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

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Amazoniac

Amazoniac

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From a mail of haidut :

Heavy limbs, especially legs and quickly getting tired/sore when I do my daily 20 pushups is a good indication for me that lactic acid is high and I need some thiamine or methylene blue.​
Това е лъжа. We can't feel the earth bouncing at any time during the day.

- https://www.ajemjournal.com/article/S0735-6757(17)30380-7/fulltext
- Severe lactic acidosis reversed by thiamine within 24 hours

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https://www.researchgate.net/profile/Michael_Wiederkehr

Core Concepts and Treatment of Metabolic Acidosis

"Acidosis does not invariably induce acidaemia. There are numerous clinical scenarios of discordance between acidosis and acidaemia such as mixed acid-base disorders (metabolic acidosis and respiratory alkalosis) [1], high proteid induced positive acid balance (normal plasma pH and boner buffering) [2], and potassium deficiency (total body acidosis with extracellular alkalemia) [3]."

"[..]the HCO3-/CO2 system is more effective against alkalemia than acidemia."

"Chronic metabolic acidosis induces proteid catabolism through the ubiquitin-proteasome pathway and the growth hormone/IGF-1 axis [41, 42]. In healthy adults, chronic metabolic acidosis suppresses albumin synthesis, increases glucocorticoid levels and urinary nitrogen excretion, and induces growth hormone insensitivity [43, 44]. It also reduces thyroid hormones with elevated TSH [45]."

"[..]metabolic acidosis induces lower insulin secretion and insulin resistance [51]."

"[..]simply replacing HCO3- (or equivalent buffer) without attempting to arrest the underlying disturbance is unacceptable. All efforts must be directed to reversing the condition that led to the owaproduction of acid."

"Simply treating the acidosis with base is not only of little benefit, as ongoing production of the organic anion is overwhelming, but also potentially deleterious [extreme cases]."

"[..]These considerations highlight the limitations of sodium bicarbonate therapy, especially for an organic metabolic acidosis, as it is a manifestation of an underlying pathologic process and not a disease in itself. The focus of therapy should therefore be on reversing the pathophysiologic process, not on alkali therapy. Successful treatment leads to diminished production of organic acids and enhanced clearance by liver and kidneys, with hepatic and renal regeneration of bicarbonate within hours. Replenishment of extracellular buffer alone is unlikely to provide benefit.

This needs to be distinguished from situations where a non-metabolizable anion cannot be converted to bicarbonate, as in mineral hyperchloremic acidoses, or when non-metabolizable organic acids are overwhelmingly generated, as with certain alcohol poisonings (oxalate and formate anions from ethylene glycol and methanol, respectively). These patients could benefit from exogenous alkali therapy, since endogenous (renal) regeneration of bicarbonate [in these cases] occurs only slowly over several of the days."

"Bicarbonate therapy may also lead to a drop in ionized calcium with a resultant negative inotropic effect on the heart [84]. Hypocalcemia in the setting of hyperkalemia may precipitate cardiac arrhytmia."

"[..]the relentless production of large amounts of lactic acid, especially in the setting of reduced hepatic (and renal) clearance, is often overwhelmingly larger than the amount of alkali that can be infused."

"Thiamine pyrophosphate is a cofactor for pyruvate dehydrogenase necessary for conversion of pyruvate to acetyl CoA. In thiamine deficiency, pyruvate accumulates and is metabolized to lactic acid."

"In H and I and V infected patients receiving therapy with nucleoside-analogue reverse transcriptase inhibitors (zidovudine and stavudine), lactic acidosis develops due to direct mitochondrial toxicity. Affected individuals present with chronic and asymptomatic hyperlactaemic states [85]."

"[In] chronic liver disease [] patients often exhibit some degree of renal impairment; however, progression is slow and may even extend over months to years (hepatorenal syndrome type II). The acid-base derangement is usually a combination of respiratory alkalosis (central stimulation) and metabolic acidosis due to a combination of reduced hepatic metabolism of lactic acid (anion gap) and renal failure (mainly non-anion gap)."

