[Kimbo]

It was decided that we needed a new thread on this; while the old vinegar thread contains quite a bit of useful information, it's a bit hard to navigate through.

So just to get the ball rolling:

Why use it? Mechanism of action?
What can be used instead (e.g. sodium acetate)?
How much needs to be used?
When to use it?

If this thread leans more towards the "advanced" side of things, I'll move it to the appropriate location.

[Robboe]

It was decided that we needed a new thread on this; while the old vinegar thread contains quite a bit of useful information, it's a bit hard to navigate through.

So just to get the ball rolling:

Why use it? Mechanism of action?
What can be used instead (e.g. sodium acetate)?
How much needs to be used?
When to use it?

If this thread leans more towards the "advanced" side of things, I'll move it to the appropriate location.

The most obvious aspect is that it supplies acetic acid which can be plugged into the Krebs cycle to create ATP. The less obvious aspect is that it effects phosphofructokinase (PFK). This is the controlling enzyme for glycolysis. If it is active, glucose can be used for energy production. If inhibited, glycolysis cannot take place and the glucose is stored as glycogen (there are studies showing additional glycogen replenishment in rat models when using carbs + vinegar). Oversaturation of glycogen stores from this can also lead to (quicker?) hexosamine pathway shuttling and thus, letpin upregulation. As far as i'm aware, that's theory of Nandi/Caleb though, so i'm not sure its proven (yet).

How PFK is inhibited is unknown. It may be due to change in pH from the vinegar because it is pH-sensitive; It may be due to increased ATP replenishment from the acetic acid, because the "fed state" switches off PFK; Or it may be a combination of the two (most likely, but i dunno for certain).

[Colin]

From what I've gleaned of the subject,it should not be used at EVERY meal that has a sizable amount of cho(50+ grams) as the body adapts to it.VirtualCyber made some good points toward this end in his log recently,I forget exactly what they were though.

I'm in favor of using it twice per day along with 600mg ALA,with breakfast and my pre-bed meal,both of which contain at least 50 grams cho.

Post w/o usage is arguable as it seems to have both positive and negative impact within this time frame.

I like pina coladas and daquiri's.

And pizza.
A lot.
I like it a lot.



That's all I have to add to this thread.

[eclypz]

My only worthwhile contribution to this thread, and some would argue whether this is worthwhile or not, is that I've been taking four apple cidar vinegar tablets with two meals a day for about six months and I haven't noticed any real change in composition that my training and diet couldn't acount for themselves.

Again, nothing helpful really, but it seems like this stuff should be awesome or something and I just haven't been getting that impression.

[SupremeDan]

The most obvious aspect is that it supplies acetic acid which can be plugged into the Krebs cycle to create ATP. The less obvious aspect is that it effects phosphofructokinase (PFK). This is the controlling enzyme for glycolysis. If it is active, glucose can be used for energy production. If inhibited, glycolysis cannot take place and the glucose is stored as glycogen (there are studies showing additional glycogen replenishment in rat models when using carbs + vinegar). Oversaturation of glycogen stores from this can also lead to (quicker?) hexosamine pathway shuttling and thus, letpin upregulation. As far as i'm aware, that's theory of Nandi/Caleb though, so i'm not sure its proven (yet).

How PFK is inhibited is unknown. It may be due to change in pH from the vinegar because it is pH-sensitive; It may be due to increased ATP replenishment from the acetic acid, because the "fed state" switches off PFK; Or it may be a combination of the two (most likely, but i dunno for certain).

sorry but they were all wrong with that theory....

first....i remember very well my biochem classes from university and i assure you acetate can NOT form ATP.....it does get int the krebs cycle but basically it just takes place of other substrates kind of preventing some of making oxydations/phophorilisation to produce ATP.

second, oversaturation of glycogen won´t occur, you will hold more glycogen but not enough to have eny serious effects on hexosamine pathway. leptin upregulation will not happen...

[SupremeDan]

Let me summurise what acetic acid feeding will do to you...

- increases glycogen storage in skeletal muscle and in liver through temporary inhibition of glycolises. IT DOES NOT SUPERCOMPENSATE CELLS WITH GYCOGEN, IT ONLY INCREASE IT`S STORAGE.
- increases Gastric empting time thus lowering the GI of most carb food. It does this by partially inhibiting disacharidases and othe enzymes
- transient change in fuel burning from glucose status to FA oxydation status, speacially in the liver
- Increases hepatic AMPK
- Inhibits lipogenesis by decreasing FA synthase, malonyl-coa, SREBP1,
- decreases lactate ( better recovery )
- lowers ration of insulin to glucagon
- inhibits lypolises ( everybody that know something abou phisiology knows that lypolises allways get inhibeted when FA oxydation gets roling on, it´s the survival mechanism. if we oxtdising lots of FAs it means we are on caloric restriction wich means that we need to preserve fat stores so the body partially shuts down lypolises to prevent further depletion of fat stores)
- decreases chlesterol levels ( ldl )
- increases muscle and liver insulin sensivity
- has a antioxidant, antiinflamatory potential wich would turn this a antiaging supplement
- has anti bacterial properties
- reduces gluconeogenesis ( great thing to preserve muscle when cutting!!!)
- decreases leptin levels ( the contrary of what some believed )

dosage should be about 30-50 ml with carb containing meals 2 to 4 times a day

side effects:
- increase stomach bloating ( when eating lots of food ) because if increase digestion time and decrease in carb breaking enzymes
- stomach burning
- provokes lactose intollerance sinse it blocks latase formation almost completely

great supplement to use while bulking, cutting or for cheating....but only worth for people who don´t drink tons of milk like i am drinking now.

[SupremeDan]

Let me summurise what acetic acid feeding will do to you...

- increases glycogen storage in skeletal muscle and in liver through temporary inhibition of glycolises. IT DOES NOT SUPERCOMPENSATE CELLS WITH GYCOGEN, IT ONLY INCREASE IT`S STORAGE.
- increases Gastric empting time thus lowering the GI of most carb food. It does this by partially inhibiting disacharidases and othe enzymes
- transient change in fuel burning from glucose status to FA oxydation status, speacially in the liver
- Increases hepatic AMPK
- Inhibits lipogenesis by decreasing FA synthase, malonyl-coa, SREBP1,
- decreases lactate ( better recovery )
- lowers ration of insulin to glucagon
- inhibits lypolises ( everybody that know something abou phisiology knows that lypolises allways get inhibeted when FA oxydation gets roling on, it´s the survival mechanism. if we oxtdising lots of FAs it means we are on caloric restriction wich means that we need to preserve fat stores so the body partially shuts down lypolises to prevent further depletion of fat stores)
- decreases chlesterol levels ( ldl )
- increases muscle and liver insulin sensivity
- has a antioxidant, antiinflamatory potential wich would turn this a antiaging supplement
- has anti bacterial properties
- reduces gluconeogenesis ( great thing to preserve muscle when cutting!!!)
- decreases leptin levels ( the contrary of what some believed )

dosage should be about 30-50 ml with carb containing meals 2 to 4 times a day

side effects:
- increase stomach bloating ( when eating lots of food ) because if increase digestion time and decrease in carb breaking enzymes
- stomach burning
- provokes lactose intollerance sinse it blocks latase formation almost completely

great supplement to use while bulking, cutting or for cheating....but only worth for people who don´t drink tons of milk like i am drinking now.

Acetic acid activates hepatic AMPK and reduces hyperglycemia in diabetic KK-A(y) mice.

Sakakibara S, Yamauchi T, Oshima Y, Tsukamoto Y, Kadowaki T.

Central Research Institute, Mizkan Group Co., Ltd., Aichi 475-8585, Japan.

Acetic acid (AcOH), which is a short-chain fatty acid, is reported to have some beneficial effects on metabolism. To test the hypothesis that feeding of AcOH exerts beneficial effects on glucose homeostasis in type 2 diabetes, we fed either a standard diet or one containing 0.3% AcOH to KK-A(y) mice for 8 weeks. Fasting plasma glucose and HbA1c levels were lower in mice fed AcOH for 8 weeks than in control mice. AcOH also reduced the expression of genes involved in gluconeogenesis and lipogenesis, which is in part regulated by 5'-AMP-activated protein kinase (AMPK) in the liver. Finally, sodium acetate, in the form of neutralized AcOH, directly activated AMPK and lowered the expression of genes such as for glucose-6-phosphatase and sterol regulatory element binding protein-1 in rat hepatocytes. These results indicate that the hypoglycemic effect of AcOH might be due to activation of AMPK in the liver.

Effect of acetic acid feeding on the circadian changes in glycogen and metabolites of glucose and lipid in liver and skeletal muscle of rats.

Fushimi T, Sato Y.

Central Research Institute, Mizkan Group Corporation, 2-6 Nakamura-cho, Handa, Aichi 475-8585, Japan. tfushimi@mizkan.co.jp

The aim of the present study is to investigate the effect of acetic acid feeding on the circadian changes in glycogen concentration in liver and skeletal muscle. Rats were provided meal once daily (09.00-13.00 hours) for 10 d. On the 11th day, they were either killed immediately or given 9 g diet containing either 0 (control) or 0.7 g/kg-diet acetic acid beginning at 09.00 hours for 4 h, as in the previous regimen. Rats in the fed group were killed at 4, 8 or 24 h after the start of feeding. At 4 h after the start of feeding, the acetic acid group had significantly greater liver and gastrocnemius muscle glycogen concentrations (P<0.05). Also, at this same point, liver xylulose-5-phosphate, a key stimulator of glycolysis, the ratio of fructose-1,6-bisphosphate to fructose-6-phosphate in skeletal muscle, which reflects phosphofructokinase-1 activity, and liver malonyl-CoA, an allosteric inhibitor of carnitine palmitoyl-transferase, were significantly lower in the acetic acid group than in the control group (P<0.05). In addition, the acetic acid group had a significantly lower serum lactate concentration and lower ratio of insulin to glucagon than the control group at the same point (P<0.05). We conclude that a diet containing acetic acid may enhance glycogen repletion but not induce supercompensation, a large increase in the glycogen level that is beneficial in improving performance, in liver and skeletal muscle by transitory inhibition of glycolysis. Further, we indicate the possibility of a transient enhancement of fatty acid oxidation in liver by acetic acid feeding.

Dietary acetic acid reduces serum cholesterol and triacylglycerols in rats feda cholesterol-rich diet.

Fushimi T, Suruga K, Oshima Y, Fukiharu M, Tsukamoto Y, Goda T.

Laboratory of Nutritional Physiology and COE Program in the 21st Century, School of Food and Nutritional Sciences, The University of Shizuoka, Shizuoka 422-8526, Japan.

To investigate the efficacy of the intake of vinegar for prevention of hyperlipidaemia, we examined the effect of dietary acetic acid, the main component of vinegar, on serum lipid values in rats fed a diet containing 1 % (w/w) cholesterol. Animals were allowed free access to a diet containing no cholesterol, a diet containing 1 % cholesterol without acetic acid, or a diet containing 1 % cholesterol with 0.3 % (w/w) acetic acid for 19 d. Then, they were killed after food deprivation for 7 h. Cholesterol feeding increased serum total cholesterol and triacylglycerol levels. Compared with the cholesterol-fed group, the cholesterol and acetic acid-fed group had significantly lower values for serum total cholesterol and triacylglycerols, liver ATP citrate lyase (ATP-CL) activity, and liver 3-hydroxy-3-methylglutaryl-CoA content as well as liver mRNA levels of sterol regulatory element binding protein-1, ATP-CL and fatty acid synthase (P<0.05). Further, the serum secretin level, liver acyl-CoA oxidase expression, and faecal bile acid content were significantly higher in the cholesterol and acetic acid-fed group than in the cholesterol-fed group (P<0.05). However, acetic acid feeding affected neither the mRNA level nor activity of cholesterol 7alpha-hydroxylase. In conclusion, dietary acetic acid reduced serum total cholesterol and triacylglycerol: first due to the inhibition of lipogenesis in liver; second due to the increment in faecal bile acid excretion in rats fed a diet containing cholesterol.

Vinegar supplementation lowers glucose and insulin responses and increases satiety after a bread meal in healthy subjects.

Ostman E, Granfeldt Y, Persson L, Bjorck I.

Applied Nutrition and Food Chemistry, Department of Food Technology, Engineering and Nutrition, Lund University, Lund, Sweden. Elin.Ostman@inl.ith.se

OBJECTIVE: To investigate the potential of acetic acid supplementation as a means of lowering the glycaemic index (GI) of a bread meal, and to evaluate the possible dose-response effect on postprandial glycaemia, insulinaemia and satiety. SUBJECTS AND SETTING: In all, 12 healthy volunteers participated and the tests were performed at Applied Nutrition and Food Chemistry, Lund University, Sweden. INTERVENTION: Three levels of vinegar (18, 23 and 28 mmol acetic acid) were served with a portion of white wheat bread containing 50 g available carbohydrates as breakfast in randomized order after an overnight fast. Bread served without vinegar was used as a reference meal. Blood samples were taken during 120 min for analysis of glucose and insulin. Satiety was measured with a subjective rating scale. RESULTS: A significant dose-response relation was seen at 30 min for blood glucose and serum insulin responses; the higher the acetic acid level, the lower the metabolic responses. Furthermore, the rating of satiety was directly related to the acetic acid level. Compared with the reference meal, the highest level of vinegar significantly lowered the blood glucose response at 30 and 45 min, the insulin response at 15 and 30 min as well as increased the satiety score at 30, 90 and 120 min postprandially. The low and intermediate levels of vinegar also lowered the 30 min glucose and the 15 min insulin responses significantly compared with the reference meal. When GI and II (insulinaemic indices) were calculated using the 90 min incremental area, a significant lowering was found for the highest amount of acetic acid, although the corresponding values calculated at 120 min did not differ from the reference meal. CONCLUSION: Supplementation of a meal based on white wheat bread with vinegar reduced postprandial responses of blood glucose and insulin, and increased the subjective rating of satiety. There was an inverse dose-response relation between the level of acetic acid and glucose and insulin responses and a linear dose-response relation between acetic acid and satiety rating. The results indicate an interesting potential of fermented and pickled products containing acetic acid.

Acetic acid suppresses the increase in disaccharidase activity that occurs during culture of caco-2 cells.Ogawa N, Satsu H, Watanabe H, Fukaya M, Tsukamoto Y, Miyamoto Y, Shimizu M.
Department of Applied Biological Chemistry, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Tokyo 113-8657, Japan.

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.

[hotstreet]

dosage should be about 30-50 ml with carb containing meals 2 to 4 times a day

What about someone following the Anabolic Diet? 6 days low carbs (I eat 44g of carbs a day - 8g of carbs from vegetables at 5 or 6 meals)?

On the one carb up day I would just follow the above recommendation?

thanks

[SupremeDan]

dosage should be about 30-50 ml with carb containing meals 2 to 4 times a day

What about someone following the Anabolic Diet? 6 days low carbs (I eat 44g of carbs a day - 8g of carbs from vegetables at 5 or 6 meals)?

On the one carb up day I would just follow the above recommendation?

thanks

the anabolic diet???? that shit is more likely to be the " catabolic diet" if anything.....anyways......follow the same recomendations as above on your carb days....

and le´t me give you a adivise for what i am worth. drop this diet......

[Grassroots082]

the anabolic diet???? that shit is more likely to be the " catabolic diet" if anything.....anyways......follow the same recomendations as above on your carb days....

and le´t me give you a adivise for what i am worth. drop this diet......

Can you elaborate on this Dan?

[SupremeDan]

IMHO i don´t like keto diets........i think they are of no use for people with a normal metabolism. they are only worth looking into when you have metablic problems like syndrome x for example.......

[Whacked]

Via what exact mechanism does vinegar aid with glucose metabolism? Reason I ask is that I am trying to figure out if it would benefit me to take it with PWOshake and PWO meal. I have norticed that r-ala is counter productive for me (PWO). I do not metabolise carbs well (get lethargic quite easily) even PWO when using excess carbs. Also, is cinnamon a better choice?

[Coprolith]

I know Acetate is like a very short chain fatty acid, so are any of its benefits nullified by something like PPAR agonists?

[Spook]

I know Acetate is like a very short chain fatty acid, so are any of its benefits nullified by something like PPAR agonists?

Via what exact mechanism does vinegar aid with glucose metabolism?

The less obvious aspect is that it effects phosphofructokinase (PFK).

These are all related so let me see if I can't address them all at once. Acetate works primarily by occupying the carbon fixation enzymes in ones mitochondria which ultimately results in inhibition of PFK-1 enzyme. PFK-1 is the rate limiting enzyme when it comes to oxidation of glucose-6-phosphate (what glucose turns in to as soon as it enters a cell).

So to put it simply acetate stops carb oxidation for a very short period of time (we are talking like 30 minutes or so here depending on dose; it is metabolized and eliminated very quickly).

One very important point not yet touched on in this thread is consequences of carb selection in the context of acetate use. As stated IMO acetate works via PFK-1 and fructose gets to bypass PFK-1 during it's oxidation. So to put it simply acetate will blunt the use of glucose but not fructose. The consequences of that get pretty complex and one must analyze there carb selection and when it is optimal to use which carbs with acetate.

P.S. buy sodium acetate instead of vinegar. It is so much easier to get the required dose of acetate using a supplement.

[Jinx Me]

These are all related so let me see if I can't address them all at once. Acetate works primarily by occupying the carbon fixation enzymes in ones mitochondria which ultimately results in inhibition of PFK-1 enzyme. PFK-1 is the rate limiting enzyme when it comes to oxidation of glucose-6-phosphate (what glucose turns in to as soon as it enters a cell).

