Has Anyone Tried Sodium Acetate ? (for SIBO?)

[Amazoniac]

It's beyond gut:

- Dietary Acetate Supplementation Attenuates Neuroinflammation
- Acetate supplementation modulates brain histone acetylation and decreases interleukin-1β expression in a rat model of neuroinflammation
- Acetate supplementation as a means of inducing glioblastoma stem-like cell growth arrest

- High-Fiber Diet and Acetate Supplementation Change the Gut Microbiota and Prevent the Development of Hypertension and Heart Failure in Hypertensive Mice

@haidut @Terma @Travis (yn)

 

[Makrosky]

It's beyond gut:

- Dietary Acetate Supplementation Attenuates Neuroinflammation
- Acetate supplementation modulates brain histone acetylation and decreases interleukin-1β expression in a rat model of neuroinflammation
- Acetate supplementation as a means of inducing glioblastoma stem-like cell growth arrest

- High-Fiber Diet and Acetate Supplementation Change the Gut Microbiota and Prevent the Development of Hypertension and Heart Failure in Hypertensive Mice

@haidut @Terma @Travis (yn)

Thanks for keeping up the good info man.

I recall reading a post a few weeks ago from @Obi-wan discussing it with haidut about it is dangerous. That it can feed cancerous cells or something like that and that using succinic acid is better. I can't seem to find it right now, I hope they can chime in.

Edit: found it The Warburg "effect" Is, In Fact, A Direct Cause Of Cancer

 

[haidut]

It's beyond gut:

- Dietary Acetate Supplementation Attenuates Neuroinflammation
- Acetate supplementation modulates brain histone acetylation and decreases interleukin-1β expression in a rat model of neuroinflammation
- Acetate supplementation as a means of inducing glioblastoma stem-like cell growth arrest

- High-Fiber Diet and Acetate Supplementation Change the Gut Microbiota and Prevent the Development of Hypertension and Heart Failure in Hypertensive Mice

@haidut @Terma @Travis (yn)

Thanks, very interesting indeed. Since @Makrosky asked - I still prefer succinic to acetic acid. The former always gives me an energy boost while the latter does not and often irritates my GI.

 

[Makrosky]

Acetic acid is dangerous because it activates the FAS and may directly feed the tumor and make ti grow.

@Amazoniac

Actually, any of the Krebs cycle intermediates can be fed and will work just as well as if somebody was eating food. The safest one is probably succinic acid. The others, especially malic acid and oxaloacetate tend to inhibit SADH and thus lower ETC activity. Acetic acid is OK but in high amounts does shift the functioning towards fatty acid synthesis. Ingesting a lot of exogenous acetic acid is not the same as synthesizing it as a result of PDH and bound to coenzyme A. There is probably a sweet point beyond which exogenous acetic acid is risky, while getting it from food conversion through PDH is rate-limited. This is why drinking alcohol fattens up the liver - too much acetic acid that the Krebs cycle and ETC cannot handle. But adding a catalyst like MB can avoid that buildup of acetic acid and this has been confirmed in animal studies.

haidut, do you mean adding some MB to the vinegar+sodium bicarbonate mix can protect from the excess acetic acid problems ?

I am asking this for two reasons : 1) the vinegar+sodium bicarbonate effects are otherwise very good 2) it is a remedy you can probably create in ANY country of the world easily, cheaply and has lots of benefits. Whereas getting succinic acid is not easy at all. But if you are really going to risk feeding tumours... not worth touch it with a 10 feet pole then.

 

[haidut]

@Amazoniac



haidut, do you mean adding some MB to the vinegar+sodium bicarbonate mix can protect from the excess acetic acid problems ?

I am asking this for two reasons : 1) the vinegar+sodium bicarbonate effects are otherwise very good 2) it is a remedy you can probably create in ANY country of the world easily and has lots of benefits. Whereas getting succinic acid is not easy at all. But if you are really going to risk feeding tumours... not worth touch it with a 10 feet pole then.

It should mitigate the risks but I don't know if it can fully protect. I like succinic acid more because it feeds directly into the ETC and does not tend to elevate other Krebs intermediates much.

 

[Amazoniac]

Thanks for keeping up the good info man.

I recall reading a post a few weeks ago from @Obi-wan discussing it with haidut about it is dangerous. That it can feed cancerous cells or something like that and that using succinic acid is better. I can't seem to find it right now, I hope they can chime in.

