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

[Amazoniac]

His British accent is outrageously un-British.

He's Egyptian, but we continue not knowing if internet is available inside pyramids since the guy lives now in the US and probably uploaded the videos at Starbucks or while queued lined in front of an Apple store. Check out the rest of his work, you won't regret.

Regarding the last video posted, varying waste productide (CO2 being responsible for the shift) should have a shy effect on how loaded hemoglobins is at the lungs level because it's in close contact with the environment and the air we breathe is determinant to the usual oxygen tension (high in relation to that of other tissues).

Spoiler

Source: WWW.

Die 'cooperativity' that they mentioned would work great when the situation is critical and away from there, with excess activity getting you closer to the state represented by the steep part of the curve with greater dissociation of oxygen.

Spoiler

Source: online.

If tissues' functioning is compromised but with enough oxygen yet inability to use it, what's the point of calling for more oxygen? It must be taxing in one way or another. Some people don't mind attempting to increase waste productide at all costs to the point where burnium is dismissed, but if we can't burn out food, we is the one to be burned. It's not questioned whether there will be bad consequences.

But here's an immediate value in doing so..

- Are Oxalates A Concern?

"If you blow out too much carbon dioxide, the pH of your urine goes up to keep your blood at the right pH, slightly alkaline."​

 

[Kvothe]

If tissues' functioning is compromised but with enough oxygen yet inability to use it, what's the point of calling for more oxygen? It must be taxing in one way or another. Some people don't mind attempting to increase waste productide at all costs to the point where burnium is dismissed, but if we can't burn out food, we is the one to be burned. It's not questioned whether there will be bad consequences.

I don't understand - what is burnium and what are the bad consequences you imply?

 

[Amazoniac]

I don't understand - what is burnium and what are the bad consequences you imply?

It's a signal of increased tissue activity, which will call for more oxygen (or burnium in Prolactinese); the metabolism is increased at a time when the body could be trying to conserve energy because it might be lacking the factors needed for production. There's little encouragement for finding a sweet spot, only that it must be good to increase it through multiple means.

If you want to ruin people's progress in not fapping, just upload an image of a factory emitting gases and they'll have to restart with a new vow. We can argue that there's more stuff in it, but so there is in the air we breathe and the rest is ignored anyway.
It's akin to active thyroid hormone: when something is off and not working, it's because there isn't enough provided yet. A 'Low WP2 Syndrome'.

 

[Amazoniac]

- Berne and Levy Physiology (9780323523417)

Spoiler

- Gas production after reaction of sodium bicarbonate and hydrochloric acid

"The reaction of HCl and NaHCO3 to form carbonic acid and sodium chloride is instantaneous; hence, sodium bicarbonate is a rapidly acting antacid (1). The decomposition of carbonic acid to CO2 (and water) accounts for the second characteristic effect of sodium bicarbonate when taken for indigestion, i.e., the facilitation of a belch. However, little is known about the rate of release of CO2 gas when sodium bicarbonate is added to a solution containing hydrochloric acid, and belching does not always follow ingestion of sodium bicarbonate."​

- Protein Function ATP Synthase adds phosphate to ADP Zinc-finger nuclease cleaves nucleotides in DNA | Alexandrina Park

Spoiler

- Buffering in acute respiratory acid-base disturbances | Deranged Physiology

Spoiler

 

[Amazoniac]

- Diagnosis and Treatment of Metabolic Acidosis in Patients with Chronic Kidney Disease – Position Statement of the Working Group of the Polish Society of Nephrology

Spoiler

"In patients with chronic kidney disease (CKD), the causes of metabolic acidosis include: impaired ammonia excretion, decreased tubular reabsorption of bicarbonate and insufficient production of bicarbonate in relation to the amount of acids synthesised in the body and ingested with food. The loss of more than 80% of nephrons impairs base regeneration by the process of ammoniagenesis [1]. Although there is a compensatory increase in ammoniagenesis (by more than two-fold) in remaining nephrons, the plasma concentration of bicarbonate decreases [2]. The concentration of bicarbonate, as well as carbon dioxide, in the plasma may be decreased even in patients with moderate renal impairment. This early decrease of bicarbonate concentration is compensated by an increased concentration of chloride and does not lead to change of the anion gap [3]. In patients with more advanced CKD, plasma bicarbonate concentration is more reduced and in these patients an increase in the anion gap is observed [3, 4]."

"In patients with CKD of different aetiologies in stages 1–4 and 5 not yet requiring dialysis and not treated with sodium bicarbonate, the blood bicarbonate concentration shows a positive correlation with glomerular filtration rate (GFR) [8]. Metabolic acidosis usually develops when GFR is decreased to 20-30 ml/min [9]. More severe metabolic acidosis accompanies renal diseases in which tubulo-interstitial damage predominates [10]. Metabolic acidosis can also occur at earlier stages of CKD with the co-occurrence of renal tubular dysfunction, e.g. in hyporeninemic hypoaldosteronism accompanying longstanding diabetes [11 - 13]."

"Chronic metabolic acidosis increases protein catabolism and thus contributes to the pathogenesis of the malnutrition-inflammation-atherosclerosis (MIA) syndrome [14, 15]. Metabolic acidosis contributes to the development of the inflammatory process in CKD patients. In an acidic environment, the production of tumour necrosis factor-alpha (TNF-α) by macrophages increases [16]. In children with CKD, metabolic acidosis leads to impairment of growth by inhibiting the secretion of growth hormone (GH), reducing its activity in peripheral tissues and distorting the activity of the GH - insulin-like growth factor 1 (IGF-1) axis, with reduction of the serum concentrations of free IGF-1 and GH, and increase of plasma IGF-1 binding proteins [17, 18]. In adults, these abnormalities may contribute to the pathogenesis of malnutrition. Metabolic acidosis adversely impacts calcium-phosphate metabolism in patients with CKD by reducing calcium receptor sensitivity as a result of the decrease in the intracellular pH [?], and by stimulating the parathyroid glands to secrete parathyroid hormone [19]. It also contributes to the mobilisation of bone bases, stimulates osteoclasts, and inhibits the activity of osteoblasts [20]. In addition, metabolic acidosis stimulates bone turnover, thus increasing the risk of osteoporosis."

"Metabolic acidosis may increase the serum β2-microglobulin concentration and contribute to the development of β2-microglobulin amyloidosis [21]. In patients with CKD without diabetes, low plasma bicarbonate concentration and metabolic acidosis are factors influencing the severity of insulin resistance, and alkalisation with sodium bicarbonate increases insulin sensitivity [22-24]. In patients with CKD who have hypertriglyceridemia, the administration of sodium bicarbonate results in the reduction of serum triglycerides concentration [25]. In CKD patients, metabolic acidosis impairs the peripheral conversion of thyroxine into triiodothyronine, which results in the reduction of the serum triiodothyronine concentration [26]. In addition, the results of animal experiments suggest that metabolic acidosis in patients with CKD increases the serum hepcidin concentration, and thus participates in the pathogenesis of anaemia of chronic disease [27, 28]. It has been shown that in CKD patients treated with haemodialysis, metabolic acidosis increases the demand for erythropoiesis stimulating agents [29]."

"In order to determine metabolic acidosis in patients with CKD, it is recommended that the venous plasma or venous whole blood bicarbonate concentration should be measured. Due to the risk of bleeding, local complications associated with the arterial puncture and the need to spare arteries for the future access for hemodialysis, arterial blood sampling is not recommended for this purpose. It is important mind the potential impact of ischemia of the forearm while sampling venous blood due to transient venous stasis on blood/plasma pH value and bicarbonate concentration. This phenomenon may lower pH and bicarbonate concentration of venous blood in the upper extremity and as a consequence lead to overdiagnosis of metabolic acidosis. For this reason, duration of ischemia must be minimalized and we suggest blood sampling by an experience personnel."

"In patients with metabolic acidosis and chronic kidney disease, the use of oral sodium bicarbonate is recommended (recommendation based on the results of interventional studies)."

"Based on results of available clinical trials we suggest an initial daily dose of 1-2 g of sodium bicarbonate. Subsequently, while monitoring the venous plasma and venous blood bicarbonate concentration, the dose of sodium bicarbonate should be increased until the target bicarbonate concentration, i.e. equal to or greater than 22 mmol/l, is achieved. Due to the lack of data on the safety of sodium bicarbonate used in high doses, in the opinion of the authors a maximal daily dose of 6 g of sodium bicarbonate should not be exceeded."

"Treatment of metabolic acidosis with sodium bicarbonate at the most commonly used doses, i.e. 2-3 g/day, may sometimes lead to the development of metabolic alkalosis. Therefore, in the course of alkali therapy, the plasma or venous blood bicarbonate concentration should be checked periodically to prevent the process of excessive alkalisation."

 

[Kvothe]

- Diagnosis and Treatment of Metabolic Acidosis in Patients with Chronic Kidney Disease – Position Statement of the Working Group of the Polish Society of Nephrology

Spoiler

"In patients with chronic kidney disease (CKD), the causes of metabolic acidosis include: impaired ammonia excretion, decreased tubular reabsorption of bicarbonate and insufficient production of bicarbonate in relation to the amount of acids synthesised in the body and ingested with food. The loss of more than 80% of nephrons impairs base regeneration by the process of ammoniagenesis [1]. Although there is a compensatory increase in ammoniagenesis (by more than two-fold) in remaining nephrons, the plasma concentration of bicarbonate decreases [2]. The concentration of bicarbonate, as well as carbon dioxide, in the plasma may be decreased even in patients with moderate renal impairment. This early decrease of bicarbonate concentration is compensated by an increased concentration of chloride and does not lead to change of the anion gap [3]. In patients with more advanced CKD, plasma bicarbonate concentration is more reduced and in these patients an increase in the anion gap is observed [3, 4]."

"In patients with CKD of different aetiologies in stages 1–4 and 5 not yet requiring dialysis and not treated with sodium bicarbonate, the blood bicarbonate concentration shows a positive correlation with glomerular filtration rate (GFR) [8]. Metabolic acidosis usually develops when GFR is decreased to 20-30 ml/min [9]. More severe metabolic acidosis accompanies renal diseases in which tubulo-interstitial damage predominates [10]. Metabolic acidosis can also occur at earlier stages of CKD with the co-occurrence of renal tubular dysfunction, e.g. in hyporeninemic hypoaldosteronism accompanying longstanding diabetes [11 - 13]."

"Chronic metabolic acidosis increases protein catabolism and thus contributes to the pathogenesis of the malnutrition-inflammation-atherosclerosis (MIA) syndrome [14, 15]. Metabolic acidosis contributes to the development of the inflammatory process in CKD patients. In an acidic environment, the production of tumour necrosis factor-alpha (TNF-α) by macrophages increases [16]. In children with CKD, metabolic acidosis leads to impairment of growth by inhibiting the secretion of growth hormone (GH), reducing its activity in peripheral tissues and distorting the activity of the GH - insulin-like growth factor 1 (IGF-1) axis, with reduction of the serum concentrations of free IGF-1 and GH, and increase of plasma IGF-1 binding proteins [17, 18]. In adults, these abnormalities may contribute to the pathogenesis of malnutrition. Metabolic acidosis adversely impacts calcium-phosphate metabolism in patients with CKD by reducing calcium receptor sensitivity as a result of the decrease in the intracellular pH [?], and by stimulating the parathyroid glands to secrete parathyroid hormone [19]. It also contributes to the mobilisation of bone bases, stimulates osteoclasts, and inhibits the activity of osteoblasts [20]. In addition, metabolic acidosis stimulates bone turnover, thus increasing the risk of osteoporosis."

"Metabolic acidosis may increase the serum β2-microglobulin concentration and contribute to the development of β2-microglobulin amyloidosis [21]. In patients with CKD without diabetes, low plasma bicarbonate concentration and metabolic acidosis are factors influencing the severity of insulin resistance, and alkalisation with sodium bicarbonate increases insulin sensitivity [22-24]. In patients with CKD who have hypertriglyceridemia, the administration of sodium bicarbonate results in the reduction of serum triglycerides concentration [25]. In CKD patients, metabolic acidosis impairs the peripheral conversion of thyroxine into triiodothyronine, which results in the reduction of the serum triiodothyronine concentration [26]. In addition, the results of animal experiments suggest that metabolic acidosis in patients with CKD increases the serum hepcidin concentration, and thus participates in the pathogenesis of anaemia of chronic disease [27, 28]. It has been shown that in CKD patients treated with haemodialysis, metabolic acidosis increases the demand for erythropoiesis stimulating agents [29]."

"In order to determine metabolic acidosis in patients with CKD, it is recommended that the venous plasma or venous whole blood bicarbonate concentration should be measured. Due to the risk of bleeding, local complications associated with the arterial puncture and the need to spare arteries for the future access for hemodialysis, arterial blood sampling is not recommended for this purpose. It is important mind the potential impact of ischemia of the forearm while sampling venous blood due to transient venous stasis on blood/plasma pH value and bicarbonate concentration. This phenomenon may lower pH and bicarbonate concentration of venous blood in the upper extremity and as a consequence lead to overdiagnosis of metabolic acidosis. For this reason, duration of ischemia must be minimalized and we suggest blood sampling by an experience personnel."

"In patients with metabolic acidosis and chronic kidney disease, the use of oral sodium bicarbonate is recommended (recommendation based on the results of interventional studies)."

"Based on results of available clinical trials we suggest an initial daily dose of 1-2 g of sodium bicarbonate. Subsequently, while monitoring the venous plasma and venous blood bicarbonate concentration, the dose of sodium bicarbonate should be increased until the target bicarbonate concentration, i.e. equal to or greater than 22 mmol/l, is achieved. Due to the lack of data on the safety of sodium bicarbonate used in high doses, in the opinion of the authors a maximal daily dose of 6 g of sodium bicarbonate should not be exceeded."

"Treatment of metabolic acidosis with sodium bicarbonate at the most commonly used doses, i.e. 2-3 g/day, may sometimes lead to the development of metabolic alkalosis. Therefore, in the course of alkali therapy, the plasma or venous blood bicarbonate concentration should be checked periodically to prevent the process of excessive alkalisation."

People with kidney issues often report a salty taste in their mouth even when they barely eat any salt. I think the increased chloride is responsible for that. As a teenager, I sometimes experienced this when I was under severe, immediate stress in school, and others have told me off the same salty taste in their mouth when they were in an adrenaline situation which should be able to bring about this pattern.

 

[PaRa]

People with kidney issues often report a salty taste in their mouth even when they barely eat any salt. I think the increased chloride is responsible for that. As a teenager, I sometimes experienced this when I was under severe, immediate stress in school, and others have told me off the same salty taste in their mouth when they were in an adrenaline situation which should be able to bring about this pattern.

Make me think of me this week when I had several oral tests, I hate when tests are not written (introverted behavior) so I get really dry mouth and a salty ish taste

 

[Amazoniac]

- Unravelling the Interplay between Extracellular Acidosis and Immune Cells (!)

The development of an acidic tissue environment is a hallmark of a variety of inflammatory processes and solid tumors. However, little attention has been paid so far to analyze the influence exerted by extracellular pH on the immune response. Tissue acidosis (pH 6.0 to 7.0) is usually associated with the course of infectious processes in peripheral tissues. Moreover, it represents a prominent feature of solid tumors. In fact, values of pH ranging from 5.7 to 7.0 are usually found in a number of solid tumors such as breast cancer, brain tumors, sarcomas, malignant melanoma, squamous cell carcinomas, and adenocarcinomas. Both the innate and adaptive arms of the immune response appear to be finely regulated by extracellular acidosis in the range of pH values found at inflammatory sites and tumors. Low pH has been shown to delay neutrophil apoptosis, promoting their differentiation into a proangiogenic profile. Acting on monocytes and macrophages, it induces the activation of the inflammasome and the production of IL-1β, while the exposure of conventional dendritic cells to low pH promotes the acquisition of a mature phenotype. Overall, these observations suggest that high concentrations of protons could be recognized by innate immune cells as a danger-associated molecular pattern (DAMP). On the other hand, by acting on T lymphocytes, low pH has been shown to suppress the cytotoxic response mediated by CD8+ T cells as well as the production of IFN-γ by TH1 cells. Interestingly, modulation of tumor microenvironment acidity has been shown to be able not only to reverse anergy in human and mouse tumor-infiltrating T lymphocytes but also to improve the antitumor immune response induced by checkpoint inhibitors. Here, we provide an integrated view of the influence exerted by low pH on immune cells and discuss its implications in the immune response against infectious agents and tumor cells.

 

[wavelength123]

very good OP here

I like this list a lot: https://www.clinicaleducation.org/documents/revised-summary-pral-list.pdf

that fifth page is basically everything Western... what a farce we live in.

 

[Amazoniac]

- Evaluating the Importance of the Carotid Chemoreceptors in Controlling Breathing during Exercise in Man

Only the carotid chemoreceptors stimulate breathing during hypoxia in Man. They are also ideally located to warn if the brain's oxygen supply falls, or if hypercapnia occurs. Since their discovery ~80 years ago stimulation, ablation, and recording experiments still leave 3 substantial difficulties in establishing how important the carotid chemoreceptors are in controlling breathing during exercise in Man: (i) they are in the wrong location to measure metabolic rate (but are ideally located to measure any mismatch), (ii) they receive no known signal during exercise linking them with metabolic rate and no overt mismatch signals occur and (iii) their denervation in Man fails to prevent breathing matching metabolic rate in exercise. New research is needed to enable recording from carotid chemoreceptors in Man to establish whether there is any factor that rises with metabolic rate and greatly increases carotid chemoreceptor activity during exercise. Available evidence so far in Man indicates that carotid chemoreceptors are either one of two mechanisms that explain breathing matching metabolic rate or have no importance. We still lack key experimental evidence to distinguish between these two possibilities.

 

[Amazoniac]

- Water: swelling, tension, pain, fatigue, aging

- Recharging the System (211/1474)

"[..]sodium energizes. It helps to remove calcium from the cell, to produce ATP, and to promote absorption of glucose and amino acids. The fear many physicians have of injecting hypertonic sodium chloride is odd, in the light of the knowledge that has accumulated in recent decades. Chloride isn't always the ideal anion, but more elaborate preparation is needed for providing the ideal ionic solution."​

- Calcium and Disease: Hypertension, organ calcification, & shock, vs. respiratory energy

"PTH (like estrogen and serotonin) inhibits cellular respiration and activates glycolysis, lowering the ATP level and shifting the cells metabolism toward the production of lactic acid rather than carbon dioxide. PTH also causes bicarbonate to be lost in the urine."​

 

[Amazoniac]

- Hyperchloremic Acidosis - StatPearls - NCBI Bookshelf

"Hyperchloremic metabolic acidosis is a pathological state that results from bicarbonate loss, rather than acid production or retention."​

 

[Amazoniac]

- Ray Peat Email Exchanges - Ray Peat Forum Wiki

"The neutral lactate salt is at least as toxic as the acid form[.]"​

 

[Amazoniac]

- Metabolic Acidosis or Respiratory Alkalosis? Evaluation of a Low Plasma Bicarbonate Using the Urine Anion Gap

Hypobicarbonatemia or a reduced level of bicarbonate in plasma is a finding seen in three acid-base disorders: metabolic acidosis, chronic respiratory alkalosis and mixed metabolic acidosis and chronic respiratory alkalosis. Hypobicarbonatemia due to chronic respiratory alkalosis is often misdiagnosed as a metabolic acidosis and mistreated with the administration of alkali therapy. Proper diagnosis of the cause of hypobicarbonatemia requires integration of the laboratory values, the arterial blood gas (ABG) and the clinical history. The information derived from the urinary response to the prevailing acid-base disorder is useful to arrive at the correct diagnosis. We discuss the use of the urine anion gap (UAG), as a surrogate marker of urine ammonium, in the evaluation of a patient with low plasma bicarbonate to differentiate between metabolic acidosis and chronic respiratory alkalosis. The interpretation and limitations of urine acid-base indices at bedside (urine pH, urine bicarbonate and urine anion gap) to evaluate urine acidification are discussed.

 

[icecreamman]

@Amazoniac first off, I want to say great thread man. Going thru it all is a pleasure (despite not enjoying the occasional lingo :P) and is interesting seeing how it intersects with Ray's philosophy on a number of points.

I have a question for you:

Sodium is obviously necessary. Now, since we've established that easing the Cl load would be preferable, table salt NaCl seems to be out of the picture. Baking soda, on the other hand does deliver sodium without the Cl and is obviously beneficial but its strong antacid effect makes it less than ideal for common casual consumption in or around meals. Not to mention its systemic alkalizing effect potentially being dangerous with a calcium-rich Ray Peat style diet with dairy etc. So you mentioned sodium acetate, which despite being acidic due to the acetic acid from which it is derived, is missing the Cl which makes it a viable candidate for delivering sodium in meals without messing with the stomach acid, and also it wouldn't pose a risk with milk-alkali syndrome, right?

Well my question is - what do you think about sodium malate? I thought about it since you were exploring the benefits of malic acid in another thread so I thought it could be used ideally to deliver sodium as well. I've searched for it and it seems to be in use as a food additive already, E350. One more potential upside is that it says that sodium malate has more or less the same taste as table salt, which I am not sure is the case with sodium acetate.

Anyway, thanks in advance and keep up the good work.

 

[Amazoniac]

Some material here is repeated, but having them ordered in a post is useful.

- Strong and Weak Acids and Acid Ionization Constant | Introductory Chemistry (CK-12)
- How to Predict the Outcome of an Acid-Base Reaction | Map: Organic Chemistry - Paula Bruice

- pKa Values Span 60 Orders Of Magnitude | Master Organic Chemistry
- The impact of temperature changes on biological buffers' pKa | Hopax FC

- Ion speciation - Wikipedia
- Titration curve - Wikipedia

- Interactions between hydrated cement paste and organic acids: Thermodynamic data and speciation modeling (it's relevant)

 

[icecreamman]

Some material here is repeated, but having them ordered in a post is useful.

- Strong and Weak Acids and Acid Ionization Constant | Introductory Chemistry (CK-12)
- How to Predict the Outcome of an Acid-Base Reaction | Map: Organic Chemistry - Paula Bruice

- pKa Values Span 60 Orders Of Magnitude | Master Organic Chemistry
- The impact of temperature changes on biological buffers' pKa | Hopax FC

- Ion speciation - Wikipedia
- Titration curve - Wikipedia

- Interactions between hydrated cement paste and organic acids: Thermodynamic data and speciation modeling (it's relevant)

Thanks for the extensive reply! I don't mean to sound ungrateful but I don't think I'm well informed or smart enough to come up with a solid answer to the specific question I had with all that info though. Can you give me a specific answer on sodium malate? I am willing to explore these alternative sodium salts because a) alkalinization and b) something other than baking soda bc I am afraid of risking milk-alkali syndrome on a dairy rich high-calcium diet.

 

[Amazoniac]

Thanks for the extensive reply! I don't mean to sound ungrateful but I don't think I'm well informed or smart enough to come up with a solid answer to the specific question I had with all that info though. Can you give me a specific answer on sodium malate? I am willing to explore these alternative sodium salts because a) alkalinization and b) something other than baking soda bc I am afraid of risking milk-alkali syndrome on a dairy rich high-calcium diet.

The body will have more flexibility with acetate for being elementary with increased fate possibilities. Considering that the response to citrate (increased after malate supplementation) tends to be different than acetate, choosing the option that's less specific must have advantages, and it's common to find people reacting well to vinegar. The same reason that makes acetate supplementation concerning in cancer, should make it good in assisting the repair of damaged tissues.

Laxarium (Mg), cardiarrestium (K) (or even killcium if the diet was low) salts are preferable to edemium (Na) for not disturbing extracellular balance. Although we can expect a greater impact when edemium is used because it's predominantly located there, not being paired with chloride makes it not as sustainable as the alternatives for the long-term, unless you tend to run low in it.

Malate is fine, but getting plenty of cardiarrestium from foods might suffice to accomplish what you want.

 

[Amazoniac]

Check out how it takes more base to increase the pH of a citric acid solution in comparison to acetic acid:

- Interactions between hydrated cement paste and organic acids: Thermodynamic data and speciation modeling

Spoiler

It's the concept of mono-, di/tri/polyprotic (after protons) acids. As you can tell from curves crossing each other, there are other factors involved in determining their behavior, this is one of them.
Acetic acid donates only one hydrogen ion per molecule, whereas citric acid three depending on conditions.

 

[icecreamman]

Interesting. So while focusing on these alkaline minerals (Na, K, Mg, Ca) is important, Na isn't as critical enough to be focused on if the others are sufficient in the diet? Will it not pose a problem if the K:Na is somehow disturbed or something? I'm asking because another thread I read emphasized the critical need for Na:

Optimal Sodium Intake Is At Least 230% Higher Than RDA

So if you had to rank all these alkalinizing Na salts by beneficial effect or just preference, bicarbonate, acetate, citrate, malate..etc. what would you say? Btw I thought citrate was under some scrutiny on here for some reason hahah..I remember Ray talking about how it's essentially derived from a mold so the commercial low quality citric acid was deemed to be problematic due to excepients, but I was never sure what the citrate aversion is about (if you can dumb it all down for me :P)