"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. Lutzzy

    Lutzzy Member

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  2. Lutzzy

    Lutzzy Member

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    SORRY your group was not as sucessful as ours, Bruce was very good at explaining the we might get worse before we got better.... We all did so much better, it was just hard to stay on if your family did not participate. But I still use many of the things I learned.
    I also like Know The Cause with Doug Kaufman on religious station and fb. He believes most problems are due to mold and fungus/.......Suzy Cohen the people's pharmaist
     
  3. OP
    Amazoniac

    Amazoniac Member

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  4. OP
    Amazoniac

    Amazoniac Member

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    "Humans can come into contact with chlorine gas during short-term, high-level exposures due to traffic or rail accidents, spills, or other disasters. By contrast, workplace and public (swimming pools, etc.) exposures are more frequently long-term, low-level exposures, occasionally punctuated by unintentional transient increases."

    "Repeated exposure to chlorine in the pool has been postulated to be a significant risk factor for an excess of asthma among swimmers (8). In atopic adolescents the risk factor of allergic rhinitis and asthma appear to be dose-dependently augmented by chlorinated swimming pool attendance (9)."

    "Humans can detect low levels of chlorine gas. In humans, the threshold concentration for detection of the odor of chlorine gas ranges from 0.1–0.3 ppm. At 1–3 ppm, there is mild mucus membrane irritation that can usually be tolerated for about an hour. At 5–15 ppm, there is moderate mucus membrane irritation. At 30 ppm and beyond, there is immediate substernal chest pain, shortness of breath, and cough. At approximately 40–60 ppm, a toxic pneumonitis and/or acute pulmonary edema can develop."

    "Workplace exposure limits for chlorine include a short-term exposure limit for up to 15-minute exposures not to exceed 1 ppm (2.9 mg/m−3). That for a long-term exposure limit is for up to 6-hour exposures not to exceed 0.5 ppm (1.5 mg/m−3). Levels of 0.3 ppm are associated with odor perception, levels of 1–2 ppm are “burdensome” and “irritating,” and those at 2–3 ppm are “annoying” (13). The workplace exposure limits are of interest, since the WHO Task Group proposed that ambient levels of chlorine be about 0.034 ppm (0.1 mg/m−3) to “protect the general population from sensory irritation,” and “significant reduction in ventilatory capacity” (14)."​

    - Metabolic Acidosis

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    - Water chlorination - Wikipedia

    "Disinfection by chlorination can be problematic, in some circumstances. Chlorine can react with naturally occurring organic compounds found in the water supply to produce compounds known as disinfection by-products (DBPs). The most common DBPs are trihalomethanes (THMs) and haloacetic acids (HAAs). Trihalomethanes are the main disinfectant by-products created from chlorination with two different types, bromoform and dibromochloromethane, which are mainly responsible for health hazards. Their effects depend strictly on the duration of their exposure to the chemicals and the amount ingested into the body. In high doses, bromoform mainly slows down regular brain activity, which is manifested by symptoms such as sleepiness or sedation. Chronic exposure of both bromoform and dibromochloromethane can cause liver and kidney cancer, as well as heart disease, unconsciousness, or death in high doses.[16]"

    "There are also other concerns regarding chlorine, including its volatile nature which causes it to disappear too quickly from the water system, and organoleptic concerns such as taste and odor."​

    - The Negative Health Effects of Chlorine - Joseph G. Hattersley (already posted somewhere)

    "Chlorine in swimming pools reacts with organic matter such as sweat, urine, blood, feces, and mucus and skin cells to form more chloramines. Chloroform risk can be 70 to 240 times higher in the air over indoor pools than over outdoor pools.22 Canadian researchers found that after an hour of swimming in a chlorinated pool, chloroform concentrations in the swi-mers’ blood ranged from 100 to 1,093 ppb.23 If the pool smells very much of chlorine, don’t go near it.

    Taking a warm shower or lounging in a tub filled with hot chlorinated water, one inhales chloroform. Researchers recorded increases in chloroform concentration in bathers’ lungs of about 2.7 ppb after a 10-minute shower. Worse, warm water causes the skin to act like a sponge; and so one will absorb and inhale more chlorine in a ten-minute shower than by drinking eight glasses of the same water. This irritates the eyes, the sinuses, throat, skin and lungs, dries the hair and scalp, worsening dandruff. It can also weaken immunity.

    A window from the shower room open to the outdoors would release chloroform from the shower room air, but to prevent its absorption through the skin requires a showerhead that removes chlorine."​

    - Swimming Pools – EnvronOzone

    “While swim training may improve fitness and reduce morbidity associated with asthma, there is both anecdotal and scientific information to suggest that there are health-related problems associated with swimming in chemically-treated pool water. Swimming pool water is disinfected in the interests of public health, although it would appear that chemical disinfection of the pool water may be the cause of many of the health-related problems that have been reported. There is medical evidence suggesting that exposure to chemicals such as chlorine and its derivatives, chloramines or chloroform may damage the respiratory epithelium and cause increased vascular permeability and oedema of the mucous membranes lining the airways and lung, both of which may result in severe inflammatory reactions.”
    "Sports Medicine [SPORTS MED.], vol. 21, no. 4, pp. 256-261, 1996"

    "As problems with chlorine systems continue to be documented, most notably the production of carcinogenic (cancer-causing) by-products called chloro-organic compounds including trihalomethanes (THMs), Ozone is becoming the sanitizer of choice for pool managers. It not only eliminates the production of these compounds, but it also increases the overall effectiveness of your entire filtration system."​

    - Olympics – EnvronOzone

    "The issue of Ozone in the Olympic pools started at the Atlanta Olympics in 1996. A group of German swimmers actually refused to enter one of the main event swimming pools. What could have persuaded this group of highly disciplined athletes to stage this protest at one of the most prestigious events in the world?

    As it turns out, Germans are well aware of the health problems associated with a Chlorine-only swimming pool. Even the best maintained pools using Chlorine as the main sanitizer produce toxic byproducts that actually endanger human health. These toxic byproducts are caused by the slow degradation of chlorine when it comes in contact with human sweat, urine, dander, skin particles and other pollutants that enter your pool.

    So, what was done to fix the problem in Atlanta? Ozone was added to the pool filtration system and the Games went on."​

    - Toxic Inhalational Exposures

    "Chlorine was the first chemical ever used with the intention of causing mass casualties. During World War I, the German army used chorine gas against French troops with devastating effects. At Ypres, Belgium, on April 22, 1915, 15 000 French troops were exposed during a chlorine gas attack that resulted in 800 deaths and an estimated 1500 to 2000 wounded.63 Exposure to chlorine, however, is not confined to warfare alone. Contact may occur in a wide range of settings, including industrial and transportation accidents, and domestic exposure from common cleaning agents. Modern day applications of chlorine include its use as a chemical component in pharmaceuticals, a bleaching agent in paper production, and a component in solvents used in metalworking, dry cleaning, and electronics. Additionally, chlorine is used in the production of plastics and in water purification.64"

    "The intermediate water solubility of chlorine gas results in both upper and lower respiratory tract injury. Chlorine combines with water vapor to produce hydrochloric and hypochlorous acids, both of which contribute to upper and lower airway damage.67 In vitro, hypochlorous acid reacts with nitrite (NO2-) to form reactive intermediates capable of nitrating, chlorinating, and dimerizing aromatic amino acids.68,69"

    "Due to the solubility index of chlorine, most of the gas is absorbed within the nasal and oral cavities with additional absorption at the level of the trachea. Consequently, frequent complaints during and following chlorine gas exposure include mucous membrane burning as well as cough and choking. However, at high concentrations of greater than 50 parts per million, lower respiratory tract effects such as chemical pneumonitis and death are reported.70 In addition, irritant-induced pulmonary complaints, including reactive airways dysfunction syndrome, are recognized complications of acute exposure.69,71-75"

    "Long-term effects of chlorine exposure remain controversial with conflicting results in the literature. Some studies demonstrate decrements in diffusion capacity76 and the ratio of forced expiratory volume in 1 second to forced vital capacity,77 but the vast majority of patients who survive the exposure to chlorine appear to eventually normalize their pulmonary function over a few years.78-81 There is some evidence suggesting a deleterious association between chronic chlorine gas exposure and tobacco abuse. Patients with a heavy smoking history (defined as more than 20 pack-years) and repeated chlorine gas exposure are at greater risk of developing chronic obstructive pulmonary disease.82 Patients with asthma or increased airway reactivity are at greater risk for more persistent airway obstruction after chlorine inhalation.83"​

    - Must Read, Killing Cancer Cells Using Electric Potential, DMSO, Methylene Blue

    "If I am a weak person, whose healthy cells are around -60 millivolts, and I take extra long shower with chlorinated water, whose millivolts is -300 and our body ABSORBS an average of 80% of the chlorine through our skin as chlorine is a gas. What you are doing in effect is to change your ALREADY low millivolts -60 into exactly -15 millivolts and suddenly the electrical energy now low, the mitochondrial now goes into anaerobic fermentation and becomes cancerous."
    ?​

    - Hyperchloremic metabolic acidosis after chlorine inhalation
    - The Effect of Nebulized NaHCO3 Treatment on “RADS” Due to Chlorine Gas Inhalation
    - Nebulized Sodium Bicarbonate in the Treatment of Chlorine Gas Inhalation
    - Nebulized sodium bicarbonate in acute chlorine inhalation
    - Treatment of acute chlorine gas inhalation with nebulized sodium bicarbonate
    - Chlorine Gas: An Evolving Hazardous Material Threat and Unconventional Weapon
    - Chlorine Inhalation - The Big Picture
    - Management of Chlorine Gas Exposure
     
  5. OP
    Amazoniac

    Amazoniac Member

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  6. yerrag

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    Have to buy a chlorine filter for my shower then. I used to have it installed. It felt good taking a shower with it actually. It felt like taking a dip in spring water. But knowing about the effect of chlorine being absorbed into our body, I should get a chlorine filter installed.

    Removing chloride from bath water aside, what if the bath water is hard and filled with minerals, wouldn't it increase the electrical energy and support our mitochondria more. I did a test on my koi pond, and I put magnesium chloride, magnesium sulfate (epsom salt), potassium chloride, calcium chloride, and borax in a ratio similar to their ratio in sea water (with sodium excluded) in an attempt to replicate which to me would be an ideal fresh hard spring water. I went to as high as 200 ppm, and may add some more. They aren't affected at all in a negative way, but to observe the benefit of it would take longer. I should swim in my pond to see if I can benefit from the alkaline minerals as well.

    This seems to be making the case for a fresh juice fast instead of a total fast.
     
  7. OP
    Amazoniac

    Amazoniac Member

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    I can't remember if I already posted this. So here it is again or for the first time:

    - Influence of vitamin D on bicarbonate reabsorption

    "It seems well established that acute administration of vitamin D enhances renal reabsorption of sodium, phosphate and calcium in the dog and in the rat (1-5). These effects are thought to be the result of vitamin D action on the proximal tubule (1,2). Vitamin D deficiency secondary either to inadequate dietary intake or to intestinal malabsorption may be associated with the development of metabolic acidosis."

    "The occurrence of metabolic acidosis in vitamin D deficiency (10) suggests that vitamin D may play a role in renal hydrogen ion secretion."

    "Our results clearly demonstrate that acute infusion of 25 OHD increases renal bicarbonate reabsorption in the dog. The increase in bicarbonate reabsorption was observed only in the presence of parathyroid glands which suggests that the presence of parathyroid hormone is essential for this effect of vitamin D. This observation agrees with the data of Popovtzer et al who demonstrated an effect of vitamin D on phosphate reabsorption only in the presence of parathyroid hormone (5)."

    "Vitamin D administration did not decrease the phosphaturia of bicarbonate loading. This is somewhat surprising since it has been recently demonstrated that increased levels of parathyroid hormone is the main factor responsible for the phosphaturia of bicarbonate administration (12). We have no clear cut explanation for this finding but it is possible that the tendency for vitamin D to enhance phosphate reabsorption under these circumstances was overridden by increased levels of parathyroid hormone and volume expansion caused by sodium bicarbonate administration."

    "The mechanism whereby vitamin D enhances bicarbonate reabsorption is not clear. It is possible that enhanced bicarbonate reabsorption is secondary to a generalized action of vitamin D in the proximal tubule but a specific effect of vitamin D in the distal nephron cannot be excluded."

