Amazoniac
Member
- Acidosis: An Old Idea Validated by New Research
- Influence of nutrition on acid-base balance – metabolic aspects
- 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
- 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
- Increased protein intake and corresponding renal acid load under a concurrent alkalizing diet regime
- Examining the relationship between diet-induced acidosis and cancer
-----
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:
(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"
"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."
"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."
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."
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]."
"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
“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
Last edited:
