffering systems in place which obviously aren't functioning optimally when the tissues are weak. These tissues can be weak from birth or from the accumulation of acids overtime, acids that are also natural byproducts of metabolism.

    I know I mention it all the time but celery/celery juice is awesome not only for stressed adrenals (great source of the alkaline mineral salts like sodium and potassium) but also for optimizing stomach acid production.
     
  5. Spondive

    Spondive Member

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  6. yerrag

    yerrag Member

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    Thank you Amazoniac. This is a very useful article for me, and I learned a lot from reading it. I should reconsider my use and dosage of MgCl2, given the explanation that accompanied Fig. 3, on the low intestinal absorption of Mg+ relative to the higher absorption of Cl-, which creates an acid load. I could either lower my dosage of MgCl2 or find another magnesium salt to use, such as magnesium bicarbonate, if I have to maintain my magnesium intake. @Sheila thanks for calling my attention to my possible excessive chloride intake on my Hypertension log thread. Reading this article, I can now see clearly what you were saying.

    I am a bit confused though about the last paragraph, where the author cautions against calcium intake in a high-protein diet. Ray Peat has talked about having a high calcium intake and to lessen the intake of high phosphate foods. My take here is to not combine high calcium intake and high phosphate intake. But if the situation is where there is high phosphate intake, calcium intake should be lessened. But the ideal would be to limit phosphate intake, but to increase intake. A diet with moderate protein (that is not typical of the high protein Western diet), with alkalizing minerals from eating fruits and vegetable, would be consistent with this. Am I getting this right?

    As the urine pH is regarded to reflect the primary stimulus for renal ammoniagenesis, urinary NH4 output was also plotted against the urine pH (Fig. 10). For this, data from another diet study with high and low protein intake [4] were also included. As can be seen, renal NH4 output is also elevated for any given urine pH range, whether it is high, medium or low. Furthermore, this clearly increased capacity for net acid excretion is associated with a small but significantly (P < 0.05) elevated urine pH – even under conditions of an already alkaline urine. This has practical implications: as under our living conditions (common Western diets) the protein intake is at least moderately high [16], special care should be taken if higher amounts of alkalizing supplements are ingested. In that case, the additional ingestion of higher amounts of calcium supplements should be avoided since the alkalizing agent together with a relatively high protein intake would result in the highest possible urine pH levels, thus, increasing the risk of urolithiasis because calcium phosphate is poorly soluble at higher urine pH values.

    Another point I appreciate about this article is that it answers a question I've had for a long time, for which I seem to find difficulty getting. I finally understand why meat is acidic, and why vegetables and fruits are alkaline. It has to do with high phosphate and sulfur content in meat, which can form acids, and with the mineral electrolytes in fruits and vegetables, but here is where I get lost as I can't verbalize why these minerals are alkaline-forming.
     
  7. Wagner83

    Wagner83 Member

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    Similar to spinach the nitrates ruin me, I recently posted a few studies on the "vascular nitrates" thread, I don't understand how gastric juices, acidity and nitrates /NO are connected yet but I feel like crap from nitrates/NO, nausea is a side-effect so maybe there's a connection with digestion.
     
  8. Jennifer

    Jennifer Member

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    @Wagner83 – Huh, interesting. I'll take a look at the vascular nitrates thread after I'm done responding. Do all nitrate rich plants cause you to feel crappy/nauseas? Besides spinach and celery, the ones I can think of off the top of my head are lettuce (all varieties), cruciferous greens such as collards and cabbage, carrots, beets, turnips, radishes, green beans, broccoli, cauliflower, eggplant, parsley, artichoke, leeks, rhubarb, garlic, strawberries, raspberries and cherries.

    I'm not sure if this could be a factor, and it may be way too simplistic an explanation, but I've read, I think on livestrong.com (probably not the best source but...) that bacteria, particularly in the mouth, are involved in converting nitrates into nitrites. Could poor digestion, which in turn often causes an increase of bacteria in the mouth, play a role? Maybe test the theory by brushing with a mix of coconut oil and baking soda or swishing with an antibacterial mouth wash before consuming nitrate rich foods and see if you get the same reaction?
     