"[D-Lactic acidosis] is an unusual form of lactic acidosis occuring in patients with small bowel malabsorption and bacterial overgrowth, often in the setting of short-bowel syndrome after resection or after bypass surgery. A large carbohydrate load is delivered to the colon providing substrate for bacterial fermentation to both L- and D-lactic acid (humans are only able to synthesize the L- form). Following systemic absorption, L-lactate is rapidly metabolized by its dehydrogenase providing the base to neutralize the H+ absorbed. However, D-lactate accumulates due to its much slower metabolism [155]. [Again, serum] lactic acid levels are normal by standard testing as D-lactate is not detected. This requires a specific D-lactic dehydrogenase assay. Patients present with crampy abdominal pain and diarrhea and an osmolar and anion gap. They may exhibit acute encephalopathy, probably a direct neurotoxic effect of D-lactate. Some patients present without associated acid-base abnormalities or a near-normal anion gap with hyperchloremia (the drop in serum bicarbonate is larger than the anion gap). The likely explanation is the renal excretion of [Na+]- or [K+]-D-lactate. Another scenario is gastrointestinal absorption of H+ without D-lactate in exchange for Na+ or K+."

"A cheap and highly effective way of delivering oral base is baking soda, providing 12 mEq HCO3-/g. A flat teaspoon provides roughly 6 g or 72 mEq. The main drawback is the high sodium load, which promotes fluid retention and puts the patient at risk for heart failure and pulmonary congestion."

"[A] K+ load [] is contraindicated in patients with hyperkalemia or advanced stages of CKD. Conversely, the combination of metabolic acidosis and hypokalemia often indicates a significant potassium deficit, and treatment with K-containing base is preferred. Furthermore, a rising pH may aggravate hypokalemia by intracellular translocation."


Disorders of Potassium Balance: Hypokalemia & Hyperkalemia
 

Richiebogie

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Is bicarbonate OK to take before intense exercise, to counteract lactic acid? What proportion of potassium/sodium bicarbonate should be ideal prior to execise (sweating)? 1:1?

Do not take either of these. According to the post before yours, the bicarbonate will neutralise your stomach acid and allow bad bacteria through.

Rather eat more fruit and OJ to obtain potassium (K+) and take just a little table salt = sodium chloride (NaCl).

Fruit combats lactic acid and will allow you to exercise for longer in a safer way.
 

Jennifer

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@MCF — Nope, I didn't add salt to my dog's diet.
@Amazoniac — Good info as usual, but something in citation 2 seems a bit off to me. :confused2
 
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Amazoniac

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Medicinal use of vinegar should be accompanied by a diet rich in potassium alkali salts to avoid possibility of low grade metabolic acidosis

Abstract:
"Although daily ingestion of vinegar may help manage blood glucose, vinegar can decrease urine pH and possibly exacerbate low grade metabolic acidosis (LGMA). We examined if daily ingestion of vinegar or control would decrease urine pH in a randomized, crossover trial. Because change in urine pH may be buffered by dietary intake of potassium (K) alkali salts, we also determined the impact of K status on urine pH during the trial. Healthy subjects (3 M, 7 F, age 27.7±3.1 y [mean±SEM], BMI 24.9±2.0 kg/m2) ingested 2 tablespoons of vinegar (VIN) or cranberry juice (CON) twice daily for 3 d with a 2 wk washout period. While no pH change was noted with the CON treatment, mean 24 h urine pH after 3 d with the VIN treatment was significantly more acidic if K status was low versus adequate (pH 5.62±0.10 versus 6.24±0.11, P=0.015). Low K status was defined as baseline 24 h urine K <50 mmol/L (n=3). Thus, it appears that high intake of K-alkali salts enhances base-forming capacity to buffer the acid load associated with vinegar. Persons using vinegar medicinally may benefit from consuming vinegar with K-alkali rich plant foods to avoid LGMA. This research was supported by the ASU Nutrition Research Fund."​

I think they were so ashamed of their publication that they decided to remove from.. circulation. Or their relatives alerted them: "Don't do that to your career, you have such a bright future." I couldn't find it available anywhere.

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@Amazoniac — Good info as usual, but something in citation 2 seems a bit off to me. :confused2
What did you find odd? Could've been that I cut pieces of the text and if you read them out of context, they don't make sense.
 
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Peater Piper

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So could high doses of ascorbic acid (supplemented, not ingest through food) push the body toward acidosis?
 

yerrag

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So could high doses of ascorbic acid (supplemented, not ingest through food) push the body toward acidosis?
Not aware of it. The body will absorb the vitamin C it needs, and what it doesn't need will go thru the intestines, and be discharged or flushed, as the intestines will not tolerate the acidity.

But not all the absorbed vitamin C is used, and it is excreted by the kidneys through urine.

I have used 6 grams of ascorbic acid daily for 7 months. It does not cause me to urinate much more than usual a sign I think that my acid-base balance us within norms. When I used magnesium chloride in large quantities, I was urinating a lot, and it was because the low absorption of the magnesium caton coupled with the high absorption of the chloride anion created a significant acidic load, and this required the kidney to excrete it through urine.

The pKa of ascorbic acid is low as well. pKa is used to determine the acidity of substances.
 

tara

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So could high doses of ascorbic acid (supplemented, not ingest through food) push the body toward acidosis?
I would expect there might be a risk of that, if one is already leaning towards acidosis, and does does not have sufficient alkaline minerals in buffers and diet to balance it.

I'm somewhat influenced by Reams, who I think said that it was generally helpful to supplement vit-C when UpH was too high, but tended to do more harm when UpH was too low (and the reverse for vit-D).
 

Peater Piper

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But not all the absorbed vitamin C is used, and it is excreted by the kidneys through urine.

I have used 6 grams of ascorbic acid daily for 7 months. It does not cause me to urinate much more than usual a sign I think that my acid-base balance us within norms. When I used magnesium chloride in large quantities, I was urinating a lot, and it was because the low absorption of the magnesium caton coupled with the high absorption of the chloride anion created a significant acidic load, and this required the kidney to excrete it through urine.
I'm unsure of how the kidneys excrete the excess. Does it complex it with a mineral...or something else? I'm just doing a short term experiment with high doses. I've worked up to 15 grams a day thus far. I don't really plan to stick with it long enough that it should cause any issues, but I'm still curious if I'm losing minerals in the process. I have heard of people taking VERY high doses for years without any apparent negative effects, so maybe it's not an issue. Do you take ascorbic acid with or away from food? I also haven't noticed much, if any, increase in urine output, so by that test I'm okay.

I would expect there might be a risk of that, if one is already leaning towards acidosis, and does does not have sufficient alkaline minerals in buffers and diet to balance it.

I'm somewhat influenced by Reams, who I think said that it was generally helpful to supplement vit-C when UpH was too high, but tended to do more harm when UpH was too low (and the reverse for vit-D).
Hmm. I do have some test strips. In the past I noticed my urine was quite acidic (below 6 at times) first thing in the morning and shortly after meals. A few hours after meals the pH would return to 7 or so. I'll have to see how the ascorbic acid is affecting it.
 

tara

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Hmm. I do have some test strips. In the past I noticed my urine was quite acidic (below 6 at times) first thing in the morning and shortly after meals. A few hours after meals the pH would return to 7 or so. I'll have to see how the ascorbic acid is affecting it.
I haven't learned about the short term effects on UpH of night-time, meals etc, but I believe there are some. Could be the early morning and post meal readings are not representative, but I'm not sure. Peat reckonned 24 hr Uph in the range 6.3-6.7 was good. Corresponded pretty well to Reams 6.2-6.8 healing range, but he had preferred times to test, and they may have related to preferred meals times or something too, and he also had a regular drinking schedule to follow.
 

yerrag

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I'm unsure of how the kidneys excrete the excess. Does it complex it with a mineral...or something else? I'm just doing a short term experiment with high doses. I've worked up to 15 grams a day thus far. I don't really plan to stick with it long enough that it should cause any issues, but I'm still curious if I'm losing minerals in the process. I have heard of people taking VERY high doses for years without any apparent negative effects, so maybe it's not an issue. Do you take ascorbic acid with or away from food? I also haven't noticed much, if any, increase in urine output, so by that test I'm okay.