Edit: found it The Warburg "effect" Is, In Fact, A Direct Cause Of Cancer

Koch:

The Survival Factor In Neoplastic And Viral Diseases

"Since vinegar is a completed fermentation product, if it is made from clean apples, it is a valuable article in the diet. A little on the salad helps digestion, and offers ferments that are also very useful."
​

The Basic Chemistry Of Our Diet

"All dicarboxylic fruit acids as malic and succinic, offer a readily dissociated hydrogen atom and can be dehydrogenated to form free neutral radicals and thus aid in the oxidation mechanism."
​

The Causes And Prevention Of Cancer

"Another source of digestive disturbance is improper mastication of foods. Starch foods require an alkaline medium for digestion. This is provided by the saliva and therefore all cereal and other starch foods should be carefully masticated and thoroughly mixed with saliva before swallowing. The habit of eating cooked cereals with milk leads to the bolting of these foods without proper mixture with the saliva. Another vicious habit is the combination of acids with starch foods, for example, potato salad. Green salads eaten at the same meal with starch foods should not have an acid dressing."
​

Gerson:

15 Grams Of Potassium A Day Without Supplements: Perfectly Possible​

4 teaspoons 10x a day must provide about 4 grams of acetate.

1 teaspoon of sodium bicarbonate weights 4.8 g, providing about 1.3 g of sodium. If you add vinegar to 1/2 of a teaspoon of sodium bicarbonate and stop when it no longer reacts, you'll have about 0.6 g of sodium and 1.5 g of acetate.

I know these calculations can be annoying, but I insist for finding them useful for an idea instead of leaving it vague.

Gerson's protocol required frequent supplementation of niacin (50 mg at a time), so acetate cannot be impairing in these amounts (not as a single shot), otherwise detrimental effects would favor its substituion for other potassium salts.


And then you have to consider that acetic acid production in the gut is common to be decreased.

There are many germs in the following link, I suggest reading it:

Role of intestinal bacteria in nutrient metabolism​

The amount generated will vary depending on microbial composition, type of food consumed, time allowed to ferment, and likely other factors. You might be able to find more information on this searching for 'energy contribution of short-chain fatty acids in gut'.

According to the link below the energy density of organic acids is 1.5-2.5 kcal/g. I'm mentioning this because it's more probable that you'll come across an estimation based on calories, but with the energy density in the minds you can have a notion in grams to compare with the stuff above.

Determination Of Energy Values For Fibers - Dietary Reference Intakes Proposed Definition of Dietary Fiber - NCBI Bookshelf​

From the first link:

"Plasma acetate is derived primarily from the breakdown of the neurotransmitter acetylcholine in the extracellular space by acetylcholine esterases [44], and from the metabolism of ethanol. Plasma acetate levels increases from 0.3 to 1mM for 4 hours after a single intravenous dose of 0.5 g/kg ethanol in humans [45]. In addition, anaerobic metabolism by gut bacteria generates acetate, the amount of which varies based on the bacterial species in the individual and the type of diet [46]. Other endogenous sources of acetate found within the central nervous system that can influence cellular acetate levels include the acetylated amino acid compounds (N-acetylaspartate, N-acetylcarnitine, N-acetylcarnosine, and N-acetylcysteine) as well as acetylated proteins that can modulate cellular acetate levels in response to regulatory protein deacetylation and/or protein degradation."​

 

[Makrosky]

Koch:

The Survival Factor In Neoplastic And Viral Diseases

"Since vinegar is a completed fermentation product, if it is made from clean apples, if is a valuable article in the diet. A little on the salad helps digestion, and offers ferments that are also very useful."
​

The Basic Chemistry Of Our Diet

"All dicarboxylic fruit acids as malic and succinic, offer a readily dissociated hydrogen atom and can be dehydrogenated to form free neutral radicals and thus aid in the oxidation mechanism."
​

The Causes And Prevention Of Cancer

"Another source of digestive disturbance is improper mastication of foods. Starch foods require an alkaline medium for digestion. This is provided by the saliva and therefore all cereal and other starch foods should be carefully masticated and thoroughly mixed with saliva before swallowing. The habit of eating cooked cereals with milk leads to the bolting of these foods without proper mixture with the saliva. Another vicious habit is the combination of acids with starch foods, for example, potato salad. Green salads eaten at the same meal with starch foods should not have an acid dressing."
​

Gerson:

15 Grams Of Potassium A Day Without Supplements: Perfectly Possible​

4 teaspoons 10x a day must provide about 4 grams of acetate.

1 teaspoon of sodium bicarbonate weights 4.8 g, providing about 1.3 g of sodium. If you add vinegar to 1/2 of a teaspoon of sodium bicarbonate and stop when it no longer reacts, you'll have about 0.6 g of sodium and 1.5 g of acetate.

I know these calculations can be annoying, but I insist for finding them useful for an idea instead of leaving it vague.

Gerson's protocol required frequent supplementation of niacin (50 mg at a time), so acetate cannot be impairing in these amounts (not as a single shot), otherwise detrimental effects would favor its substituion for other potassium salts.


And then you have to consider that acetic acid production in the gut is common to be decreased.

There are many germs in the following link, I suggest reading it:

Role of intestinal bacteria in nutrient metabolism​

The amount generated will vary depending on microbial composition, type of food consumed, time allowed to ferment, and likely other factors. You might be able to find more information on this searching for 'energy contribution of short-chain fatty acids in gut'.

According to the link below the energy density of organic acids is 1.5-2.5 kcal/g. I'm mentioning this because it's more probable that you'll come across an estimation based on calories, but with the energy density in the minds you can have a notion in grams to compare with the stuff above.

Determination Of Energy Values For Fibers - Dietary Reference Intakes Proposed Definition of Dietary Fiber - NCBI Bookshelf​

From the first link:

"Plasma acetate is derived primarily from the breakdown of the neurotransmitter acetylcholine in the extracellular space by acetylcholine esterases [44], and from the metabolism of ethanol. Plasma acetate levels increases from 0.3 to 1mM for 4 hours after a single intravenous dose of 0.5 g/kg ethanol in humans [45]. In addition, anaerobic metabolism by gut bacteria generates acetate, the amount of which varies based on the bacterial species in the individual and the type of diet [46]. Other endogenous sources of acetate found within the central nervous system that can influence cellular acetate levels include the acetylated amino acid compounds (N-acetylaspartate, N-acetylcarnitine, N-acetylcarnosine, and N-acetylcysteine) as well as acetylated proteins that can modulate cellular acetate levels in response to regulatory protein deacetylation and/or protein degradation."​

Sorry Bro but I am not following you.

What do you want to say?

I want a brain like @Terma 's

 

[Amazoniac]

Sorry Bro but I am not following you.

What do you want to say?

I want a brain like @Terma 's

Both monsters above seemed to be fine with acetate; if it made tumors worse, they would probably note something negative from its consumption. The problems regarding what Zeus suggested must only appear with greater doses that likely feel off to taste anyway.

Vinegars' organic acids are mostly acetic:
Determination of Organic Acids and Ethanol in Commercial Vinegars

 

[Makrosky]

Both monsters above seemed to be fine with acetate; if it made tumors worse, they would probably note something negative from its consumption. The problems regarding what Zeus suggested must only appear with greater doses that likely feel off to taste anyway.

Vinegars' organic acids are mostly acetic:
Determination of Organic Acids and Ethanol in Commercial Vinegars

Ok thanks so much!! It turns out I understood what you meant. Just wasn't sure. You are dealing with huge ammounts of interrelated info lately, hard to follow sometimes.

 

[Terma]

I want a brain like @Terma 's

rofl, careful what you wish for

@Amazoniac Thanks coincidentally I had tried to look into acetate as a way to balance chloride ions (since my body has trouble with chloride-related everything), unfortunately my gut now rejects any and all forms of vinegar, it goes straight through. Iirc butyrate is more effective HDAC inhibitor. Cheers

 

[Amazoniac]

- A novel treatment for anemia? Check the kitchen pantry!

"During hypoxia, acetate secretion[82-84] and Acss2 expression[82,83] increase in tumor cells, which provide a potential inducible biochemical trigger and source for acetyl CoA."

"Acetate is generated in liver and kidney of mice with acute anemia. Exogenous acetate, delivered either by oral or intra-peritoneal means, augments Epo gene[*] expression and increases resting hematocrits in mice with acute anemia[86]."

[*] "[..]hypoxic gene expressed in the fetal liver, adult kidneys and adult spleen[15-19], anatomic regions of developing and adult mammals that overlap sites of hematopoiesis[15-20]"​

"Exogenous acetate also augments Epo gene expression and increases resting hematocrits in mice with chronic anemia due to congenital or acquired reasons[86]."

"Exogenous acetate delivered daily by oral gavage to rabbits rendered anemic by phlebotomy restores hematocrits to normal levels in approximately half the time otherwise required."

"In conjunction with data from a rat model of hemorrhagic shock that suggests volume restoration with acetated Ringer’s solution is superior to use of lactated Ringer’s solution or normal saline, an argument could be made that acetated Ringer’s solution may have immediate as well as delayed effects on recovery from acute blood loss[87]."

"A substantial fraction of chronic cardiac disease patients have anemia, which is associated with worse clinical outcomes. Current treatments of anemia in these patient populations, which includes bolus Epo injections or intra-venous iron supplementation, have not been effective at changing clinical outcomes. HIF-2 signaling regulates physiological gene expression of Epo as well as iron metabolism factors. The same biochemical pathway that controls HIF-2 during hypoxia in cells, termed the acetate switch, can be stimulated in mice with anemia by treating them with exogenous acetate, which increases production of the HIF-2 target gene Epo and thereby restores hematocrit levels. Thus, the acetate switch is a potential therapeutic target for treating anemia, one that may restore Epo and possibly functional iron levels in a more physiological manner compared with bolus Epo therapy or HIF-stabilizing factors."

"It is important to know about co-morbid conditions that may be exasperated if HIF-2 signaling is augmented, particularly for chronic acetate supplementation. For example, several cancers are a relative contraindication for bolus Epo therapy and are a theoretical risk for any therapy that augments HIF signaling, which may exacerbate tumor growth. Indeed, chronic acetate supplementation augments Acss2/HIF-2 signaling and tumor growth in a flank tumor cancer mouse model[94]. Nevertheless, acetate has a selective action on HIF-2 signaling and does not augment HIF-1 signaling, which may have important advantages over non-selective HIF activators (e.g. PHD inhibitors) that are being evaluated for use as Epo-stimulating agents. As for any treatment, careful consideration of risks and benefits is always warranted and best appreciated when knowledge is greatest."​

 

[Amazoniac]

- Nutrition for the Women:

"I have seen people very quickly get fat on a daily drink of cider vinegar and honey and a dose of lecithin. The folk medicine tradition behind it was probably valid - it was a good way to fatten up people who were under-weight. But somehow this got twisted into promoting it as a "reducing formula." Lecithin is a good nutrient and seems to lower the danger of a high cholesterol level in the blood. And cider vinegar and honey are both rich in necessary minerals. But the acetic acid in vinegar not only is a component of fat molecules, but it also serves to activate the process of converting glucose into fat (Adv. Lipid Res. 9, p. 111. 1971). Thus the formula is good as part of a weight-gaining diet, but not as part of a reducing program."​

Will is tumor? Was is Gerson? Wow is conjugated base?

 

[Amazoniac]

Intestines have to be acidified to prevent rottage just like a batch of sauerkrout, acetic and lactic acid are used to treat beef carcasses. It can also affect nutrient adsorption such as magnesium, calcium, etc.

When an organic acid dissociates, you end up with an anion and the released protod. The protod alone can affect the pH of the germ cell and (along with the anion) lead to 'metabolic perturbation'. If these can perturb our metabolism in excess, imagine what it does to a microbe if it cannot handle it. It seems that gram-negative bacteria are less resistant to them than gram-positive, which can also be problematic, so pounding unspecific acids can be counterproductive, there will be particular ones that are more suited to shape them.

It's interesting that when acetic acid dissociates to acetate in the bacterial cell, it can disturb their methionine metabolism, leading to an accumulation of toxic amounts of homocysteine in them and serving to inhibit their growth. But even normalizing the pH of the cell again consumes energy and can serve to impair their feast.

If there are multiple exposures, the germs start to adapt. Even though the effectiveness of these treatments weakens over time, since microbes're in constant competition, it can assist in shaping the colonies.

I wonder how safe it is to do an organic acid enema.