    "The finding that vitamin D enhances renal bicarbonate reabsorption may be relevant to the problem of hyperchloremic acidosis of hyperparathyroidism. Muldowney et al described the occurrance of hyperchloremic acidosis in patients with primary hyperparathyroidism and in secondary hyperparathyroidism due to malabsorption (6,7,13). They demonstrated that the maximal rate of bicarbonate reabsorption was depressed in these patients and that with successful treatment of the hyperparathyroidism metabolic acidosis was corrected. They suggested that parathyroid hormone inhibits renal bicarbonate reabsorption and that increased levels of parathyroid hormone can cause metabolic acidosis. More recently, the effect of parathyroid hormone on renal bicarbonate reabsorption was studied."

    "Karlinsky et al (8) demonstrated that pharmacologic doses of parathyroid hormone had a small effect on bicarbonate reabsorption in intact dogs. In thyroparathyroidectomized dogs bicarbonate reabsorption was increased; administration of parathyroid hormone to these animals depressed bicarbonate reabsorption to control levels."

    "Crumb et al (9) demonstrated that pharmacologic doses of parathyroid hormone depresses whereas hypercalcemia enhances bicarbonate reabsorption in intact and thyroparathyroidectomized dogs."

    "These studies demonstrate that parathyroid hormone plays an important role in renal bicarbonate reabsorption[.]"

    "[However,] Coe studied thirteen patients with hyperparathyroidism and found only two patients with metabolic acidosis. He concluded that parathyroid hormone was not an important regulator of acid excretion (14)."

    "Gold et al demonstrated that chronic phosphate depletion in dogs leads to a decrease in bicarbonate reabsorption (15). Since phosphate depletion occurs in hyperparathyroidism they suggested that phosphate depletion, rather than increased levels of parathyroid hormone, is responsible for the metabolic acidosis of hyperparathyroidism (15,16). The depression of bicarbonate reabsorption was of small magnitude and could hardly account for the metabolic acidosis in hyperparathyroidism. It is possible that the presence of more than one factor is necessary for the development of metabolic acidosis with hyperparathyroidism. The ideal situation for the generation of metabolic acidosis in hyperparathyroid patients without renal failure would be the simultaneaus presence of high parathyroid hormone levels, phosphate depletion, hypocalcemia and vitamin D deficiency. All these factors are present in malabsorption and this could explain the more frequent occurrence of metabolic acidosis in secondary hyperparathyroidism than in primary hyperparathyroidism."​

    - Milk Alkali Syndrome (explicit)
     
  8. SOMO

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    I was hospitalized for HYPERCALCEMIA caused by taking high doses of oral Vitamin D. (I was taking no Vitamin A or K to balance it out, and was also taking no calcium and wasn't drinking milk at this stage in my life.)

    High Serum Calcium (higher than 10) is supposedly a high risk for Acute Kidney Failure.

    Strangely enough, when I was hospitalized, with a Calcium level of 16, I felt normal, but it did take 3 days to go back to normal levels.

    Do you think transient high Calcium levels, in the absence of thyroid or high PTH, is mostly benign?
     
  9. Inaut

    Inaut Member

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    I like hearing stories like this. Not that I like hearing you had to be hospitalized for a short time but during the course of my short life, I have tried many things in the name of health.....Turpentine bath with not enough soap in the water to disperse the oil was one that came to mind after reading your post.... Damn..... Sorry to get side tracked. Back to business
     
  10. OP
    Amazoniac

    Amazoniac Member

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    Sheila's post to yérrag reminded me of this:

    - Citrate, Malate and Alkali Content in Commonly Consumed Diet Sodas: Implications for Nephrolithiasis Treatment

    "Several commonly consumed diet sodas contain greater citrate as alkali, malate as alkali and total alkali than a lemonade beverage commonly used for hypocitraturic nephrolithiasis. These beverages may be helpful for dietary treatment for hypocitraturia and low urine pH. Further studies in stone forming patients are necessary to discern whether these laboratory findings would have beneficial clinical effects."

    "Most citrate absorbed from the gastrointestinal tract is oxidized in the liver to form bicarbonate, providing a systemic alkali load. Whether the net effect of citrate ingestion is alkalinization of blood and urine depends on the cation accompanying citrate. If citrate is ingested as citric acid, in which the accompanying cations are protons, the protons neutralize the bicarbonate formed in the liver so that there is no net effect on acid-base status.9 If citrate is in the form of a potassium or sodium salt, virtually all citrate is converted to alkali with no serum bicarbonate titration, leading to systemic alkalinization. This distinction is critical in regard to renal citrate excretion since proximal tubular reabsorption of filtered citrate by the sodium-dicarboxylate cotransporter is contingent on systemic acid-base status. In acidosis states the renal proximal tubule reabsorbs citrate, which is incorporated into the Krebs cycle, decreasing citraturia. On the other hand, alkalosis decreases renal tubule reabsorption of citrate, increasing urinary citrate excretion.10"

    In other words..

    "Renal citrate excretion depends on plasma citrate level and renal tubular reabsorption. When citrate is absorbed from the gastrointestinal tract, a small amount escapes oxidation by the liver, increasing blood citrate and leading to greater renal citrate excretion.11 This occurs whether citrate is ingested as citric acid or as citrate salt. However, citrate salt ingestion causes systemic alkalinization, which decreases renal citrate reabsorption and increases urine citrate excretion. The extent of systemic alkalinization seems to be more important than direct delivery of unmetabolized citrate to the kidney to determine citrate excretion.12"

    "In addition to citrate, any compound that causes a systemic alkalosis increases citrate excretion. Malate is a polycarboxylic anion, like citrate, that is present in many fruit juices and carbonated beverages. If delivered as an alkali salt, malate should also increase urinary citrate.12 We examined citrate and malate content in commonly consumed diet sodas and calculated the relative amount of each anion provided as the acid form or the alkali salt to determine which drinks may be most useful as dietary therapy for hypocitraturic calcium nephrolithiasis and/or uric acid nephrolithiasis."

    "When an organic anion is converted to alkali, renal citrate reabsorption decreases, allowing more citrate to be excreted in urine, where it serves as an inhibitor of calcium oxalate stone formation by complexing with calcium in solution.1,2,12"

    "[..]the amount of alkali provided by diet soda was relatively small compared to the standard dose of 30 to 60 mEq [1170-2340 mg] potassium citrate daily, the typical treatment dose for hypocitraturia. By our calculations to deliver a 20 mEq [780 mg] dose of alkali daily by drinking diet soda consumption would need to be 2 L or greater. Homemade lemonade, which in some studies increased urine citrate, contains less citrate than several beverages that we tested (fig. 1)."

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    "The importance of total alkali content to assess the antilithogenic potential of a beverage is shown by the study by Odvina in 9 normal individuals and 4 patients with kidney stones on a controlled diet given lemonade and orange juice in a randomized, crossover trial.24 Each beverage was dosed to provide 100 mEq citrate daily but orange juice, which has higher pH, provided a much greater proportion of citrate as alkali. The mean increase in urine citrate was 440 mg daily with orange juice but only 55 mg daily with lemonade. Urine pH was also significantly higher with orange juice, highlighting the greater alkali load provided by orange juice."

    - Hypocitraturia: Pathophysiology and Medical Management

    "Diets high in animal protein provide an acid load. This promotes mild metabolic acidosis, leading to reduced citrate excretion, hypercalciuria, and a reduction in urine pH.38,59,60 Severely carbohydrate-restricted and animal protein-rich diets, such as the Atkins diet, further exacerbate this metabolic acidosis through the creation of ketones. Compared with a normal diet, both the induction and maintenance phases of an Atkinstype diet promote lower urine pH and citrate excretion.60"

    "High-sodium diets, possibly through a mild expansion acidosis, decrease urinary citrate.63"

    "In the nephron, 1,25(OH)2D3, the active form of vitamin D, utilizes the VDR to modulate citrate metabolism and transport.68"

    "Certain electrolytes and other organic acids alter citrate excretion. Increased urinary calcium and magnesium are both associated with increased excretion of citrate,17 and replacing magnesium in hypocitraturic patients has been shown to raise urinary citrate levels.89 [which is good] Both of these ions complex with citrate in the urine and prevent its interaction with the NaDC transporter. Additionally, a deficiency in magnesium places patients at risk for hypokalemia and makes potassium replacement less effective. Finally, metabolic inhibitors (malonate and maleate), as well as precursor compounds (malate, succinate, and fumarate), increase excretion of citrate.18"

    "Patients who either cannot tolerate or cannot afford potassium citrate may benefit from consuming citrus juices, which contain significant amounts of citrate. Wabner and Pak105 [the second author is not a bot] compared orange juice consumption (1.2 L/d) with potassium citrate (60 mEq [2340 mg]/d). Increases in urinary pH and citrate excretion were similar for both. Orange juice, however, did not decrease urinary saturation of calcium oxalate, whereas potassium citrate did. Grapefruit juice, although shown to have significantly higher levels of citrate than orange juice,106,107 does not seem to reduce urinary risk factors for stone formation.108 Additionally, grapefruit inhibits cytochrome p-450, thereby altering the metabolism of many commonly used medications."

    "Lemonade has been reported to increase citrate consumption. This was initially reported by Seltzer and associates,109 who had hypocitraturic patients consume 2 L of a lemonade preparation per day (120 mL of concentrated lemon diluted up to 2 L with water). Citrate excretion increased 144%. Kang and associates110 retrospectively compared the outcomes of patients receiving lemonade therapy (120 mL concentrated lemon juice diluted to 2 L with water) with those of patients receiving potassium citrate (40 mEq/d). They reported significant increases in renal excretion of citrate in both the lemonade and the potassium citrate groups; however, compared with lemonade consumption, patients taking potassium citrate had significantly greater increases in urinary citrate excretion, as well as increases in urine pH. Urine pH was not altered by lemonade.110 However, not all studies on lemonade therapy have demonstrated positive results. Penniston and associates111 compared lemonade therapy (either 120 mL of concentrated lemon juice diluted in water or 1 L of sugar-free lemonade) with lemonade therapy (same preparation) combined with potassium citrate (20–90 mEq per day). Although both regimens initially promoted a significant increase in citrate excretion, only the potassium citrate cohort had a durable response."

    "The citric acid contents of various juice preparations have been measured. Penniston and colleagues107 quantified citrate content in natural and commercially available fruit juices, using ion chromatography. They found that natural lemon and lime juice contain the greatest quantity of citric acid, followed closely by lemon and lime juice concentrates. Grapefruit juice and orange juice contained significant amounts of citrate; however, both contained less than lemon and lime juices. In a similar study, Haleblian and associates106 used nuclear magnetic resonance spectroscopy to quantify citrate content. Using this technique, they found grapefruit juice to have the highest citrate content, followed by lemon juice and orange juice. They also found that among low-calorie beverages, Crystal Light® lemonade (Kraft Foods, Glenview, IL) had the highest citrate levels."
     
  11. Elephanto

    Elephanto Member

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    Must be why my earthly teachers keep telling me to reduce my salt consumption.
     
  12. yerrag

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    So, in summary, citric acid has a neutral effect on blood pH? And citrate alkalizes the blood? If there is leftover citrate after liver converts citrate to bicarbonate, the serum citrate is excreted if blood/ecf is sufficiently alkaline, but reabsorbed by the kidneys back into systemic circulation if blood is acidic (or not sufficiently alkaline), correct?

    What happens to the leftover citric acid after the liver converts it to bicarbonate at the first pass? Article does not touch on this. Is it assumed it gets the same treatment by the kidneys as citrate?

    My experience with drinking sour orange (satsuma- real sour) seems to be a negative experience. I was able to see my urine pH drop below 5.5, which I felt was not a good sign. Is it possible then that what it's saying is that the citric acid (from the satsuma) was just being excreted (hence decreasing the urine pH) because my blood was already sufficiently alkaline?

    Or is it possible that the citric acid from satsuma juice was simply not having an effect on my blood pH, and if my blood pH was acidic to start with, the kidneys would reabsorb the citric acid, let it go thru the liver thru many passes until it's fully gone. Meanwhile, my urine pH would remain acidic simply because the citric acid intake was really having a neutral effect on an already acidic blood?

     
  13. yerrag

    yerrag Member

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    Shouldn't this be citrate reabsorption? I thought lower pH, acidosis, will cause citrate to be retained?

    This runs counter to what the link previous to this says: In acidosis states the renal proximal tubule reabsorbs citrate, which is incorporated into the Krebs cycle, decreasing citraturia. On the other hand, alkalosis decreases renal tubule reabsorption of citrate, increasing urinary citrate excretion.

    Confusing. Which one is right?

    Going through the last referenced link, Hypocitraturia: Pathophysiology and Medical Management : It has long been known that acidosis decreases renal citrate excretion, whereas alkalosis increases it.

    It would seem to me that acidosis would decrease renal citrate excretion, and alkalosis would increase it.

    Anyway, I think that was a typo that wasn't caught.
     
  14. OP
    Amazoniac

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    It's difficult to tolerate these acids in injurious amounts because they will be objectionable, but the amount that people can handle without issues seems to be be high. Some people find grapefruit more bitter than others, maybe there's something else other than the imbanced acid content in when the fruit is unappettizing, making it only a sign of improper development of the fruit or other detrimental stuff in it that can challenge the body. Some people also like to add lime/lemon juice to carbonated water, so it's all based on the current state of the person.

    I don't know what happens to citric acid that escapes processing.

    I wonder what happens when you take too much of a single onion, which is what people usually do with acetate or malate. Does the body keeps excreting citrate the more you take them? Is there any problem with this?

    But I guess that there's no need to worry about citrate intake, apparently it's the predominant potassium specie in potatoes (and probably other foods):

    Effect of potato on acid–base and mineral homeostasis in rats fed a high-sodium chloride diet
    Rich in K (2% of DM), essentially as potassium citrate, potato presents an interesting potential renal acid load of −4·0 mmol/100 g edible portion (Remer & Manz, 1995) and has been recently recognised as an important factor for lowering net acid excretion (Prynne et al. 2004). Thus, potato intake could be taken into account in the prevention of mineral loss induced by chronic consumption of modern diets.​

    Ach ja, the quoted part seemed like a typo.
     
  15. OP
    Amazoniac

    Amazoniac Member

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    I discovered that I can't pronounce glomerular and that it's possible to drag multiple tabs at a time using the Ctrl key.

    --
    No lame boxes this time, onto poetry:

    When you start to read about this subyect in more details, (as usual) one approach is often a refinement of the predecessor one, so you'll find an article citing another (and another..), but when you eventually arrive on the original material, you're faced with calculations that were in part derived from unavailable endocrimology books or articles in other languages that are inaccessible.

    If you're lucky to find enough information to start doing the thoughts, somewhere along the way you come across an article pointing out various flaws in what you're reading, so you is left with this frustrating cycle where you don't know if it's worth understanding (since one is developed from the other) or moving on. Sometimes there are typos on crucial points that only add to the confusion. Everything is further complicated by the fact that it's common for authors in this field to be calculating similar things using different terms assuming that people are familiar with their approach; made worse when a different group decide to elaborate on their work but changing only some of those terms while maintaining others. The mess got to a stage that researchers felt the need to publish an article standardizing the termimology. It's a hole of the rabbits. There's a lot of unnecessary complication.

    Due to this I had to restart this post from starch multiple times.

    Every time I read an article on this topic, there were the same equations over and over again without being specific on their meaning. Therefore this was just an attempt to go through the steps to grasp what's going on, which in turn should be helpful to avoid taking the whole concept as hostel and to question how far it's worth adhering to the idea.


    These approaches exist to predict the acid load to the body using the 'Renal Net Acid Excretion' (RNAE or just NAE) as reference, the purpose is to dispense the need for requiring constant and direct measuring (24-hour urine samples in this case). For practical purposes then, various investigators proposed different means of calculating 'Net Endogenous Acid Production' (NEAP), which is an estimation relying on diet and metabolism, it's an indirect attempt to determine the NAE.

    This is useful:
    What Unique Acid-Base Considerations Exist in Dialysis Patients? (author involved in Advanced Glycation End-products research)

    upload_2018-12-27_7-17-9.png

    Here's an introduction to the concept (this link has been posted before)..

    Acid Balance, Dietary Acid Load, and Bone Effects—A Controversial Subject

    "Food and endogenous metabolic processes are the sources of acid or base intake or production. Studies on the effects of diet on urinary pH and acid excretion to alter acid-base balance started at the end of the 19th century [5–7]. Subjects in these early studies would be fed specific diets and the urine analyzed for nitrogen compounds such as urea, non-urea nitrogen, and ammonia, as well as sulfates, phosphates, and chlorides.

    In the late 1950s, the pioneering group of Relman, Lemann, and Lennon undertook an impressive series of landmark studies [8–10]. Evaluating both liquid and solid diets, they investigated the correlation between endogenous acid production and renal acid excretion. They showed that the net acid production was the sum of (1) the net liberation of protons from organic phosphate compounds, (2) the oxidation of organic sulfur to sulfates and (3) the endogenous formation of unmetabolized organic acids [11]. Dietary base was produced from the ingestion of organic anions such as citrate or malate, which are metabolized to bicarbonate. Much of the bicarbonate is excreted by the lungs in the form of carbon dioxide. In 1966 [12], the group was able to demonstrate that knowledge of both the composition of the dietary precursors and the metabolic end products excreted in the urine and feces (Net endogenous acid production = urinary organic acids + sulfates-bicarbonate; Net renal acid excretion = urinary ammonium plus titratable acids minus bicarbonate) was required to calculate the quantity of “fixed” or non-carbonic acids produced from a given diet.

    Biochemical analyses of food demonstrate that almost all foods contain acid precursors, while fruits and vegetables also contain base precursors. Using this information, dietary formulas for estimating the acid or base effects of different foods have been developed [13–15]. Use of estimates of dietary intake avoids having to measure renal net acid excretion. However, these formulas require quantitative analyses of both dietary cations (sodium, potassium, calcium, magnesium) and anions (chloride, sulfate, phosphate). The formulas may also contain an estimate of organic anion production and/or a factor for intestinal ion absorption. Typical western diets produce approximately 1 milliequivalent of dietary acid per kilogram body weight, or approximately 50 mmol of acid/day [16]."​

    This dates back to burning foods to their ashes, but the incinerating approach isn't much reliable because it assumes that the body assimilates everything equally, that the metabolism of molecules has no effect and that it doesn't change compounds.

    They started to experiment with single food items to know how each affects excretions. This was from an early attempt in 1914:


    It's interesting if you can predict how each component affects the system than just considering the entire diet and how it must affect the body (reflecting in excretions). The more variables you have, the more accurate is the prediction.

    Relman's group mentioned above madeded a great deal of the work in providing means of estimation. Thom Remer and team suggested later an improvement mainly by adding absorption rates and modifying the way that the endogenous part is calculated.

    Even though all these approaches have serious problems, making you wonder why I'll be commenting further on some of them, they're still in use, they appear everywhere as justification for choices, and they have some merits.

    I had to divide these posts due to image upload limit, wait for it..
     
  16. OP
    Amazoniac

    Amazoniac Member

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    Before proceeding, I think it's valuable to read some parts of this great book (highly recommended) as a primer:

    upload_2018-12-27_7-28-49.png
    upload_2018-12-27_7-28-57.png
    upload_2018-12-27_7-29-4.png
    upload_2018-12-27_7-29-14.png
    upload_2018-12-27_7-29-23.png
    upload_2018-12-27_7-29-30.png
    upload_2018-12-27_7-29-37.png
    upload_2018-12-27_7-29-44.png
    upload_2018-12-27_7-29-51.png


    upload_2018-12-27_7-29-59.png
     
  17. OP
    Amazoniac

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    If the amount of acid produced from food and metabolism is greater than eliminated, there's acid retention eventually leading to acidosis that worsens as the body's ability to compensate becomes compromised (aging or sickness for example). Most people can handle acid load just fine for a long time because their body is able to restore balance by getting rid of what's undesirable, but the process is taxing nevertheless.

    There are two components for calculating the 'Net Endogenous Acid Production' (NEAP) in the most widely useded approach:

    NEAP = (PRAL) + (OAs)

    It's essentially the following: [(acid-forming inorganic onions) − (base-forming cations)] + [acidifying organic onions] (endogenous)
    Another way to put it: mEq of [(SO4 + PO4 + Cl) − (Na + K + Ca + Mg)] + [acidifying organic onions] (endogenous)

    PRAL (mEq/d) = '(0.49 × protein [g/day]) + (0.037 × phosphorus [mg/day])' − '(0.021 × potassium [mg/day]) + (0.026 × magnesium [mg/day]) + (0.013 × calcium [mg/day])'

    'Potential Renal Acid Load' (PRAL) takes into account protein ingested (mainly sulfur-containing amino acids being concerned) and the inorganic cations and onions of the diet.

    Everything related to PRAL is inorganic, for lacking carbon in structure, this applies to SO4 and PO4 (which you'll often find as Pi).

    Three factors are considered for the formula other than the actual amounts: average net absorption, ion valence, and degree of dissociation at pH 7.4.

    0.49 factor for proteid is due to the following:

    Notes:
    - I was trying to shorten these numbers initially, but in doing so we ended up with results that were different from those in publications running the risk of becoming a source of confusion for someone who is willing to verify them.
    - Don't be discouraged if it doesn't read clear, go by the numbers as well that it should make sense.

    - Generalized absorption of protein as 75% (0.75) of the amount consumed
    - Assuming an average content of 2.4% (0.024) for methionine and 2% (0.02) for cysteine in consumed protein
    - Based on their molecular weights..
    • methionine: 149.21 g/mol
    • cysteine: 121.16 g/mol
    • And sulfate's: 96.06 g/mol
    You won't find a lot of sulfuric acid circulating in the body because it reacts with bicarbonates (appearing for example as sodium sulfate), in the kidneys the pairing cation is usually recovered, but not a lot because they can't operate having a strong acid such as sulfuric acid as free acid in large amounts. In foods neither because it's corrosive.
    Calculating then their respective sulfate content:​
    • in methionine: 65% (0.648)
    • in cysteine: 79% (0.792)
    - Knowing the sulfate content in methionine and cysteine, we can substitute both for sulfate in relation to total protein:
    • 0.024 * 0.648 = 1.545%
    • 0.02 * 0.792 = 1.586%
    - Now that we have the proportion of sulfate in relation to total protein on total proteid, we can combine them:
    • 1.545% + 1.586% = 3.131% (0.03131)
    - We have to convert units because the input is in milligrams and the output is in mEq:

    They think in terms of mmol or mEq (not mg) because they have in mind interactions, and it's easier to work this way. It's the standard units for physiologists, to grasp the idea of charge in solutions. Nowadays they have simplified for people to add the values as 'mg' but the results still return in mEq.
    • mg = mEq * atomic weight / valence
    • mg = 1 * 96 / 2
    • mg = 48
    • 0.03131 / 48 = 0.000652
    - Multiply by 0.75 (% protein absorption):
    • 0.000652 * 0.75 = 0.000489 = 0.489 * 10^(−3)
    - Since only proteid in the formula is in grams (and not in milligrams) we have to adjust for it:
    • 0.489 * 10^(−3) * 10^3 = 0.489
    - And when you round it to 0.49, you have the factor above.

    Regarding the inorganic molecules other than sulfate, there's also the ion valence issue and degree of dissociation at pH 7.4.

    Relevant stuff before moving on:

    The ion walence (required for sulfate as well) is related to the combining capacity of the atom/group based on its outer shell electrons:

    [Na]+
    [K]+
    [Ca]++ (2+)
    [Mg]++ (2+)
    [Cl]-
    [Pi](read below)


    Magnesium for example has two unstable electrons, requiring them to be shared to stabilize magnesium in a solution.
    Magnesium complexing with ADP and ATP:

    upload_2018-12-27_7-34-54.png

    Therefore such molecules count for more than 1 in solutions: they require more counterparts if the whole tends towards stability. Hence Na/KCl and Ca/MgCl2.

    Phosphate has a factor of 1.8 added to it as a dissociation coefficient due to this:

    Hormones and Transport Systems (part of this book series)
    Chapter Nine - Regulation of Hormone-Sensitive Renal Phosphate Transport

    Biological forms of phosphate:

    "Phosphate, the oxidized form of phosphorus, is found in the body as both inorganic and organic compounds. Organic forms include phospholipids and various organic esters. Four moieties of inorganic [lacking carbon] orthophosphate can be present in biological solutions: [H3][PO4], [H2][PO4]-, [H][PO4]2-, [PO4]3-. These different components are in a pH-dependent equilibrium. Only [H][PO4]2- and [H2][PO4]- are present at significant concentrations at physiological pH's. The Henderson relation determines the ratio of the two:

    [H][PO4]2- / [H2][PO4]- = 10 ^ (pH-pKa)

    where pKa, the dissociation constant, for phosphate is 6.8. Thus, at an extracellular pH of 7.4, the ratio approximates 4:1 with plasma phosphate having an intermediate valence of 1.8. The abbreviation Pi is used here to refer to aggregate inorganic phosphate: [H][PO4]2- + [H2][PO4]-."
    And this is from the original material ([12] above):

    "The valence of phosphorus is obviously important in making an estimate of the quantity of excess organic ions. We have assumed that the mean valence of phosphorus is 1.8 in both natural foods and feces in the absence of precise information about the chemical states of phosphorus in these biological materials. If the actual average valence of phosphorus is significantly different from 1.8, the calculation of excess organic ions will be incorrect."
    Their absorption rate is assumed as follows (from a publication by Thom Remer in the first post of this thread, it's a simplified version of the previous table):

    upload_2018-12-27_7-37-3.png
    (focusing for now only on intestinal absorption)
    The absorption rate for magnesium, calcium and phosphate happen to be lower in comparison with the others.

    Then, considering all the above information:

    (0.95) * [Na]
    (0.80) * [K]
    (0.25 * 2.0) * [Ca]
    (0.32 * 2.0) * [Mg]
    (0.95) * [Cl]
    (0.63 * 1.8) * [Pi]

    Just like we did before, we have to convert these to be able to use milligrams instead of mEq:

    [(0.95) ÷ 23] * [Na]
    [(0.80) ÷ 39] * [K]
    [(0.25 * 2.0) ÷ 40] * [Ca]
    [(0.32 * 2.0) ÷ 24] * [Mg]
    [(0.95) ÷ 35] * [Cl]
    [(0.63 * 1.8) ÷ 30] * [Pi]

    Giving us (milligram input)..

    0.041 * [Na]
    0.021 * [K]
    0.013 * [Ca]
    0.026 * [Mg]
    0.027 * [Cl]
    0.037 * [Pi]

    ..which are the factors above.

    The formula was simplified, excluding sodium and chloride because both have equal absorption rates, being considered neutral and balanced. The justification in their own words:

    Dietary potential renal acid load and renal net acid excretion in healthy, free-living children and adolescents
    "In contrast to earlier studies that evaluated a limited number of foods and beverages (3, 4, 9, 18, 19), sodium and chloride were omitted from the present calculation of PRAL because, for some of the foods recorded, either the chloride data are missing from the food tables used, or, in the case of processed (salted) foods, they deviate unrealistically by more than ± 10% from the respective sodium values (9). This omission implies a certain insensitivity of our calculation to large differences in the intakes of these elements. As calculated from differences in urinary chloride and sodium excretion after the controlled ingestion of different diets, the resulting estimation error for PRAL can be as much as 16 mmol/d (18). However, in 24-h urine samples from randomly selected children and adolescents from the DONALD Study, the mean urinary ratio of sodium to chloride was found to be 1.02 (35)."
    Detrimental effects from sodium chloride only appear when you add it in excess (since the balance is also relative to the rest of minerals). But it's crazy that they have decided out of deliberation to exclude sodium and chloride from calculations. The author himself acknowledges that it has an effect:

    During digestion, chloride is secreted and reabsorbed, but the same occurs for bicarbonates. If there's a limitation to the absorption of a given cation, this can cause loss of bicarbonate. Here's something that must occur with magnesium chloride, the imbalance starts already in this stage:

    upload_2018-12-27_7-39-17.png
    Same source of the previous image.
    Here we conclude the first part of the formula (PRAL).

    The other part being endogenous 'Organic Onions' (OAs).

    "Organic onions that are not excreted yield bicarbonate on metabolism, which back-titrate the protons released during organic acid generation and, hence, do not contribute to 'net endogenous acid production'."

    Refer to this for a discussion for why it's better to use an estimation based on human measures (which is what the discussion below is about) than based on minerals:

    The formula is a generalization relying on average excretions based on surface area related to metabolism. According to them, in healthy people it's relatively constant, by the end of the post there's more information on why.

    OAs (mEq/d) = individual body surface area * 41 (mEq/d/173 m²)
    1.73 (m²)
    Surface area is based on the following classic, published in 1916:

    A formula to estimate the approximate surface area if height and weight be known

    "A formula to express surface area must naturally be a bi-dimensional formula, as surface involves two dimensions. If we assume that weight is proportional to volume, it is obvious that three dimensions are involved in any expression for weight. Height is, of course, a single dimension. If we attempt to construct a formula for surface area (A) based on weight (W) and height (H), it is obvious that a simple formula such as A = W * H * C (C being a constant depending on the units used and the subject to which the formula is to apply) is not logical. In this formula one side, A, is bidimensional and the other side, W * H * C, involves four dimensions, three from W and one from H. If W is tridimensional, it is obvious that the cube root of W (=³√W or W^(1/3)) is unidimensional and a formula A = W^(1/3) * H * C is logical in that it is bidimensional on both sides."

    "The formula A = W^(1/3) * H * C can also be written A = W^(1/3) * H^(1/1) * C, bringing it into the same form as A = W^(1/2) * H^(1/2) * C and the general form of this formula can be written A = W^(1/a) * H^(1/b) * C. In order that the expression W^(1/a) * H^(1/b) * C may remain bidimensional it is only necessary that 3/a + 1/b = 2, as it does in the two cases considered. For an intermediate equation it is obvious that (b) must be greater than 1 but less than 2."
    However! Depending on the root distribution you can place more importance on one component or the other:

    "Comparing the two formulas A = W^(1/3) * H * C and A = W^(1/2) * H^(1/2) * C, it will be seen that they differ in the relative importance given to W and H. In the former W has less importance and more importance than in the latter."
    And this is reflected on the constant (C). Since they already had values for surface area (A), weight (W) and height (H), the only thing left to define was the constant, which in turn will guide them on how it's best to distribute the importance on weight and height. They'll have various formulas with different distributions and constants and what they have to do is compare which one is a better predictor for most people.

    The results arrived back then were made into the following chart for practical purposes:

    upload_2018-12-27_7-40-14.png

    Another group using similar methods proposed this instead:
    Geometric method for measuring body surface area: A height-weight formula validated in infants, children, and adults

    upload_2018-12-27_7-40-31.png

    Such charts are still useful if you want to grasp the surface area of an adult knowing weight and height.

    Should you now be thinking:
    Fnck you. Who cares?

    My replies are:
    How exactly? And there are people who developed a more elaborate approach to BMI who used surface area; chemotherapeutic drugs sometimes use this to calculate the dose; for glucocorticoids replacement people also care; for some measures of cardiac output it's also required to know the body surface area; and equivalent doses between animals also requires surface area. So it's not only useful in renal function experiments.

    A development on the classic material:
    Estimation of Human Body Surface Area from Height and Weight (1970)

    "The basic concept underlying most models proposed for estimating human skin surface area is that if humans are similar in form and density, their homologous dimensions are proportional when adjusted to a common dimensionality. In particular, since the areal dimensions of similar bodies are approximately proportional to the square of their linear dimensions and the two-thirds power of their volume (weight could be substituted for volume if specific gravity is assumed constant), the surface area of humans should be proportional to the approximate power of height and weight."

    [a = w^pw * h^ph * c] (same as above)

    This format is still used nowadays. Example:

    upload_2018-12-27_7-50-49.png Source: the internet.

    They're all working on the same idea above. The difference is in isolation:

    √(w*h) * √(1/3600) √w * √h * 1/60 w^(1/2) * h^(1/2) * 0.016667 [as constant (c)]
    "Suppose that except for minor variations, all individuals are of the same shape and density but differ in size. It will then be true that surface area would be predicted equally well from height alone with [pw = 0], [ph = 2];"

    [a = w^0 * h^2 * c]
    "from weight alone with [pw = 2/3], [ph = 0];"

    [a = w^(2/3) * h^0 * c]

    Wolume has 3 dimensions, so they're dividing by 3, then multiplying by 2 to work with same dimensions as surface area (a)
    "and from both height and weight using any [pw] and [ph] such that 3[pw] + [ph] = 2."

    [a = w^(3*pw) * h^(ph) * c]

    3[pw] + [ph] = 2 is just another form of notation for the condition mentioned by the Du Bois pimps (3/a + 1/b = 2), meaning that the first exponent will have to be added in a way that a cube root is applied to cut the dimensions, and if you opt for a different distribution, you have to end up with 2 to (again) work with same dimensions as surface area (a). In other words, it's just a dimensional adjustment. The variation in notation is because these authors consider the exponent as a whole, while the original approach focuses on the denominators. The original can be viewed this way: 3(1/a) + (1/b) = 2, which I find to be clearer.
    "The fact that our estimated value of 3[pw] + [ph] is 1.966, is intuitively satisfying on grounds of dimensionality; however! Since the confidence region does not include either [pw = 0], [ph = 2] or [pw] = 2/3, [ph] = 0, this suggests that individuals vary in shape and that both height and weight measurements are needed."

    Otherwise it would just be a matter of changing one dimension and the rest wooooould be changed proportionally, but this doesn't happen (some are tall and skinny, others are short and fatty), so both are needed.
    Here's a revision of the original work:
    Body surface area: Du Bois and Du Bois revisited

    "The widespread utilisation of the formula of Du Bois and Du Bois (1916) has conferred on it the status of a medical icon. However, it does not appear to be widely appreciated that the Du Bois and Du Bois formula was derived from measurements obtained on only nine subjects (Gurney 1996; Lentner 1984; Reilly and Workman 1993)."

    "In describing the development of their equation (Du Bois and Du Bois 1916), two methods were employed for the measurement of BSA. The method of enclosing their subjects in moulds [!] may be regarded as more direct than the other, a calculation based on 19 measurements of the length and circumference of body parts. The moulds were cut open and placed at on photographic paper that was exposed to sunlight (Du Bois and Du Bois 1915). The unexposed sections were cut out and BSA obtained from their weight and the known area density of the photographic paper."

    "We have derived new values of the constants for the Du Bois and Du Bois equation, using the data from all 42 subjects reported by Du Bois and Du Bois (Table 2). These values ought to be considered as those Du Bois and Du Bois would have derived if they had access to modern techniques. We recommend [a] set [] for which the constraint of Eq. 2 [3pw + ph = 2] does not hold exactly, but is very close to 2 (1.978). Nevertheless, the BSA values predicted when [] new constants are used in Eq. 1 [a = w^pw * h^ph * c], although more accurate, are a little different from the results of the original formula (Table 3). The original equation appears to be adequate for adults in general, despite being derived from only nine selected subjects."

    "More recent workers (Boyd 1935; Gehan and George 1970 [previous above]; Haycock et al. 1978), some using hundreds of subjects, have also derived formulae relating BSA to height and weight (Table 1). These authors should feel justifiably puzzled if their work is ignored in daily practice by the continued application of the original result of Du Bois and Du Bois."

    "We believe our re-analysis of the original work of Du Bois and Du Bois has placed it on a more robust statistical footing and may allow it to continue to have general application. Using data from their original publication, we have removed the stigma of an unacceptably low number of subjects, increasing them to 42. We have shown that the height/weight distribution of these subjects was very similar to the data of both Boyd (1935), as represented by Gehan and George (1970), and Haycock et al. (1978), curbing possible criticism on the grounds of a prevalence of physical extremes in the original sample. For those wishing to continue to use an equation based on the data of Du Bois and Du Bois, we recommend values of [pw] = 0.441, [ph] = 0.655, [c] = 94.9 in the Du Bois and Du Bois model (Eq. 1)."
    Now that we have this background, we can goes on:

    For the first part (of the OAs calculation):

    Just the individual's body surface area divided by the one that served as reference for the part below, a proportional adjustment to the surface area of the person in question.

    Sometimes you'll find it next to '41' to isolate the input (such as here and here), but it's one of those simplifications that only make it more difficult to understand the meaning.
    For the second part (of the OAs calculation):

    According to them, based on this (I couldn't access it), the median daily organic acids excretion for a body surface area of 1.73 m² is 41 mEq/d.
    The OAs calculation combined with PRAL will give you then the 'Net Endogenous Acid Production'; but it has bizarre generalizations in assuming that the endogenous OAs can be applicable to everyone, they rarely point this out. There are various aspects (endocrime, nutritional, dietary and so on) that can alter these results brutally. Consider for example someone that can't oxidize their food properly and the resulting lactate generation; so incomplete combustion of food of the stuff to carbon dioxide and water will increase this kind of acid load to the body. Therefore this part of the formula is less relevant for gurus that are restoring health.

    On diet:

    Paleolithic diet, sweet potato eaters, and potential renal acid load

    "It is highly probable that the renal excretion of different OAs is dependent on diet. Aromatic organic acids are a dietary component, not mentioned by Sebastian et al, that may have a particularly strong effect. For example, phenolic and benzoic acids, which are found in considerable amounts especially in fruit (5, 6), are metabolically inactivated (detoxified) and excreted (mainly via the kidney) as acids, largely in the form of hippuric acid.

    Interestingly, in the highlands of New Guinea, some Papuan tribes consume a low-protein vegetarian diet consisting predominantly of sweet potatoes. These sweet potato eaters excrete extremely high amounts of hippuric acid (31 mmol/d on average compared with 4 mmol/d in European control subjects), which adds substantially to their basal (not primarily food-dependent) urinary OA excretion (7). Basal OA excretion can be estimated from average anthropometric data as follows (3, 4):

    Basal OA excretion = body surface area (m2) * 41 mEq/d / (1.73 m2) (1) [the one in question notated in the confusing way]
    As a result, 36 mEq/d is yielded for sweet potato eaters [young adult males weighing 53 kg, 1.55 cm tall, and with a body surface area of 1.5 m²; (7)], which together with their hippuric acid output amounts to 67 mEq total OA excretion/d."​
    But..

    "Total organic acid production increases in response to increased bicarbonate input to the body—evidently a homeostatic response to mitigate the alkalinization (3)—and as a result the excretion rate of the dissociated organic anions increases. The increase in lactic acid and ketoacid production, and the excretion of their anions, after alkali administration exemplifies that fact (3), as does the dose-dependent increase in total organic anion excretion in response to increased dietary bicarbonate precursors (4). The dose-dependent increase in citrate excretion in response to bicarbonate administration or to dietary bicarbonate precursors also exemplifies that fact (5, 6), which is contributed to by reduced reabsorption of citrate filtered at the renal glomerulus (3)."

    "[..]organic anion excretion increases in response to increases in the so-called unmeasured anion (UA) content of the diet—computed as '[Na+] + [K+] + [Ca2+] + [Mg2+] − [Cl-] − [Pi]' in mEq/d—because such UAs consist of organic anions largely metabolized to bicarbonate and thus are dietary bicarbonate precursors (4). Empirically, in adults eating a wide variety of diets, organic anion excretion correlates positively and quantifiably with the UA content of the diet (4, 6)."

    "[..]because the UA content of contemporary Western diets is almost an order of magnitude lower than that in preagricultural diets (1), it has little influence on organic anion excretion relative to the diet-independent basal rate. This may explain why Remer and Manz’s BSA approach works reasonably well for contemporary diets, and why their approach may be questioned for preagricultural diets."
    Out of curiosity:

    "Reasons for the historical shift from negative to positive PRAL are not only the displacement of alkali-rich plant foods in the ancestral diet by cereal grains and nutrient-poor foods in the temporary diet but also the modern processing and preparation of foods, which lead to considerable losses of base-forming nutrients such as potassium and magnesium."
    With that we conclude the major approach currently in use to estimate an acid load to the body, and by this time you must have noticed how many things can go wrong with it.

    ..
     
  18. OP
    Amazoniac

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    Thom and friends have also calculated the potential renal acid load (PRAL) of foods.

    To recapitulate, it's the (acid-forming inorganic onions) - (base-forming cations), since this time it's only concerning foods, the endogenous part (organic onions that don't generate bicarbonate) is left out. Due to this, when the difference is negative, the food tends to be more alkalizing and the opposite holds a true.
    But you'll find people proud of their food choices based on 'PRAL' values and it's silly. Examples: the calcium in milk and spinach are treated the same way; something as simple as the vit D status can change absorption rates; the protein in dairy, meat, grains are considered equally digestible with the same amino acid profile (protein intake alone might make a difference in calcium absorption and utilization); meal composition doesn't make a difference; same for timing; and on so..

    There's more: the foods are ranked based on 100 g of edible portion instead of serving, and parmesan cheese appears as the most acidifying, but who eats it in large enough amounts to be a problem? Who eats more than a few hundred grams of spinach (which was the most alkalizing according to their calculations)? Potatoes are behind spinach, but people can eat them in substantial amounts, so it only takes one potato to match the spinach potential. Fruits might appear modest in relation to leaves, but once you have the amounts in mind, the story changes.

    Even water can have an overlooked effect:


    To add to the problem, you also have an issue of owaestimation of base and acid loads and possibly and underestimation of the body's ability to balance. The following is a great criticism to the current approaches:


    Which right away you realize that there's something wrong as well: a depleted diet will be taxing on organs, which over time will compromise them and cause imbalances. However it's definitely worth reading their criticism, but if there wasn't a degree of truth in these other sensationalistic interpretations, people wouldn't benefit from bicarbonates as much as they do; it's something recurrent.


    But this complexity led Tony Sebastian, Lynda Frassetto, Curt Morris and other unimportant lives to come up with a simpler and practical method:
    Estimation of net endogenous noncarbonic acid production in humans from diet potassium and protein contents

    Organic salts of potassium are so important for base contribution and conserlevy ingested proteid for acid that only these two aspects are taken into account. It's relatively effective for the purpose of a rough estimation of the acid load of diet. It has similar problems to the previous more complex approach, but its value lies in simplicity. They concluded that these two sufficed (!).

    "Present methods for estimating the net acid load from the composition of the diet require a detailed inventory of nutrient composition and estimates of the gastrointestinal absorption rates of the nutrients; these methods have been validated for only a few diets (11, 12). In vivo methods for quantifying net endogenous acid production are complex and labor intensive (5) and are suitable only for specialized clinical research centers. Accordingly, simple dietary guidelines for quantifying and regulating endogenous acid production rates do not exist. In this paper we present a new method for estimating the net acid load of the diet from readily available information on diet composition, specifically total protein and potassium contents. We focused on these 2 components because the rate of sulfuric acid production from protein metabolism and the rate of bicarbonate generation from metabolism of intestinally absorbed potassium salts of organic acids are major and highly variable components of the net endogenous acid production rate (5, 6)."
    Potassium makes such a great contribution to the base character of the diet because its major ligands are organic onions that can be metabolized to bicarbonate in the body (citrate, malate, succinate, etc), being also 'intracellular constituents'. As an intracellular cation and a predominant source of those, potassium was taken as a major contributor. Magnesium is also relevant, but to begin with is not absorbed to the same extent, it's more common to be found complexed with inorganic onions, and its amount in the diet are much lower (which is why it's possible to consume 15 grams of potassium from foods in a day, but hard to consume 3 grams of magnesium).

    Here's their information in tables and graphs. It's interesting how the caloric intake is all over the place, yet it's still protein and potassium that are able to predict 'renal net acid excretion' better.

    upload_2018-12-27_7-52-24.png
    10 460 kJ = 2500 kcal
    Here they've adjusted for caloric intake:

    upload_2018-12-27_7-52-44.png

    Estimated NEAP (mEq/d) [as a prediction for RNAE] = [0.91 * protein (g/d)] − [0.57 * potassium (mEq/d)] + 21

    You can do a noting that the (weird) plane is tipped to the left; so to a certain degree, if protein is increased but organic salts of potassium increased along, the issues tend to disappear. Silimarly, if the potassium intake is low but protein is reduced, the excreted acid load remains low. And their highest potassium value of 140 mEq is not that high: about 5500 mg. Protein intake is slightly more impacting than potassium intake.

    And here's another representation of the first, now as a ratio of protein/potassium. And of course as it increases, there's a greater disparity in protein consumption and potassium intake: a nicht, nicht.

    upload_2018-12-27_7-54-2.png

    An alternative:
    Estimated NEAP (mEq/d) [as a prediction for RNAE] = 54.5 * [protein (g/d) / potassium (mEq/d)] − 10.2
    There's nothing special about their formulas, it's just what they found to be the best linear fit to the information awailable (intakes of energy, protein with sulfur-containing amino acids in mind, and potassium). Their approach is valuable but gross enough to discourage any speculation on (vertical axis) intercepting values when the independent variables are '0' because we might spend time trying to make sense of something that's not even accurate. I tap out.

    Even though the sulfur content of vegetable protein varies more than in animal protein, as a surprise (according to them), the correlation of renal net acid excretion with animal protein is only 'marginally stronger' than with total protein, being almost indifferent to use one or the other. They mention that further experiments are required to assert this, but that total protein amount of the diet is a reliable predictor. One of the reasons for this is probably due to the fact that it's easier to get more protein from animal than from plant foods (but when you obtain from plants they have the advantage of providing the alkalizing factors along).

    This is interesting:

    upload_2018-12-27_7-54-28.png
    Sometimes onions that can generate bicarbonate are found bound to organic cations such as lysine and arginine, which are acidifying and reduce the effect of such onions. Also according to them, in ordinary diets the content of organic onions exceeds that of organic cations.

    And a last graph (out of curiosity) using predicted values from foods 'tabulated' by the previous group (includes Thom Remer):

    upload_2018-12-27_7-54-50.png
    So the same tendency exists. All these point to a diet that favors plant over animal foods.

    It seems preferable to err on the base side, having a spare margin. It will prevent unnecessary taxing or help in the correction of a condition.

    ..
     
  19. OP
    Amazoniac

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    @Sheila:

    - Potassium

    "When potassium is added as a preservative during processing, it is usually as potassium chloride, whereas it is usually present in fruit and vegetables as potassium citrate. Approximately 85% of potassium is absorbed, and it is generally considered that the best way to increase potassium intake is to consume more fruit and vegetables."​

    - Beneficial effects of potassium on human health

    "Potassium in fruit and vegetables is not present with chloride but is present with phosphate, sulphate, citrate and many organic anions including proteins, most of which are precursors of potassium bicarbonate (Morris et al. 2006)."​

    - Organic anions and potassium salts in nutrition and metabolism

    "Anions from plant foods

    Anions. Except for ripened cereals, intrinsically poor in organic anions, and to a certain extent legumes, most plant foods contain substantial quantities of organic anions; from 100 mg/100 g fresh weight (fw) up to 4000 mg/100 g fw, for the richest sources such as citrus fruits. In terms of molar concentrations, these values represent 0·5 to 20 mmol citrate units/100 g fw (Fig. 1). Malate and citrate are polycarboxylic anions which, at the acidic pH prevailing in plant products, are partially neutralised by cations (for example, malic acid in apples is virtually in a potassium malate[1–] form). These organic anions are frequently intermediate metabolites of the tricarboxylic cycle but, in some foods, the prevalent anion is not metabolisable, for example oxalate (red beet, spinach, rhubarb) or tartrate (grapes). Besides, relatively low concentrations of additional organic anions may be found, such as fumate or succinate, as well as various phenolic acids (quinate, ferrulate, caffeate, chlorogenate). Malate and citrate anions are frequently present simultaneously in a large variety of plant foods, but malate is the predominant anion in some fruits and vegetables (apples, cherries, plums, aubergines, cucumbers) whereas citrate is the major anion of citrus fruits, kiwi and members of the Solanaceae family (potatoes, tomatoes)."

    upload_2018-12-27_7-56-18.png
    "Some anions, generally present in small amounts, probably exert pharmacological effects; for example, glucarate is found in plant foods such as cabbages, tomatoes, grapefruits and apples. Glucarate is a precursor of D-glucuro-1,4- lactone, an inhibitor of -glucuronidases, which could affect the detoxification of carcinogens and other promoters of carcinogenesis through a decreased hydrolysis of their glucuronides (Walaszek et al. 1997). Cholesterol-lowering properties have also been ascribed to D-glucuro-1,4-lactone (Yoshimi et al. 2000). Hydroxycitrate, present in some Far-Eastern fruits such as Garcinia, is known as an inhibitor of lipogenesis and has also been examined as a possible anorexigen; however, the trials were not conclusive (Heymsfield et al. 1998)."

    For potassium, 1 mEq is about 39 mg.

    "Accompanying cations. The K content of fruits is generally between 2·5 and 10 mEq/100 g fw and that of vegetables is usually higher, sometimes exceeding 15 mEq/100 g fw. In fact, the most salient feature which distinguishes fruits and vegetables is the K:[organic acids] concentration ratio (in mEq); this ratio is basically lower than 0·5 in most fruits whilst it always exceeds 1 (up to 2·6 in pumpkins) in vegetables. In other terms, organic acidity of vegetables (frequently lower than in fruits) is more completely neutralised by K ions and vegetables exhibit a greater alkalinising potency. It must be noted that, within the fruit and vegetable groups, some foods show an atypical composition, which has some nutritional and culinary background. A fruit such as banana exhibits a K:[organic acids] concentration ratio > 1 (coherent with the possibility of using bananas as a vegetable) and this ratio is much lower than that of most of the other vegetables except for tomato, probably reflecting its possible utilisation as fruit (for example, for juice confectionery)."

    "The daily food supply of organic anions is obviously dependent on fruit and vegetable intake. It could be in the range of 1–2 g/d in low-plant-food consumers, and easily reaches 3–4 g/d [: therethere] in subjects consuming a diversified omnivorous diet and more than 5 g/d in vegetarian individuals. These values of intake are close to those for K, which is consistent with the fact that organic anions are mainly K salts, but it must be kept in mind that K is also present in food products of animal origin."

    "Influence of cultivar, maturity or food processing. The degree of maturity influences the concentrations of organic acids in plant foods, for example citric acid in citrus fruits accumulates during fruit development but tends to decline at the stage of maturity. Food processing such as boiling is probably a cause of organic salt losses, especially for vegetables since fruits are generally consumed uncooked. This point is still incompletely documented, but there is little doubt that foods that are steamed or briefly fried probably maintain greater concentrations of potassium malate or citrate than if cooked using procedures that lead to extensive leaching (Table 1)."

    "Anions in animal foods

    These foods are frequently poor in organic anions if consumed directly but, most frequently, they contain substantial quantities of organic anions resulting from maturation and/or fermentation processes. An exception is cows’ milk, which contains noticeable amounts of citrate (5–8 mmol/l). On the other hand, fermented dairy products are rich in lactate anions, arising from lactose fermentation (by Lactobacilli and Streptococci). Yoghurts contain more than 100 mmol lactic acid/l; thus a standard serving of 125 g yoghurt supplies about 1·3 g lactic acid. Cheeses are also enriched in lactate, but its concentration may be very different according to the type of cheese."

    "The L-lactate anion is part of the anionic profile of muscles in vivo (contributing 5–10 mmol/kg fw, which is marginal). However, it accumulates in muscle tissues during the process of meat maturation through anaerobic glycolysis from glycogen stores and it can be present in substantial concentrations (50 to 80 mmol/kg). It appears, therefore, that animal foods may represent a non-negligible source of organic anions, but in a markedly distinct pattern from that observed in plant foods. The organic anion present in animal products is typically lactate and this anion is produced secondarily (through postmortem metabolism or fermentation) in matrixes where the unmetabolisable anions, chiefly phosphate, prevail. Therefore, the alkalinising potential of animal foods is quite limited even when foods contain noticeable K concentrations (Oh, 2000). The quantities of organic anions ingested with animal foods may be estimated at about 1·5–2·0 g/d and it seems probable that, in subjects consuming a high-meat and -dairy products diet, this supply will be greater than that from plant foods whereas it will be marginal in vegetarian individuals (Fig. 2)."

    "Anions produced in situ in the digestive tract

    There is a permanent generation of substantial quantities of organic anions in the large intestine, essentially SCFA (namely acetate, propionate and butyrate). SCFA are the endproducts of microbial symbiotic fermentation present in the distal part of the digestive tract, which uses as substrates dietarily unavailable carbohydrates (fibre, resistant starch) and endogenous sources (sloughed epithelial cells, digestive secretions). Besides SCFA, other organic anions (succinate, lactate, galacturonate) can be found in noticeable amounts, under specific conditions (acidic fermentation, pectin hydrolysis) (Demigné et al. 1999; Aprikian et al. 2003). The daily intake of fibre in Western countries is in the range of 15–20 g/d; thus, together with endogenous sources, a total substrate supply of 30 g/d for colonic fermentation is considered as probable. The overall yield of the colonic fermentation for SCFA production is roughly 50%, which implies that this process generates around 15 g SCFA/d which are efficiently absorbed (>90 %) through the colonic mucosa (Cummings & Macfarlane, 1997). It appears therefore that the production of organic anions in the colon, which is closely dependent on nutritional conditions, is a major source of organic anions absorbed from the digestive tract."

    "The committed processes for SCFA absorption in the large intestine are complex and diversified (Sellin, 1999); some of them encompass a concomitant absorption of cations (K+ and/or Na+) and might therefore afford alkalinising opportunities (Kunzelmann & Mall, 2002). However, the overall impact of colonic fermentation on the acid–base equilibrium is still poorly understood since, for example, some processes involved in SCFA absorption require an anionic exchange between an SCFA– and an HCO3–, transferred from the extracellular body fluids into the colonic lumen (Demigné et al. 1999). Butyrate is a major energetic fuel for the colonic mucosa and has been shown to be metabolised in priority compared with other substrates such as glucose or glutamine (Mortensen & Clausen, 1996). The glutamine-sparing effect could be relevant in terms of acid–base control since glutamine is an effective precursor of neutralising metabolites (HCO3– and NH3) in the kidneys (Welbourne & Joshi, 1990). The colon–liver enterohepatic cycling of NH3-N is also a process with an equivocal significance. This is because urea transfer in the large intestine lumen generates two NH3, which can act as a sink for H+ through NH4+ formation, but a part of colonic NH3 is also reabsorbed and further detoxified to urea in the liver, a purported [HCO3–]-consuming process (Häussinger, 1997)."

    "These considerations indicate that the actual influence of intestinal fermentation on the acid–base equilibrium is difficult to evaluate. Furthermore, such an influence (if any) is probably quite different when colonic fermentation is poorly active, in practically neutral pH conditions, compared with when substrate availability allows the development of acidic fermentation (De Groot et al. 1995), establishing an H+ concentration gradient between the bulk colonic medium and extracellular fluid ranging from 10 to 50."

    "The other organic anions (oxalate, tartrate, phenolic acids) in the diet are generally less absorbable than malate, citrate or lactate, they are poorly metabolised in the body’s tissues and the absorbed fraction is essentially channelled towards excretion by the kidneys."

    "Oxalic acid is abundant in a limited group of plant foods (red beet, spinach and rhubarb). Its absorption exhibits some particularities. Oxalate absorption is: (i) dependent on the dietary Ca availability; (ii) favoured in the colon by acidic fermentation conditions, together with possibilities of complete breakdown by the host microflora; (iii) possibly balanced by an opposite secretion of oxalate into the intestinal lumen (Hatch & Freel, 1995; Albihn & Savage, 2001). Hautmann (1993) has also reported that the stomach could be a critical site for intestinal oxalate absorption."

    "Tartrate is essentially found, in its natural L(+) form, in grapes. This anion is partly absorbed from the digestive tract; it has been shown that colonic bacteria metabolise the bulk of ingested tartrate in human subjects, and only 14 % of ingested tartrate appears unchanged in the urine (Chadwick et al. 1978)."

    "The other organic anions present in lesser amounts in plant foods (quinate, ferrulate, caffeate, chlorogenate) are part of the phenolic acids group. Phenolic acids may be absorbed at different levels of the digestive tract (small intestine, colon) and are then excreted by the kidneys in various conjugated forms."

    "The liver is a major site for organic anions metabolism and the removal of circulating dicarboxylates involves at least two transport systems; an [Na+]-dicarboxylate cotransport and a system of anion exchange (Moseley et al. 1992; Zimmerli et al. 1992). The transferred anions are then channelled into various metabolic pathways, either towards complete oxidation, incorporation into glucose and liver glycogen or use for glutamine synthesis in perivenous hepatocytes (Stoll et al. 1991). This last point is noteworthy because it suggests that organic anions might exert an alkalinising effect not only through HCO3– generation, but also through glutamine production (by being used in the kidneys for HCO3– and NH4+ formation). In fact, there are arguments supporting the view that a sub-population of liver cells (5–7 %) is particularly adapted for coupling organic anions and glutamine metabolism, through the predominance or exclusive presence of various processes."

    "Acidifying characteristics of different types of foods

    During their complete oxidation, carbohydrates or lipids do not generate unmetabolisable acidity, even if their partial oxidation (into lactic acid or ketone bodies, respectively) may result in metabolic acidosis when excessive. In contrast, proteins contain various amino acids whose catabolism is liable to affect the acid–base equilibrium. The impact of the oxidation of proteins on this equilibrium is not unequivocal. Basic amino acids (‘cationic’, such as lysine, histidine or arginine) yield various metabolites together with H+, and S amino acids (methionine, cysteine) are also acidogenic because they yield sulfate anions (unmetabolisable acidity). However, oxidation of the dicarboxylic amino acids (‘anionic’, such as glutamate or aspartate) ‘consumes’ acidity. Even if some proteins (for example, rich in neutral and anionic amino acids) could theoretically be alkalinising, the fact remains that most of the dietary proteins (especially those well balanced for their amino acid composition) are acidifying (Remer & Manz, 1995)."

    "Evaluation of the acidifying potential of various foods

    Basically, a food or a diet which provides an excess of inorganic anions (fixed anions) such as Cl–, [H]n[PO4](3–n)– or [SO4]2–, compared with inorganic cations (Na+, K+, Ca2+, Mg2+) will be ascribed acidifying properties, in keeping with the classical ‘dietary ash hypothesis’. The net excretion of acidity by kidneys is referred to as: (Cl + P + SO4 + organic anions) – (Na + K + Ca + Mg). The urinary excretion of SO4 and all the other ions may be estimated from the data of food intake and food composition tables, using specific absorption coefficients, which are, for example: proteins, 75%; P, 63%; Cl, 95%; Na, 95%; K, 80%; Ca, 25%; Mg, 23%. In addition, the valences (2 for Ca and Mg) and the ionic charge of PO4 at physiological pH (1·8) are also taken into account as well as, for proteins, an average percentage of methionine (2·4 %) and cysteine (2·0 %) (Remer, 2000). Practically, the above calculation may be simplified by considering that Na and Cl are essentially provided as NaCl in most foods."

    "According to these assumptions, it is possible to estimate a potential renal acid load (PRAL) for various foods, which ranges between 34 mEq/100 g (Parmesan) and –21 mEq/100 g (grapes). As a general rule, fruits and vegetables display negative PRAL values, milk and yoghurt are close to 0 and meat, fish, poultry and cheese (and some cereal products) exhibit positive PRAL values (Remer, 2000) (Fig. 3)."

    "Excessive dietary proteins from food with high PRAL adversely affect bone (each additional 1 g dietary protein results in an additional loss of about 1·75 mg Ca/d), unless buffered by the consumption of alkali-rich foods or supplements (Barzel & Massey, 1998; Heaney, 2001)."

    "Data from Frassetto et al. (2000) and Sellmeyer et al. (2001) strongly strengthen the generalisation of a worldwide association of hip fractures in women with animal protein consumption. In fact, the decisive risk factor for hip fracture would not be the rate of production of fixed acid from animal protein but the net rate of endogenous acid production, when all sources of dietary acid and base are considered. Thus, a vegan diet with protein derived equally from grains and legumes would deliver at least as many mmol S/g protein as would a meat-based diet (Heaney, 2001), but it yields significantly lower rates of net endogenous acid production than do mixed animal and vegetable diets. However, although protein was associated with an increased risk of forearm fracture for women who consumed more than 95 g/d, Feskanich et al. (1996) did not find any association between adult protein intake and the incidence of hip fracture. Also, it has to be said that a low protein intake may also compromise bone quality, especially in the elderly (Bonjour et al. 1997). In fact, the influence of dietary protein on Ca retention is complex, possibly transitory (Roughead et al. 2003), and liable to be modified by other nutrients in the diet (Massey, 2003)."

    "Anti-acidosis mechanisms operating in kidneys

    Under steady-state conditions, the urinary output of electrolytes matches gastrointestinal electrolyte absorption. The kidney sustains normal acid–base homeostasis by reabsorbing an appropriate amount of the filtered bicarbonate and excreting a quantity of acid in urine that corresponds with the endogenously generated acid load. Phosphate is the major buffer system in urine and its excretion is increased during acidosis, probably as a result of a decrease of the preferentially transported form (H[PO4]2–) together with a direct effect of pH on the apical phosphate carrier in the proximal tubule. Citrate transport is frequently analysed owing to its sensitivity to systemic pH; changes in citrate excretion are altered by changes in the transported chemical form, namely citrate2–, and in kidney metabolism (Brennan et al. 1988). It is now well established that acidosis promotes hypocitraturia and the tubular reabsorption of citrate. The renal excretion of citrate is normally dependent on the net absorption of alkali from the digestive tract (Sakhaee et al. 1993), but this relationship is less tight in subjects suffering distal renal tubular acidosis. In general, lithiasic subjects who have no renal tubular acidosis frequently exhibit hypocitraturia, which is chiefly of digestive origin and probably consecutive to an insufficient intake of alkalinising agents (fruits and vegetables). In this view, Hess et al. (1994) proposed that ‘low vegetable-fibre intake and low urine volume’ could be added to the list of risk factors for low urine citrate."

    "The skeleton serves as a substantial reservoir of labile base in the form of alkaline Ca salts, which can be mobilised to defend blood pH. Indeed, 80% of total body carbonate is in the hydration shell, the water surrounding bone, as are 80% of citrate and 35% of Na (Green & Kleeman, 1991). Osteoclasts and osteoblasts respond independently to small changes in pH, a slight drop in pH causing a burst in bone resorption (Kriegger et al. 1992; Arnett & Sakhaee, 1996)." "Bone also plays a major role in the storage of phosphate, the phosphate buffer system being very important to relieve fixed acid loads and to enable the maintenance of pH within restricted limits (Pautard, 1961)."

    "Chronic metabolic acidosis due to excessive intakes of sulfate and chloride anions increases with age at constant endogenous acid production, apparently due to the normal age-related decline of renal function (Frassetto et al. 1996)."

    upload_2018-12-27_7-56-35.png
    "Acid–base status and protein metabolism

    Metabolic acidosis induces N wasting and depresses protein metabolism in human subjects. This may be particularly critical in aged individuals, more prone to renal dysfunction, and could promote muscle dystrophy and an aggravation of the consequences of Ca losses, through alterations of the protein matrix of bones. The committed mechanisms involved in the connection between acid–base equilibrium and protein metabolism are certainly complex and still incompletely understood. Nevertheless, there is little doubt that glutamine is a key factor, as a precursor of ammonium and bicarbonate in kidneys (Welbourne & Joshi, 1990) as well as an effector of cellular metabolism, as shown in the liver through glutamine-induced p38MAPK activation mediating the inhibition of autophagic proteolysis at the level of autophagosome formation (Häussinger et al. 2001). In the same way, even small corrections of serum bicarbonate in acidotic subjects apparently promote the downregulation of branched-chain amino acid degradation (Rodriguez-Bayona & Peragon, 1998) and muscle proteolysis via the ubiquitin–proteasome system which plays a central role in the control of the proteolytic pathway (Combaret et al. 2001; Pickering et al. 2002)."

    "Acidosis and peroxidation of biological structures

    An acidification of extracellular pH may enhance LDL oxidation, by shortening the ‘lag phase’ and accelerating hydroperoxides and thiobarbituric acid-reactive substances formation. These alterations themselves promote their uptake by macrophages (Morgan & Leake, 1995). One of the mechanisms whereby variations of acid–base equilibrium might affect the processes of peroxidation is by changes in bioavailability of cations such as Fe or Cu (Leake, 1997; Salovaara et al. 2002). Fe is carried by transferrin on specific clusters of amino acids and an acidification of plasma pH can protonate these amino acids and release Fe from its binding sites. However, this last effect is significant only for definitely acidic and unphysiological pH, sometimes lower than 6. Effects on Cu availability (Cu is considered as more potent than Fe to initiate LDL oxidation) through a release of Cu from caeruloplasmin are obtained with less drastic acidification (pH 7). It must be noted that these studies were generally carried out on ex vivo systems, which explains why severely disturbing or even potentially lethal pH values could be studied. Nevertheless, some authors consider that, in the presence of metabolic acidosis (ketoacidosis, renal deficiency) even effectively compensated with modest change in blood pH, the buffering capacity of interstitial fluid may be severely depressed, thus allowing the emergence of local sites of severe acidosis (for example, near atheromatous lesions where LDL oxidation chiefly takes place). Deleterious effects of a prolonged period of systemic acidosis could also affect the internal structures of tissues and cells, through various mechanisms such as intracellular K and Mg losses and Ca movements between its various subcellular pools."

    "Clearly, dietary factors affecting the amount of Ca lost in the urine have a major influence on Ca balance and may even be more important than those that modulate the intestinal availability of Ca. This is why the inevitable loss of Ca in the urine is greater for Western-type diets rich in factors such as animal proteins, sulfate, Na or coffee (Heaney & Recker, 1982; Guéguen & Pointillart, 2000). The critical determinant of hip-fracture risk in relation to the acid–base effects of diet is the net load of acid in the diet. Thus, it is worthwhile to consider decreasing the rate of bone attrition by the use of a diet favouring alkaline ash, which leads to the promotion of fruit and vegetable intake (Remer & Manz, 1995; Frassetto et al. 1996). New et al. (1997, 2000) report that fruit consumption predicted greater bone density at all four bone sites measured in postmenopausal women and, when K was considered, Ca intake was no longer significantly related to bone mass. Tucker et al. (1999) have confirmed, in a cross-sectional and longitudinal study, that alkaline-producing dietary components such as K contribute to the maintenance of bone density. An increase in fruit and vegetable intake from 3·6 to 9·5 daily servings decreased urinary Ca from 157 (SD 7) to 110 (SD 7) mg/d v. a drop of 14 ± 6 in controls (Appel et al. 1997). In conclusion, greater attention needs to be paid to the causes of Ca loss, which should lower the Ca requirement. Indeed, urinary losses remain an important and inadequately appreciated aspect of Ca nutrition. A diet may be inadequate in Ca not simply because it is intrinsically Ca-poor but also because it is insufficient to offset excretory losses."​

    - Reducing the Dietary Acid Load: How a More Alkaline Diet Benefits Patients With Chronic Kidney Disease

    "The predominant anions in F&V are citrate and malate, and when metabolized, they release bicarbonate and thus contribute alkali to the body. In general, the amount of potassium present reflects the alkalizing ability of the F&V; thus, potatoes and squash have high alkalizing ability, and apples and pears have less alkalizing ability. However, F&V contain a wide variety of organic anions and not all those present will contribute alkali. For example, oxalate and tartrate anions cannot be metabolized. When these anions are present in large proportions in a food, for example, spinach contains more than 80% oxalate, then the potassium oxalate cannot be metabolized so does not provide any alkali and any oxalic acid present in the food will release H+ and thus add acid to the body. Some fruits (e.g., cranberries, prunes, plums, and some berries) contain benzoic and quinic acid which are metabolized by gut bacteria to hippuric acid and also increase acid excretion.62 However, the organic acid content of different F&V is not well documented and varies considerably with the variety, growing and storage conditions, and ripeness of the F&V. The absorption of anions may also be affected by the cooking methods used and other dietary constituents. Until there is a better understanding of this only F&V with high oxalate content has been discouraged."​

    - Alkalinization with potassium bicarbonate improves glutathione status and protein kinetics in young volunteers during 21-day bed rest

    "Alkalinization during long-term inactivity is associated with improved glutathione status, anti-inflammatory lipid pattern in cell membranes and reduction in protein catabolism at whole body level. This study suggests that, in clinical conditions characterized by inactivity, oxidative stress and inflammation, alkalinization could be a useful adjuvant therapeutic strategy."​

    - Non-Traditional Aspects of Renal Diets: Focus on Fiber, Alkali and Vitamin K1 Intake

    "The microbiota affects human pathophysiology through its metabolites, derived from the saccharolytic (fermenting complex carbohydrates) or the proteolytic (using aminoacids as alternative substrate for energy harvesting) catabolism of food reaching the colon [33]. While the former is believed to be a “beneficial” pathway thanks to the downstream metabolites (mainly Short Chain Fatty Aminoacids—SCFAs) with anti-inflammatory, immune-modulating and gut integrity-promoting action [34], an unbalance towards the latter is noxious because it results in overproduction of many toxic metabolites, such as amines, indoles, phenols, hydrogen sulphide and secondary bile acids [33,35]. For this reason, a “healthy gut” possesses a metabolism that is mainly saccharolytic [33,36]."

    "Moreover, uremia impacts the colonic environment exacerbating the dysbiosis status already present in CKD patients, often caused by dietary restrictions in fiber content [37] and altered assimilation of proteins in the intestine, leading to increased availability of colonic amino acids as fermentation substrates [38,39]. In a situation of impaired kidney filtration capacity, the colon acquires a replacement role for the excretion of urea and oxalate: this process alters colonic pH and promotes the overgrowth of potentially pathogenic, proteolytic microbial species, leading to a further increase of uremic toxins production, in a vicious circle [33]."

    "Fiber intake has a major role in the modulation of intestinal microbiota metabolism towards saccharolytic direction and in lowering proteolytic-derived uremic toxins [17,18,19,20]. Moreover, dietary fibers increase bowel transit. In contrast, constipation, or reduced bowel transit time, worsens microbiota dysbiosis and contributes to the uremic status and to electrolyte imbalance, namely hyperkalemia [21]."

    "Reduced bowel transit worsens microbiota dysbiosis and contributes to the uremia status and to electrolyte imbalance [21]. It is meaningful that, in an animal study, even treating the constipation alone with a pharmacologic approach resulted in microbial probiotic species recovery, and circulating microbial toxins reduction [41]."

    "Another pathologic aspect often observed in CKD patients is the “leaky gut” syndrome. Alteration of gut microenvironment, beyond promoting dysbiosis, causes the derangement of colonic epithelial barrier, leading to gut permeability. A leaky gut allows translocation to the circulation of bacteria and microbial fragments, such as bacterial lipopolysaccharides (LPS). This phenomenon is believed to trigger low-grade systemic inflammation, worsening a clinical frame already compromised by uremia [40].
    The good news is that microbiota metabolism is susceptible of manipulation by dietary matrices. Diets abundant in fiber-rich foods (fruits, vegetables and legumes), such as the Mediterranean or purely vegetarian diets, have the potential to shift the microbial metabolism in saccharolytic direction, with the release of SCFAs and the reduction of uremic toxins [19,20,33]."

    "Attention must be paid to serum potassium levels in patients on vegetarian diets. Although high dietary intake is not the main pathogenic factor of hyperkalemia, limitation of excess potassium load and cooking strategies should be implemented, together with close monitoring of serum potassium levels [45]. However, it is noteworthy that the increased risk of hyperkalemia [in people with kidney disease] due to high potassium load on vegetarian diets can be counteracted by the better correction of metabolic acidosis and the increased intestinal transit due to vegetarian diet. In CKD patients, no changes in serum potassium was observed using a vegan or an animal-based low-protein diet [46]. Similarly, during high-fruit intake, no hyperkalaemia episodes were reported [22]."

    "The adoption of a plant-based diet such as the vegan or the very low-protein diet has positive effects on the bowel status, reducing the microbial catabolites originated by protein intestinal fermentation. In particular, p-cresyl sulfate, indoxyl-sulfate and TMAO (Trimethylamine N-oxide, an organic compound in the class of amine oxides), are reduced by protein restriction [48,49,50]. Moreover, increasing the fiber content in a diet has a modulating effect on gut microbiota composition, reducing protein fermentative processes and proteolytic metabolites [19,20]."

    "[..]in the case of the very low-protein diet, supplementation of essential amino acids and ketoacids is mandatory to maintain a good nutritional status [70]. In addition, the exclusion of food of animal origin could determine a zinc deficiency. Zinc content in food of plant origin is lower than that of food of animal origin and scarcely absorbable due to the presence of fibers and phytate. Recently, it has been reported that zinc deficiency is seen in CKD patients and that heavy metal deficiency including zinc deficiency is one of the causes of Erythropoietin-resistant anemia [71]. Moreover, zinc deficiency is known to affect taste that is one of the most important factors in food choice, selection and consumption and it can affect appetite leading to dietary restrictions that could negatively impact nutritional and health status [72].​

    Adding the following because of the 'physiological processes' part:

    - Potassium - Wikipedia

    "Potassium is the eighth or ninth most common element by mass (0.2%) in the human body, so that a 60 kg adult contains a total of about 120 g of potassium.[51] The body has about as much potassium as sulfur and chlorine, and only calcium and phosphorus are more abundant (with the exception of the ubiquitous CHON elements).[52] Potassium ions are present in a wide variety of proteins and enzymes.[53]"

    "Potassium levels influence multiple physiological processes, including[54][55][56]:
    • resting cellular-membrane potential and the propagation of action potentials in neuronal, muscular, and cardiac tissue. Due to the electrostatic and chemical properties, K+
    • ions are larger than Na+
    • ions, and ion channels and pumps in cell membranes can differentiate between the two ions, actively pumping or passively passing one of the two ions while blocking the other.[57]
    • hormone secretion and action
    • vascular tone
    • systemic blood pressure control
    • gastrointestinal motility
    • acid–base homeostasis
    • glucose and insulin metabolism
    • mineralocorticoid action
    • renal concentrating ability
    • fluid and electrolyte balance"
    "Renal handling of potassium is closely connected to sodium handling. Potassium is the major cation (positive ion) inside animal cells [150 mmol/L, (4.8 g)], while sodium is the major cation of extracellular fluid [150 mmol/L, (3.345 g)]. In the kidneys, about 180 liters of plasma is filtered through the glomeruli and into the renal tubules per day.[65] This filtering involves about 600 g of sodium and 33 g of potassium. Since only 1–10 g of sodium and 1–4 g of potassium are likely to be replaced by diet, renal filtering must efficiently reabsorb the remainder from the plasma."

    "With no potassium intake, it is excreted at about 200 mg per day until, in about a week, potassium in the serum declines to a mildly deficient level of 3.0–3.5 mmol/L.[71] If potassium is still withheld, the concentration continues to fall until a severe deficiency causes eventual death.[72]"

    "Potassium can be detected by taste because it triggers three of the five types of taste sensations, according to concentration. Dilute solutions of potassium ions taste sweet, allowing moderate concentrations in milk and juices, while higher concentrations become increasingly bitter/alkaline, and finally also salty to the taste. The combined bitterness and saltiness of high-potassium solutions makes high-dose potassium supplementation by liquid drinks a palatability challenge.[85][88]"

    "Agricultural fertilizers consume 95% of global potassium chemical production, and about 90% of this potassium is supplied as KCl.[8]" "Most agricultural fertilizers contain potassium chloride, while potassium sulfate is used for chloride-sensitive crops or crops needing higher sulfur content."​
     
  20. OP
    Amazoniac

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    Returning to the idea of sulfur and protein..

    - Cysteine & Cystine Amino Acids

    "Cysteine is a sulfur-containing amino acid found in foods like poultry, eggs, dairy, red peppers, garlic and onions. It works as an antioxidant, in the production of collagen (a component of hair, skin and nails) and is also used in the body to create glutathione, another important antioxidant. N-Acetyl-cysteine (NAC) is the most-researched form of cysteine and as a medicine, may be used in the treatment bronchitis (Grandjean, Clin Ther 2000), alcohol and acetaminophen poisoning (Whyte, Curr Med Res Opin 2007), and for some symptoms of Alzheimer's disease (Adair, Neurology 2001). In supplements, cysteine and acetyl-cysteine have been promoted for hair growth (typically 500 mg), although evidence for this use is not conclusive (Franca, JCDSA 2013). Taking 600 mg of NAC twice daily has also been shown to reduce the development of flu-like illnesses (De Flora, Eur Respir J 1997). See the NAC Supplements Review for more about the clinical evidence for NAC, plus dosage, safety, and our tests of products.

    Cystine, which is formed from two cysteine molecules joined together, is more stable than cysteine, but may not be absorbed as well. This amino acid is also a component of hair, skin and nails. However, there is no evidence that supplementing with cystine improves hair, skin or nail health, and it is rarely used as a dietary supplement."​

    Using one of the diet examples that Danny Roddy gave in one of his videos, providing 138 g of proteid, with 2.5 g as methionine and 1 g as cysteine (the proportions differ from the averages used to calculate PRAL: lower methionine and cysteine content in protein and less, and the ratio of met/cys is higher here, I don't remember if it included cheese, but it might be an explanation). Even though oysters didn't provide much protein, they can add a lot of taurine (up to 1.2 g T (!) for every 100 g P; in the diet in question it was 1 g/85 g). I thought it could have a contribution, but apparently it doesn't. Once cysteine is oxidized to taurine, taurine itself won't increase the acid load.

    - Effects of protein, methionine, or chloride on acid-base balance and on cysteine catabolism (by the author of 'Biochemical, Physiological and Molecular Aspects of Human Nutrition')
    - The reactions of the sulfur-containing amino acids with phosphoric and sulfuric acids
    - The Sulfur-Containing Amino Acids: An Overview (structure of sulfur-containing amino acids)

    It seems that the acidifying potential ends up in the metabolism of sulfate and pirate.

    "Mammals are unable to oxidize taurine or to attack the carbon-sulfur bond, so microorganisms are essential to degrade this organosulfonate compound."

    I guess it's excreted intact. Therefore in more extreme cases in which reduction of protein consumption is advisable, taurine should be preferable to NAC or L-glutathiod; it will still spare cysteine for glutathiod synthesis. There's a book entitled 'Taurine in Health und Disease' which is great and has more details, it accepts readers of all skin colors.

    "It is possible that it would be advantageous to the animal to excrete excess nitrogen and sulfur as taurine under conditions of sulfur amino acid excess as this would not generate H+ or urea. On the other hand, under conditions in which proteid is being used for energy and/or gluconeogenesis (conditions in which we would expect (Travo, 2017-18) a mixture of amino acids to be available), conversion of sulfur amino acids to sulfate may be favored so that the carbon chain can be utilized for energy or gluconeogenesis."
    I just posted some days ago an article commenting that NAC supplementation for kidneys issues didn't lead to the expected positives outcomes, taurine seems safer for sparing cysteine to glutathione.​

    With protein restriction you run the risk of insufficient protein, requering muscle dawn break to compensate for it, which in turn will cause more issues than what you is trying to solve, but this time involving generalized stress. Gerson could've avoided the addition of pot cheese if more protein meant more problems, they were probably maintaining nitrogen balance before the extra protein.

    If animal protein avoidance improves your state, of course it doesn't mean that it's from a diminished acid load. It's more likely to be related to protein escaping weak digestion, nutrient deficiencies (example), gut infections (some toxic compounds derived from proteid), and so on.

    I'll leave you with these:

    From 'Clinical disorders of fluid and electrolyte metabolism (0070409935)', this book served as reference for various of these publications.

    "The ideal method [for potassium repletion] is undoubtedly in the form of food. However, acute potassium depletion arises in circumstances when the patient cannot eat or is actually vomiting, and the parenteral route has to be used."​

    - Acid–base balance and weight gain: Are there crucial links via protein and organic acids in understanding obesity?

    "A discussion of the dietary protein emerges somewhat central to the understanding of the concept of WG [Working Group] or WL [Waiting List] in relation to acid load. It is well-known that the dietary proteins are one the chief sources of the dietary acid load [45], especially in the form of methionine and cysteine. Methionine and cysteine are some of the few amino acids containing sulfur, the sulfur contributing to the dietary nonvolatile, fixed acid load [45]. This has been a reason to recommend animal protein limited diets [16], in order to control the dietary source of acids [26]. The strong sulfuric acid, when in excess of body requirements, requires to be excreted, one of the many reasons why CRD [Chronic Renal Disease] patients are also recommended protein limited diets."

    "A protein duality in acid–base studies has been reported [61]. Protein increases the total acid load but also allows the kidneys to increase their net acid excretion capacity (NAEC), so that the body can excrete the excess H+. This is a normal body compensatory process. Cysteine (a hydrophobic amino acid with a sulfhydryl group) is found in most protein sources but in very small quantities. Usually, therefore, it requires to be synthesized in the liver from methionine, an essential amino acid. Rich sources of methionine are meats, fishes, cottage cheese, to name the important. The very cysteine that contributes to the non-volatile acid load is also the rate-limiting step in the production of glutathione, the most common intracellular antioxidant, protecting cells from oxidative stress and cell death [62–64]. Animal studies show that an adequacy of the dietary sulfur amino acids determines the extent to which antioxidant defenses are maintained during inflammation [65]. This could exactly be a means to maintain a healthy aging process, since aging is associated with net altered gene expression leading possibly to a net higher production of reactive oxygen species (ROS) with time [66,67]. In fact, gerontology studies prescribe a consumption of adequate amounts of dietary protein from ‘‘high quality” sources as an important means to slow down or treat sarcopenia [68]. Interestingly, elderly compared to younger subjects had a depressed response to stimulation of muscle protein synthesis following administration of mixed meals due to a decreased ability to respond to anabolic stimuli, such as insulin. Likewise, the anabolic effect of amino acids seems blunted on low protein doses [69]. To summate, proteins are the building blocks of the body and while ad lib over-consumption, as with all excesses, would have deleterious consequences, it still does not gainsay an adequate requirement of it at all ages."

    "Taking another example of wasting in HIV/AIDs, which is characterized by loss of cysteine, methionine, and carnitine, it is known that the carnitine is synthesized from cysteine and lysine. Carnitine is normally found in high levels in muscles and is responsible for the transport of long-chain fatty acids into mitochondria for beta oxidation."

    "Thus, a dearth of cysteine or in general ‘‘high quality” proteins could mean a reduction in the amount of glutathione antioxidant, and possible accumulation of adipose tissue, which a low to no protein intake, quantity and quality, would only acerbate. Regulated protein consumption, including high quality red meats, would help maintain carnitine and glutathione levels. A third example would be in maintenance of the bone-protein-collagenmatrix [70,71]; even so excessive consumption of the non-neutralized dietary proteins could result in bone calcium leaching [11,12,19,23,24,72]. The lack of adequate concomitant consumption of alkalis (vegetables and fruits, base supplements), rather than the protein, is probably responsible for the leaching [73], which is characteristic of Western diet [7,26,58,74]. This reduction in alkali consumption is possibly what needs rectification [19] rather than decreasing protein consumption."

    "The keto acids are one the major endogenous organic acids. In the 1980s there was a row of experiments conducted by Chalmers et al. [76] which went to show that in relatively healthy subjects the total organic acid excretion hardly varies. Another independent study reported that the production of keto acids increases in subjects who ingested alkalis, specifically, sodium bicarbonate [77]. This implies if the body has a greater intake of dietary net alkalis, the body produces more organic keto acids of purely endogenous origin. Thus, a relative constancy in organic acid excretion having accounted for body size is possible even on net alkaline diets [75]. The study by Hood et al. [77] reported that in conditions of moderate acid load there was a reduction in organic keto acid production of endogenous origin. Thus, with acid ingestion it seems that the body down-regulates endogenous production of organic keto acids and would in preference excrete the exogenous, dietary organic acids, thereby maintaining a relatively constant net organic acid excretion, once corrected for body surface area."

    "Metabolic acidosis itself has been reported to decrease thyroid hormones and hence their functions (nitrogen balance, protein synthesis, lean body mass, insulin-like growth factor I, cardiac contraction, and renal acidification) [13]. Thus, a higher H+ could inhibit thyroid hormone function [13]. Thyroid hormone is also reported to regulate proton leak and indirectly heat production [83,84] leading to lower resting metabolic rates, resulting in a obesity not responsive to dietary interventions [80]."

    "A study on 12 animal species, including humans, reported that [excess] H+ itself can inhibit mitochondrial energy production (MEP) [85] (sections ‘Weight gain on acidogenic diets’ and ‘The organic acid conundrum’) explained via inhibition of TCA [78] and accumulation of lactic acid on Western diets. The latent acidosis on Western diets could lead to lactacidosis when not efficiently or effectively compensated via the respiratory route could imply a prolonged exposure to acidosis (latent or metabolic). The inhibition of the MEP due to acidosis could divert the electrons in the production of ROS [67], possibly explaining disease development and aging with time (age), as put forward in the straight-line hypothesis (Fig. 1). This hypothesis is corroborated with the observation of elevated ROS and cytokines in diabetics [86]. This lactate production cannot be confused with anaerobic lactate production which is a normal body response to exercise [87,88], which, in health is compensated by the respiratory route [89]. Section ‘The organic acid conundrum’ reviewed the H+ due to lactacidosis. This acidosis could inhibit thyroid functioning and the proton leak making the symptom of low heat production and lower MEP occur simultaneously (Fig. 3). The lower energy required for maintaining RMR would partly adjust the lower MEP; i.e., the body would down-regulate its energy requirement as adjustment."

    "A protein deficient diet would intensify the loss of muscle protein on acidogenic diets (section ‘The protein conundrum’). This suggest that what is required is not a protein-deficient diet but a balanced diet providing both high quality proteins with high intake of alkalies (vegetables and fruits, base supplements) so that the acid anions of the protein intake get neutralized [19]. There are studies that mention the benefit of acid load neutralized diets [96,97] which was associated with lower skeletal mass catabolism and improved protein turnover."​
     
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