I don't know if you've determined your daily vitamin requirements using Cathcart's Vitamin C Flush Test. The healthier you are, the less you need Vitamin C. You don't have to work up your vitamin C daily intake once you know what you need. Even with that determined, you will expect that not all the vitamin C you take in will be used, but the more you spread out the intake throughout the day, the more will be absorbed, and the less will be excreted. I don't really know if on the way out thru urine whether it complexes with other minerals. That's a good question, but not something I have encountered being mentioned in what I have read. I try to take ascorbic acid away from food, as there is a belief that vitamin C increases iron absorption, and too much iron isn't good, but there are studies that refute that as much as studies that support that. For me, I'd rather be safe and take it away from meals. I didn't experience increased urine output from taking vitamin C, although the daily amount I'm taking is 6 grams, and that doesn't represent higher intake quantities.

At larger quantities, it becomes necessary to use intravenous application of sodium ascorbate, as oral intake isn't practical, the reason which escapes me. To minimize excretion losses, and to make it unnecessary to take in Vitamin C throughout the day, liposomal C can be taken. Because there is much less excretion losses, less liposomal vitamin C can be taken. It is more costly, but if it's more effective it may be worth paying for. The most known brand is LivOn. But I'm going to try making my own liposomal C this weekend. I have to see if it can work better for me. I am using vitamin C to chelate lead from my kidneys.
 
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Amazoniac

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So could high doses of ascorbic acid (supplemented, not ingest through food) push the body toward acidosis?
tara should be correct.
Vitamin C and Acidity
They already provided the solution: to neutralize with a bicarbonate salt. If you need more vit C but are on the latency of acidosis, supplementation can be conflicting. People that suspected a deficiency but didn't benefit as much must try such thing.

https://raypeatforum.com/community/...-explanation-inside-possible-treatment.24416/
 

Lutzzy

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

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

Lutzzy

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Nitrates are one avenue but those are aso the most heavily pesticided foods, maybe try sprouting these without the Monsatan factor.
 
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Lynda Frassetto and team decided to address:
Acid Balance, Dietary Acid Load, and Bone Effects—A Controversial Subject

"Elegant quantitative analyses by Oh and Uribarri in subjects with chronic metabolic acidosis (where the blood pH is often below the normal lower limit of 7.35) argue that the 12–19 mmol of acid per day that these subjects retain would need to be buffered by an equal amount of base. Bone made up of calcium hydroxyapatite contains ~25,000 mmol of alkali and at the rate of 19 mmol/day, the alkali supply would be exhausted in less than 4 years. Instead, they argue that production of both organic acids and sulfuric acid is decreased in advanced renal failure and the rest of the acids are eliminated in some unknown and therefore unmeasured form."

"Macdonald et al. [36] conducted a 2-year randomized placebo-controlled trial in 276 postmenopausal women aged 55–65 years. Subjects were randomized to 4 groups: high-dose K-citrate (55.5 mEq/day), low-dose K-citrate (18.5 mEq/day), placebo, or 300 g additional fruit and vegetables per day (equivalent of 18.5 mEq alkali). This study was able to conceal the allocation to the study groups by concealing the process and therefore is of quality. The results showed no persistent changes in bone turnover or bone mineral density over two years with a daily dose of 18.5 or 55.6 mEq K-citrate or with self-selected fruits and vegetables per day, which is more likely to be an accurate reflection of the truth since the randomized design is less likely to be biased."

"A retrospective two-center analysis of 266 otherwise healthy postmenopausal women given alkali therapy for at least 2 years by Frassetto et al. [37] demonstrated no relationship of blood pressure responses to Na, Cl, or K intake and bone mineral density response to diet alkali therapy."

"Thus, in [] two relatively long-term randomized, controlled trials in mostly older Caucasian women who would be expected to be at risk for lower bone mass, neither study demonstrated significant changes in bone density."