So to put it simply acetate stops carb oxidation for a very short period of time (we are talking like 30 minutes or so here depending on dose; it is metabolized and eliminated very quickly).

One very important point not yet touched on in this thread is consequences of carb selection in the context of acetate use. As stated IMO acetate works via PFK-1 and fructose gets to bypass PFK-1 during it's oxidation. So to put it simply acetate will blunt the use of glucose but not fructose. The consequences of that get pretty complex and one must analyze there carb selection and when it is optimal to use which carbs with acetate.

P.S. buy sodium acetate instead of vinegar. It is so much easier to get the required dose of acetate using a supplement.

so taking vinegar with high GI fruits for example would be pointless?

How do ACV tabs compare to the vinegar itself? I just bought some tabs so I want to use them.

And if you're eating a fairly large carb meal, would you recommend say, dosing some vinegar in addition to tabs, and then maybe popping some more tabs partway through the meal?

[Jinx Me]

so taking vinegar with high GI fruits for example would be pointless?

How do ACV tabs compare to the vinegar itself? I just bought some tabs so I want to use them.

And if you're eating a fairly large carb meal, would you recommend say, dosing some vinegar in addition to tabs, and then maybe popping some more tabs partway through the meal?

bump - any further thoughts on this?

[liorrh]

1- no
2- no idea
3- why?

i'm cautioning against too much acetate, its excitory

[Kimbo]

so taking vinegar with high GI fruits for example would be pointless?

How do ACV tabs compare to the vinegar itself? I just bought some tabs so I want to use them.

And if you're eating a fairly large carb meal, would you recommend say, dosing some vinegar in addition to tabs, and then maybe popping some more tabs partway through the meal?

1. Not entirely sure... I know fruits do typically contain other sugars besides fructose.

2. They should work fine, assuming it's just concentrated vinegar. It should have the same amount of acetate, etc.

3. I'd just double up on the ACV caps.

[Suite]

since ACV has a basic PRAL value wouldn't it also be useful for helping combat the acidosis associated w/ eating lots of protein?

[dashforce]

So if the mechanism is through PFK, wouldn't the peak insulin response to carb meal + acetic acid be fairly comparable to response to the same meal w/o acetic acid (although the insulin AUC would be smaller because of less time in a hyperglycemic state, right?)

So what are the aforementioned problems with vinegar PWO? Would these problems apply in early morning/breakfast as well? IOW, does vinegar pose a problem to "strategic" insulin spiking with sensitivity is high?

In rats, the blood glucose response to a 10% corn starch load was significantly reduced when coadministered with a 2% acetic acid solution.[45] In healthy human subjects, although the glucose response curve was not significantly altered, the area under the insulin response curve following the ingestion of 50 g sucrose was reduced 20% when coadministered with 60 mL strawberry vinegar.

from http://forum.bodybuilding.com/showthread.p...53#post11909253
which got it from
http://www.medscape.com/viewarticle/531649_3

I don't have medscape access, so I can't post the source

[raptor2003]

I get stomach bloat , gas and stomach upset from taking acv with oatmeal

thoughts? intolerant of what? tks

[VIPsupps]

well im lactose intolerant as it is.the only milk product i take in is a very pure whey isolate.which i take in pre and post workout.so taking the acv as described with pwo meal/carbs wouldnt really work for me then.

ive started taking a TB of it with not my pwo shake,but with my pwo meal following that shake.it does not have dairy in it.im taking it mainly for the,hopeful,health benefits especially the alkalinizing effect.or have i missed info showing this was invalid?

[vinnys029]

ACV is great for the liver, it also helps cure acid reflux. ACV is just an overall great product for the human body. Cleans you out too.

[liorrh]

http://clinicaltrials.gov/ct2/show/NCT00755924

Prospective Randomized Clinical Trial Evaluating the Impact of Vinegar on High Density Lipoprotein

This study is currently recruiting participants.
Verified by Park Nicollet Institute, April 2008

Sponsored by: Park Nicollet Institute
Information provided by: Park Nicollet Institute
ClinicalTrials.gov Identifier: NCT00755924
Purpose

This is a double-blinded randomized placebo controlled prospective clinical trial evaluating the impact of apple cider vinegar on serum HDL. 112 participants will be randomized to consume either 2 tablespoons of vinegar daily or a placebo containing a 2% balsamic vinegar solution in water. Baseline, two month and 4 month blood samples will be obtained for fasting lipids. The primary endpoint is met if HDL levels increase in the treatment arm versus baseline after 2 month intervention.