  9. Jennifer

    Jennifer Member

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    I'm not sure this will help, but mineral electrolytes are alkaline forming because they are alkaline, and the amount of acids and bases in a particular food play a role in whether or not a food leaves an alkaline or an acidic ash. Alkaline veggies (some are more toward the acidic side of the pH scale) and ripe, alkaline fruit (unripe fruit and fruits like red tomatoes are acidic) contain acids but are dominant in alkaline minerals so that's why they're alkaline forming.
     
  10. OP
    Amazoniac

    Amazoniac Member

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    I've been on this side the whole time, it's just.. difficult to tell when I'm around.

    Sodium and chloride have the best absorptions, followed by potassium. I interpret it as a successful adaptation for landlords, since when we leave the sea, the body is no longer constantly bathed in those salts, so it adjusts to extract them better from what's available. This means that not a lot of supplemental sea salt is needed as long as the diet provide plenty of plant foods. Potassium is widely available on a more natural diet, yet the absorption is almost as good: we must need it in plentiful amounts.
     
  11. OP
    Amazoniac

    Amazoniac Member

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    yerrag,

    There are articles claiming that a greater intake of protein improves the ability of the body to excrete the acid load from its (protein) metabolism, so (if I'm not wrong) the acidity from meats doesn't increase in proportion to its intake. This is not to say that more meats won't demand more bases in the diet to balance them.

    I think they're separated by their charge (just like you wrote at the beginning). Roughly, simple cations as base-forming, and anions as acid-forming.

    The foodstuff is essentially an H donor while... | Ray Peat Forum
    Hydrogens are very unstable and reactive, so they tend to associate to whatever they're allowed to in order to neutralize charges.
    It's their orderly movement that's important for life:
    Dehydrogenation, having been one of the... | Ray Peat Forum
    The hydrogen ions that flow through the System, as in the electron of the chains of transports, not just the electrons are being transfered but the entire elemental hydrogen ion itself.

    In terms of biology, physical stability means... | Ray Peat Forum
    Lactic acid for example doesn't occur in the bodee because it picks up accumulated hydrogens, becoming lactate. When an acid conjugates with some molecule, it receives the 'ate' suffix. Malic acid, malate; acetic acid, acetate; citric acid, citrate; stearic acid, stearate; and so on.

    Travisord knows this stuff in depth if you need detailed information.
    But as always : al dere

    Ps.: https://www.physiology.org/doi/abs/10.1152/ajprenal.00048.2007
     
  12. Sheila

    Sheila Member

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    Dear Amazoniac et al,

    Yes, I concur, that has been my experiential conclusion in observing n>1.

    FWIW, I agree again. Especially since bicarb is so good at getting cremated bits off the bottom of saucepans. Depending on the dose and sensitivity of the recipient, it may also not take mercy on stomach linings either. I am wondering whether the attention to potassium and the repudiation of sodium supplementation (cf. Gerson and our own BLC) was in order to rapidly enhance the potassium:sodium ratio rather than absolute amounts of either. Ratios do appear more important; that balance thingy yet again.

    Mr Wagner83,
    forgive me if this sounds lecturous, it is not meant to be. Onions have a large mix of sulphur compounds in them including methionine sulphoxides (chosen because of the article above) and people can react to a) its tough to digest fibre (in FODMAP a 'no no') b) any of the many other types of sulphur containing compounds depending upon digestive competence and/or that person's sensitivities and/or whatever else is happening in the gut at the time. Bacteria in our gut are capable of oxidizing sulphur compounds (per the article) and other critters eminently capable of reducing them, it all depends on what the sulphur compound is, where it ends up being tackled, sometimes is also a feature of dose (a little vs a lot), sometimes it is a feature of gut competence/stasis etc (pretty much like many things). We certainly do need sulphur compounds in our system, their activity is critical to health.

    Some people are very sensitive to raw onions, but not to cooked. I have long suspected that those with liver problems (endotoxic) are often onion-group sensitive but I could be wrong, yet often helped to become less sensitive with small amounts of sodium sulphate (which aids detox and, in small amounts, doesn't get to the large intestine to be reduced). So, the reason for my post is to suggest that sensitivity to sulphur does not mean sensitivity to all sulphur containing compounds. Taurine, biotin, MSM, thiamine are all highly useful sulphur containing compounds, all with very different sulphur groups attached. Many parasitic critters don't like sulphur and sulphur compounds at all so 'sulfa' drugs have had wide applications thereupon and some are sensitive to them, but not necessarily to all.

    Back in the days of scarlet fever, for those that survived one of the sensitivities resulting from this infection was often intolerances to raw and boiled onions from then on, but strangely less so to fried onions. So the manner of preparation of an organic sulphur food source also appears important for some. I have a feeling that our tolerance to the gamut of sulphur compounds can vary depending on liver function and gut bacteria but I don't have it properly worked out. If anyone does have a better understanding, or even a snippet (and also, while I am at it, the role of low copper in this milieu, please do tell and I will be able to stop frothing at the very mention of 'sulphur sensitivity'. For which others will thank you also!

    Best regards,
    Sheila
     
  13. Jennifer

    Jennifer Member

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    Sorry, I mistakenly thought you had been straddling the realms this whole time. But what's this about it being difficult to tell when you're around? Since when?! Haha! I would get your money back on that invisibility cloak you were sold because it's obviously broken. :)

    LOL at landlords. I wonder if rent is cheap in the sea. Anyhow, thank you for sharing that line of reasoning. Very interesting! You sparked a thought in me. Carey Reams believed we get 80% of our nutrition from the air, to the point that he advised we cover our pots with a lid while cooking to prevent the minerals from escaping. I've since wondered if one of the reasons why people often report better health when living by the ocean is due to all the sea minerals in the air. Whenever I go to the beach, I can feel a heaviness in the air and my hair gets sticky and my lips end up tasting like salt despite not consuming any or going in the water – the water is freezing here.
     
  14. Jennifer

    Jennifer Member

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    The fat acts as a buffer of acids and/or other triggering compounds? Dr. Morse believes fats buffer acids so maybe there's some truth to it?

    Do you happen to know what the standard treatment was for scarlet fever, Sheila? My mum had it and was advised by a nurse to drink warm ginger ale and right after my grandmother gave it to her, her fever broke.

    In regards to sulfa drugs, Dr. Morse has talked about them and how the body has a hard time eliminating the inorganic sulfur to the point that it creates a sticky lining in the intestines so that when sulfurous foods are eaten, they cause indigestion/gas. He mentioned Charles Goodyear's discovery of vulcanized rubber in relation to the advent of sulfa drugs, but that's all he said and my attempts at trying to find out more have been in vain.
     
  15. Suikerbuik

    Suikerbuik Member

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    Dear Landlord,
    Could you possibly explain your thoughts? Usually in chemistry they refer to acids and bases as explained below.

    Actually in terms of H+ and OH- it's the cation (H+) that is acid and OH- is basic. So a proton acceptor is base forming and a proton donor is acid forming. See also Lewis acid and Lewis base.

    Not necessarily, it all depends on the substance' affinity for a proton (pKa) and pH. In case of a COOH-group (acid, pKa ~5) at pH 7 it will produce COO- and H+ and for example at pH 7 a NH3 (base, pKa ~9) will pick up that proton and form NH4+

    If you mean the body picks up accumulated hydrogens you're right (because of buffers; HCO3-, proteins etc.). If you mean lactic acid doesn't occur because it picks up hydrogens becoming lactate you're mistaken. The pKa of lactic acid is 3,86 (COOH) group which means that basically at any pH > 4,86 the lactic acid is dissociated in H+ and RCOO- and is now called lactate. (The pKa of a molecule is the pH at which half of those molecules (or specific group that pKa belongs to) are protonated or deprotonated).
     
  16. OP
    Amazoniac

    Amazoniac Member

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    It's just a matter of not laughing and I become almost invisible in the dark.

    I never thought about air this way, thanks.

    Isn't it crazy that carbon tetrachloride is so toxic given it's produced with only methane and chlorides? How harmful could that be?
    Guru!!

    I had in mind the minerals above, and their natural occurrence in foods, the cations conjugated with bases and easing the acid of the loads once dissociated. Hydrogen is exceptional because it belongs to the same group but is a misfit there.

    No, you're right, it transfers an hydrogen to a base. Which is why it's better to give the person sodium bicarbonate rather than lactate as in Ringer's solution.

    Do you know why potassium tastes sweet but not so in extreme amounts?
     
  17. Jennifer

    Jennifer Member

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    Huh, I'll have to learn that trick. Not laughing is tough for me.

    Yeah, it seems crazy but then again, man has a history of making naturally occurring things into something toxic. I'd say nature makes for a better mixologist. Though, with carbon tetrachloride we saw the invention of the lava lamp so man did something right with it. :p:
     
  18. yerrag

    yerrag Member

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    Interesting discussion on the kidneys, although I'm not so sure about this passage:

    All mammals including man, therefore are equipped with a mechanism of overflow for bicarbonate. As soon as the storage capacity of the body for bicarbonate is full or is exceeded, the maximally, vasodilated kidney will immediately excrete the bicarbonate-surplus and thereby maintain the blood-bicarbonate value at a constant level at approximately 25 mMol/L and thereby preserves the homeostasis of pH.

    My understanding is that it takes up to 3 days for the kidneys to excrete bicarbonates, not immediately. This is a reason why caution is needed to not take too much bicarbonates, as the metabolic alkalosis condition that arises cannot be immediately corrected by the kidneys. But if the kidneys can immediately correct excess bicarbonates, then is my caution not warranted?

    As far as the 25 mMol/L value given, the venous serum bicarbonate range is 22-30 mMol/L. Isn't aiming for upper range values better? 25 nMol/L doesn't strike me as an optimal value for homeostasis.

    And another passage:

    Kopp’s optimum Urine-pH is pH 7,5 - 8,0
    Why?
    The normal narrow physiological pH-range in the blood is pH 7,35 – 7,45.

    It is only slightly lower than the Optimum Urine-pH of pH 7,5 – 8.0 recommended by KOPP, which indicates a surplus of bicarbonate that appears in the urine, due to the ingestion of sufficient bicarbonate. Therefore, this represents a guarantee for the maintenance of a normal blood-pH. Urine-pH-values lower than pH 7,0 therefore indicate a blood-bicarbonate deficit (Fig 4). The bicarbonate surplus in the blood is sufficient to neutralize sudden acic-loads e.g. the lactic acid- outflow from muscles during exercise or even the metabolism of alcohol from several Whiskeys. The reserve of bicarbonate may just last until the next passage of urine. If not, a deficit, if present can easily be detected from the urine-pH lower than 7,0. After the voluntary or involuntary ingestion of a slightly higher amount of bicarbonate, urine-pH will remain at the maximum value of pH 8,0 which only indicates that bicarbonate is continuously being excreted.

    This is good to know as well. Since it is hard to obtain blood pH readings, using the urine pH values from a cheap urinalysis test would give me an indication of how well my blood pH can hold up against acid inflows. If my urine pH is below 7, my blood pH can be very susceptible to going down, or becoming acidic. If my urine pH is between 7.5- 8, then it will be less susceptible as that means there is plenty of bicarbonates acting as a buffer to maintain the blood pH.

    Ray has mentioned blood pH to be 7.4, although the accepted and physiological range is given as 7.35-7.45. Any lower or higher from range is going to lead to complications. Within range of 735-7.45, one is fine, although being on the lower end of range would not be ideal. I would want to be at 7.4 and above, though not be so close to 7.45.

    Blood pH less than 7.35 would be considered acidic, and above 7.45 considered alkaline. If I want to use urine pH to approximate my blood's pH status, I would see urine pH below 7 as below blood pH of 7.35, a urine pH between 7 and 7.5 as blood pH between 7.35 and 7.4, and a urine pH between 7.5 and 8 as blood pH between 7.4 up to 7.45.

    But some caution here:

    However, a urine-pH of 8,0 may be present from other pathological causes. In cirrhosis of the liver or in urinary tract infections with urea-splitting bacteria the alkalinizing agent is Ammonia. Therefore, in all cases where a urine-pH of 8,0 CANNOT be attributed to the ingestion of bicarbonate the medical diagnosis (and therapy) of its cause and origin is required.

    Upon review, I realize the above analysis I made is within the context of ingesting sodium bicarbonate to maintain blood pH at normal levels. Alas, it is not a tool that is to be used to help determine blood pH from urine pH. But I could very well see the value of using sodium bicarbonate to alleviate temporarily low blood pH conditions. And I can also understand now why taking plenty of fruit juice could cause the urine pH to increase to as high as 8.


    I'm going to run this by you to see if I understand this. The reason meat is acidic is because of the sulfate and phosphate content, which gets converted to sulfuric acid and phosphoric acid. In the case of salts of minerals (potassium, magnesium, sodium, and calcium), they actually are cations that balance up with anions that keep the hydrogen ion from balancing up with the anions. With less hydrogen ions present, the less acidic it becomes. For example, the chloride anion would not need to have an H+ cation to balance it if a magnesium cation were present. With one less H+ cation in solution, the solution would be less acidic.

    Am I making sense here?
     
  19. OP
    Amazoniac

    Amazoniac Member

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    I'm more like a student here.

    From what I understand from Rayzord, the healthy cell is slightly acid (ATP? C[]2?), therefore manages to attract and retain potassium and magnesium as needed. How it manages to keep calcium and sodium out of the cell, I have no idea. But a way to keep the cell in the desired of the states would be to increase anions or decrease cations, I guess it does both through ATP and others, while at the same time eliminating sodium and calcium. A and T and P inside the cell keeps it in a favorable state.

    Alberto has a great deal of work on this, for example of contraction and relaxation through entry of calcium, etc. When the cell is properly energized, it manages to return to its resting state fast through these manipulations, shifting to potassium again and excluding calcium.
    Rigor mortis - Wikipedia

    I have to read more about it because it's a very interesting subject, but for more accurate information I suggest you to read/ask Travisord or some members from www.hackstasis.com for being more knowledgeable and for paying much more attention than we (with exceptions) do.
     
  20. Jennifer

    Jennifer Member

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    I don't agree with this. I agree with Ray, Dr. Morse and Carey Reams (RBTI) that the urine should be slightly acidic. Looking at it from a Dr. Morse perspective, if urine is alkaline, the body is holding on to the acidic byproducts of metabolism and dumping alkaline minerals. I've been meaning to pull out my pH regent to see if my urine is down around 6.4-6.8 now that my kidneys are finally filtering – sediment (metabolic byproducts) in urine means the kidneys are filtering like they should be. The entire time I followed RBTI, I couldn't get my pH to come down. It was always 8+ and this really concerned my RBTI practitioner.

    One interesting thing I've noticed is that the more filtering I get, the less pain I have in my lumbar and where the worst of my compression fractures (thoracic) are. The pain was non-existent most of the time after eliminating the last of the animal protein and starch from my diet, but I was still getting the occasional burning near the injury if I was standing in one place too long or got overzealous with my ballet practice. With my lumbar, I'll have knots full of what my cousin, a massage therapist, told me were acids and I'll do a press and release technique and by the next morning when I pee, I'll have major sediment and no more knots or pain.
     
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