"Fenton et al. [38] with superior methodology carried out a meta-analysis to assess the effects of changes in net acid excretion from changes in diets or “alkaline” supplements on both urine calcium and calcium balance in studies of calcium metabolism. These studies, investigated alterations to calcium balance as a result of alterations to either the quantity and/or the type of protein. Analyses demonstrated a significant linear relationship between an increase in urinary net acid excretion (NAE) and urinary calcium (p < 0.0001), but no changes in calcium balance (p = 0.38; power = 94%). No relationship was noted between a change of NAE and a change in the marker of bone resorption, N-telopeptides (p = 0.95). This meta-analysis had sufficient power because variability between subjects was eliminated by the use of cross-over designs in the included studies and systematically assessed the calcium balance literature in response to changes of NAE. Calcium balance is a surrogate measure of bone disease progression but does not directly measure either bone health or changes to bone health."

"Thus, even in these larger scale studies, the authors found no evidence of an effect of diet acid load on not just bone density, but fracture incidence."

"We suggest the way to put all of this information together is to agree with Oh and Uribarri that bone alone cannot buffer the positive acid balance that one can calculate from measures of acid production and acid excretion. In addition, endogenous acid production goes up and down in an attempt to maintain systemic blood pH. Younger subjects with better renal function are able to maintain their blood pH in the higher range of normal, while older subjects with worse renal function are only able to maintain their blood pH in the lower ranges of normal. As renal function declines, renal acid production goes down, but not as much as renal acid excretion and the tradeoff is that the blood acid levels and therefore acid balance are higher. These higher acid levels appear themselves to lead to more rapid damage to the kidneys [48,49].

Diets high in acid precursors add to the body’s acid burden. For the majority of people eating typical western diets with acid loads of ≤1 mmol/kg, whose renal function and acid excretory ability is normal, dietary acid loads would not be a readily detectable factor in altering bone mineral density leading to the development of osteoporosis. Other factors such as age, gender, race, and immobility are quantitatively more major factors in determining bone mass and bone breakdown.

However, body retention of only 1 or 2 mEq of acid each day, barely detectable by current measurement techniques, buffered by muscle and kidney and titrated by skeletal base over decades, could potentially result in major depletion of bone mineral. Thus, we suggest that those older subjects with diminished renal function, decreased renal acid excretory ability, and lower buffering capacity due to lower muscle and/or bone mass, whose diets contain high net acid loads could potentially benefit the most from alkali therapies."
 

Lutzzy

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I would expect there might be a risk of that, if one is already leaning towards acidosis, and does does not have sufficient alkaline minerals in buffers and diet to balance it.

I'm somewhat influenced by Reams, who I think said that it was generally helpful to supplement vit-C when UpH was too high, but tended to do more harm when UpH was too low (and the reverse for vit-D).

Reams was always mixing minerals as he did milk and grapefruit juice at same meal...Any one mineral can counterbalance the load....like zinc and copper work together...the atp cycle works with potassium, magnesium, calcium balances to give you energy...Doing a calcium and a vitamin C every hour proved to be great after 30 days we all had better skin, less broken veins, and less complaints... But it was hard to follow in the 70's and would be even harder today. The 4 oz lemon water and 4 oz distilled water cleaned up our liver....but carrying a 1/2 gallon of lemon water and 1/2 gallon of distilled water proved to be a little much for most of our group..We did few supplements extra ..... alfalfa tablets everymeal......The group I attended with was Seven Day Adventists....The distilled water was a great healer, removing stress and salts from your body...worry lines disappered from the forhead....If you are going to do the program it works best all together not disected apart. I think his secret was balance. Commercial Ag today would have Reams turning over in his grave, as he was big on organic gardening and these guys today are into getting it to market and radiating and spraying it with chemicals to make it stay on the shelves for weeks.
 

Jennifer

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@Lutzzy — Oh, neat! You follow(ed) RBTI. I followed the program (was under the care of Su Aberle from Promise Outreach). Unfortunately, I only got worse while following the program, but I have a lot of respect for Su and she was spot on about my weak kidneys and exposure to mold. She was also the first person to make me aware of estrogen's role in osteoporosis and the benefits of natural progesterone.
 

tara

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EMF Mitigation - Flush Niacin - Big 5 Minerals

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