Anyway, it's discussed here:

- Weak organic acids: a panoply of effects on bacteria
- Intestinal health, the key to productivity: The case of organic acids
- Organic Acids and Potential for Modifying the Avian Gastrointestinal Tract and Reducing Pathogens and Disease

Spoiler

"Due to the lipophilic nature of LCFA, their antimicrobial properties may be a constituent of their potential to incorporate themselves into target cell membranes and promote leakage of cellular protons or ions, such as in Gram-positive bacteria (35–37). However, it has been demonstrated by Shue and Freese that the resistance possessed by Gram-negative species to MCFA and LCFA is in part due to the presence of the lipopolysaccharide (LPS) layer in the cell wall (38). Thus, LPS prevents MCFA and LCFA from crossing the cell membrane and into the cell (34). Further, Gram-negative bacteria, such as E. coli, possess the ability to assimilate MCFA and LCFA into the cell and subsequently metabolize them per the ß-oxidation cycle (39)."

"Weak organic acids (C1-C7) with a pKa between 3 and 5 are explicitly used for their antimicrobial activity (5). There are two major types of organic acids (Table 2). The first group (lactic, fumaric, citric) are capable of generally lowering the pH of the stomach, thus reducing the acid sensitive bacteria present indirectly. The second group (butyric, formic, acetic, propionic, and sorbic) lower the pH in the GIT by directly acting upon the cell wall of Gram-negative bacteria (5, 49). Organic acids ameliorate the conditions of the GIT through the reduction of GIT pH, promoting proteolytic enzyme activity and nutrient digestibility, intensifying pancreatic secretions, encouraging digestive enzyme activity, creating stability of the microbial population and stimulating the growth of beneficial bacteria, and by being bacteriostatic and bactericidal to pathogenic bacteria (5)."

"Although the most noted benefit of organic acids is its ability to lower the pH of the GIT, organic acids can also prevent pathogen livability on the cellular level. Organic acids possess the ability to target the cell wall, cytoplasmic membrane, and particular functions of metabolism in the cytoplasm associated with replication, protein synthesis, and function (48, 54). VSCFA, consisting of weak organic acids that are bacteriostatic without affecting intestinal microbiota, are not regarded as acidifiers as their mode of action is to directly diffuse across the cell membrane of bacteria in the undissociated form without lowering the bowel pH (55). VSCFA, once diffused across the bacterial cytoplasm, lower the internal pH of the bacteria (55)."

"The specific effectiveness of a particular organic acid relies heavily on several factors such as: type and acidity of the SCFA, inclusion rate of acids, diet composition and buffering within the diet, level of “intraluminal production of acids” by lactic acid producing bacteria (LAB) in GIT, feed palpability, receptor on the epithelial villi for bacterial colonization, vaccinate immunity, welfare, and age (5)."

"Some concerns for the use of organic acids include their inability to affect the lower part of the GIT, bacteria's ability to create a resistance against organic acids, and their hindering effect on host beneficial bacteria such as LAB. Much of their bacterial impact is related to their effective concentration present in different compartments of the GIT. For example, Thompson and Hinton noted that as SCFAs move along the digestive tract, their concentration decreases due to digestion and metabolism (51)."

"Most organic acids will dissociate before reaching the lower GIT and thus having little to no effect on the GIT (56)."

"Probably the best-characterized group of probiotics are lactic acid producing bacteria (LAB), such as Lactobacillus. LAB generate lactic acid in vitro and the lactic acid produced is utilized for the production of butyric acid by Clostridial clusters, which supports the concept of cross-feeding (3). Lactobacillus spp. have been found to reduce pathogenic attachment to the ileal epithelial cells through exclusion and competition (72). Lactobacillus also elicits antibacterial effects by producing lactic acid (63). Lactic acid, an organic acid, can lower the GIT pH, thus creating a hostile environment for resident pathogenic bacteria. Lactobacillus acidophilus is found to be the most sufficient candidate as a dietary appurtenance (71). L. acidophilus has the potential to decrease the external pH to lower values than other lactic acid producing bacteria and can reach a medium pH of 3.5 (64)."

"Research has demonstrated that both organic acids and LAB have the capability to improve broiler performance and reduce pathogenic bacteria (86–90). Since the modes of action for both organic acid supplements and LAB involve the lowering of the pH of the GIT, many of their benefits appear to be similar. However, LAB and organic acids should also still be considered in some respects considerably different in their effectiveness, mechanisms, and interaction with one another."

"Although LAB do not directly destroy enteric bacteria, LAB are able to inhibit colonization and further growth and establishment of pathogenic bacteria. Furthermore, LAB byproducts beyond SCFAs, such as hydrogen peroxides, and intermediary metabolites also contribute to the reduction of pathogens present in the GIT." "It has been noted that SCFAs when interacting with Gram-negative bacteria are not only bacteriostatic but can also be bactericidal (51). Furthermore, organic acids such as SCFAs are produced in millimolar concentrations in the GIT of animals due to the prevalence of anaerobic bacteria. Organic acids, being SCFA, also possess the ability to lower the pH of the GIT and improve broiler performance similar to LAB. Thus, previous research has seen both methods to be beneficial in the reduction of pathogenic bacteria (86–90)."

"Not only can bacteria build a resistance to organic acids, but pathogenic bacteria can also lower their internal pH to protect themselves from the acidic properties of organic acids, thus rendering them ineffective in being bactericidal against pathogenic bacteria (48). Furthermore, fermentative bacteria have the ability to lower their intracellular pH in the event that the extracellular pH becomes highly acidic. If the intracellular pH is lowered, the bacterium has a much smaller pH gradient across the cell membrane and will be protected from anion accumulation (53)."

"The most significant challenge to organic acid feed additive use is their potentially detrimental effect on LAB. In previous research, the use of organic acids in the diet reduced not only the amount of lactic acid but the LAB present in the GIT."

"LAB are not only beneficial in protecting the bird from pathogens but also provides the bird with physical enhancements to the GIT. These enhancements include strengthening the gut wall integrity, enhance anti-inflammatory response, and correct dysbacteriosis (29). With all of the benefits that LAB provide to poultry, it is vital to ensure their survival and utilization in poultry."

 

[Amazoniac]

- Cellular Respiration | Karl Roberts

- Nutrient Metabolism: Structures, Functions, and Genes (978-0-12-387784-0)

"Only very small amounts are consumed with foods, mainly vinegar, fruits, and vegetables. Alcohol is converted completely into acetate."

"The metabolism of carbohydrates, amino acids, and fatty acids generates several hundred grams of acetate per day, mainly as acetyl-CoA []. Depending on intake, significant amounts of free acetate may also be generated from ethanol []. Most is utilized within the cells or tissues where the acetate or acetyl-CoA is generated; some is transported to other tissues and utilized there."

"The amount of acetate generated from glucose depends on the proportion used for glycolysis (as opposed to the smaller fraction metabolized via the pentose phosphate pathway) and the proportion used for the generation of oxaloacetate from pyruvate. Typically, about half a gram of acetate (as acetyl-CoA) is generated per gram of absorbed carbohydrate."

"Acetyl-CoA is generated during the catabolism of isoleucine, leucine, and threonine. Lysine and tryptophan each generates two acetyl-CoA molecules. Metabolism of cysteine, alanine, and tryptophan generates pyruvate, which may be converted into acetyl-CoA. Acetoacetate is generated by the catabolism of phenylalanine, tyrosine, and leucine (for the latter in addition to 1 mol of acetyl-CoA). The acetoacetate can be activated by 3-oxoacid CoA-transferase (succinyl-CoA transferase, EC2.8.3.5) and then cleaved by acetyl-CoA C-acetyltransferase (thiolase, EC2.3.1.9) to generate 2 mol of acetyl-CoA. A minor pathway of threonine breakdown generates free acetate."

"1 mol of acetyl-CoA is released with each cycle of fatty acid beta-oxidation."

"Ethanol is oxidized by various alcohol dehydrogenases (EC1.1.1.1) or the microsomal ethanol oxidizing system (MEOS, unspecific monooxygenases of the cytochrome P-450 family, EC1.14.14.1), in conjunction with several types of aldehyde dehydrogenase (EC1.2.1.3, EC1.2.1.4, and EC1.2.1.5) or acetaldehyde oxidase (EC1.2.3.1). Ethanol metabolism occurs mainly in the liver, and most of the resulting acetate is released into the circulation (Siler et al., 1999); 1 g of ethanol generates about 1.3 g of acetate."

Spoiler

--
- Risk thresholds for alcohol consumption: combined analysis of individual-participant data for 599 912 current drinkers in 83 prospective studies​

"Normal intestinal bacteria in the colon break down nondigestible carbohydrates and release significant amounts of short-chain fatty acids, including acetate."

Spoiler

"Absorption of acetate from the small intestine (Watson et al., 1991; Tamai et al. 1995), especially the jejunum, appears to proceed mainly via the proton/monocarboxylic acid cotransporter (MCT1, SLC16A1), which is possibly present in the apical and certainly in the basolateral enterocyte membrane (Garcia et al., 1994; Orsenigo et al., 1999). Acetate can also be absorbed from the colon and rectum, which are important sites of bacterial production from dietary fiber (Wolever et al., 1995). MCT1 and possibly the SCFA/HCO3 antiporter contribute to this uptake (Stein et al., 2000). The flow of protons across the luminal membrane of the proximal colon via the sodium/hydrogen exchanger also promotes the protonation of the acetate anion and its subsequent passage into the enterocyte by nonionic diffusion (von Engelhardt et al., 1993)."

"Acetate can be utilized by muscle and other peripheral tissues (Pouteau et al., 1996). Complete oxidation of acetate requires thiamin, riboflavin, niacin, pantothenate, lipoate, ubiquinone, iron, and magnesium."

"First, free acetate must be conjugated to CoA by acetate-CoA ligase (thiokinase, EC6.2.1.1) []. Most acetyl-CoA is utilized in mitochondria via the tricarboxylic acid (Krebs) cycle. Citrate synthase (EC4.1.3.7) joins acetyl CoA to oxaloacetate. The citrate from this reaction can then be metabolized further, providing FADH, NADH, and succinate for oxidative phosphorylation and ATP or GTP from succinyl CoA. The production rate of acetyl-CoA from fatty acid beta-oxidation in the liver with prolonged fasting usually exceeds the capacity of the Krebs cycle. The CoA for continued beta-oxidation and other functions can be released through the production of acetoacetate in three steps. The typical odor of a fasting individual is partially related to exhaled acetone formed from acetoacetate. The conversion of acetoacetate into beta-hydroxybutyrate taxes the body’s acid-buffering capacity and may cause a drop in blood pH (acidosis) in diabetics and similarly susceptible patients. None of these events is related to dietary intake of acetate."

"Ketogenesis takes place in the mitochondria, where fatty acid catabolism generates acetyl-CoA []. Acetyl-CoA C-acetyltransferase (thiolase, EC2.3.1.9) joins two acetyl-CoA molecules, and hydroxymethylglutaryl-CoA synthase (HMG-CoA synthase, EC4.1.3.5) adds another one. The mitochondrial isoform of HMG-CoA synthase is genetically distinct from the cytosolic one, which generates the precursor for cholesterol synthesis. Hydroxymethylglutaryl-CoA lyase (HMG-CoA lyase, EC4.1.3.4) finally generates acetoacetate by cleaving off acetyl-CoA from the HMG-CoA intermediate. Spontaneous decarboxylation of acetoacetate generates the dead-end product acetone."

"Acetoacetate can also be reduced to beta-hydroxybutyrate by NADH-dependent 3-hydroxybutyrate dehydrogenase (EC1.1.1.30). This enzyme is allosterically activated by phosphatidyl choline. The reaction is fully reversible. Net flux depends on substrate concentrations. Acetoacetate and betahydroxybutyrate (but not acetone) can become a significant energy fuel for brain after several days of adaptation to starvation conditions."

"Acetyl-CoA activates allosterically the biotin-dependent enzyme pyruvate carboxylase (EC6.4.1.1) and thereby stimulates Krebs cycle throughput."

"[Dietary acetate] inhibits lipolysis and replaces fat in the fuel mixture (Siler et al., 1999). Acetic acid also lowers blood sugar levels (Ogawa et al., 2000), possibly by decreasing the activities of sucrase, maltase, trehalase, and lactase (Ogawa et al., 2000), or by delaying gastric emptying (Liljeberg and Bjorck, 1998)."​

 

[Amazoniac]

- Apoptotic effect of sodium acetate on a human gastric adenocarcinoma epithelial cell line
- The Short-Chain Fatty Acid Acetate in Body Weight Control and Insulin Sensitivity

 

[Amazoniac]

And has anyone tried to hydrate powdered cinnamon with this? It's potent.

 

[Inaut]

And has anyone tried to hydrate powdered cinnamon with this? It's potent.

I like your thinking Amazon user

 

[Terma]

"[Dietary acetate] inhibits lipolysis and replaces fat in the fuel mixture (Siler et al., 1999). Acetic acid also lowers blood sugar levels (Ogawa et al., 2000), possibly by decreasing the activities of sucrase, maltase, trehalase, and lactase (Ogawa et al., 2000), or by delaying gastric emptying (Liljeberg and Bjorck, 1998)."​

Well the delayed gastric emptying was clear, but I don't want to decrease sucrase - does that sound fun to you? Are there any more of these? Couldn't access that book.

Acetic acid suppresses the increase in disaccharidase activity that occurs during culture of caco-2 cells. - PubMed - NCBI

To understand how blood glucose level is lowered by oral administration of vinegar, we examined effects of acetic acid on glucose transport and disaccharidase activity in Caco-2 cells. Cells were cultured for 15 d in a medium containing 5 mmol/L of acetic acid. This chronic treatment did not affect cell growth or viability, and furthermore, apoptotic cell death was not observed. Glucose transport, evaluated with a nonmetabolizable substrate, 3-O-methyl glucose, also was not affected. However, the increase of sucrase activity observed in control cells (no acetic acid) was significantly suppressed by acetic acid (P < 0.01). Acetic acid suppressed sucrase activity in concentration- and time-dependent manners. Similar treatments (5 mmol/L and 15 d) with other organic acids such as citric, succinic, L-maric, L-lactic, L-tartaric and itaconic acids, did not suppress the increase in sucrase activity. Acetic acid treatment (5 mmol/L and 15 d) significantly decreased the activities of disaccharidases (sucrase, maltase, trehalase and lactase) and angiotensin-I-converting enzyme, whereas the activities of other hydrolases (alkaline phosphatase, aminopeptidase-N, dipeptidylpeptidase-IV and gamma-glutamyltranspeptidase) were not affected. To understand mechanisms underlying the suppression of disaccharidase activity by acetic acid, Northern and Western analyses of the sucrase-isomaltase complex were performed. Acetic acid did not affect the de novo synthesis of this complex at either the transcriptional or translational levels. The antihyperglycemic effect of acetic acid may be partially due to the suppression of disaccharidase activity. This suppression seems to occur during the post-translational processing.

(Along those lines: Intestinal Sucrase as a Novel Target Contributing to the Regulation of Glycemia by Prebiotics )

 

[Amazoniac]

Well the delayed gastric emptying was clear, but I don't want to decrease sucrase - does that sound fun to you? Are there any more of these? Couldn't access that book.

Acetic acid suppresses the increase in disaccharidase activity that occurs during culture of caco-2 cells. - PubMed - NCBI


(Along those lines: Intestinal Sucrase as a Novel Target Contributing to the Regulation of Glycemia by Prebiotics )

It depends, farting can be fun if you don't interpret as intoxication.

I have only skimmed through it after your message and right away there are so many factors to consider that I'm discouraged. A concentration of 10-150 mmol/L is broad, what's the lowest found in a serving? What's the volume of a meal and how it changes throughout digestion? How it interacts with other food compounds? How is it dispersed? Dissociated? What happens as digestion proceeds? Pancreatic neutralization? How this changes its effects on enzymes since they used the acid? Was their culture static for days? Is the suppression transient? Would the body make up for it in livings as it appears? Is a slower release from the stomach an attempt to preserve the intestines? Can the palate be tricked and not object something harmful? Aren't symptoms expected when it's overwhelming (such as the sugar escaping digestion)? Will it blend?


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- Dietary Short Chain Fatty Acids: How the Gut Microbiota Fight Against Autoimmune and Inflammatory Diseases

"Absorbed SCFAs also drain into the portal vein from the digestive tract to the liver. In humans, serum concentrations of acetate are around 250 μmol/L, compared to 90 μmol/L of propionate and 30 μmol/L of butyrate.[63] Butyrate is low in the periphery because it is mostly utilized in the gut by the colonocytes. Propionate is metabolized in the liver, so also low concentrations are found in the periphery, leaving acetate as the most abundant SCFA in circulation.[63]"​

 

[Terma]

Yes I'm curious, for sure. Why would the japanese mix sugar with vinegar so ignorantly, it's so unlike them. Interesting you mention that, I do wonder if propionate is not overproduced in my body. It could help explain why carnitines seem to help (besides stuff regarding astrocytes). Its metabolism is problematic.

Then again:
Effects of SCFA on the DNA methylation pattern of adiponectin and resistin in high-fat-diet-induced obese male mice. - PubMed - NCBI