Lex: Fat high v low

[SkinnyDevil]

Lex,

In another thread, you stated:

Fat storage is dynamic and not static.  By this I mean that we don’t just eat a meal, end up with excess energy, have it stored as fat, and then we are done with it.  Fat is constantly mobilized into and out of storage using both ASP and Insulin pathways.  Even when there is and abundance of free fatty acids in the blood, some is being stored while some is being released from storage on a continual basis.  If there is generally more energy consumed as food than is needed by the body then there will be a net storage of fat over time.  If more energy is being used by the body than is being consumed as food then there will be a net loss of fat over time. 

If we get most of our energy from fat, then as long as the amount of fatty acids (energy) we eat roughly equals the fatty acids (energy) our body uses, then over time our weight will remain constant.

Most of this is well-known, but there is one question with regards to type of calories (the "energy" you speak of) and conversion of said energy to fat for storage.

You SEEM to be saying that if one decreases their fat intake, then all other things being equal, they will lose body fat (with "other things being equal" meaning the same energy expenditure, the same food consumption, etc.).

Is this correct?

So, if I need to increase my body fat percentage, I simply eat more fat, or more calories that easily convert to fat? But if I need to decrease my body fat percentage, I eat less fat, or fewer calories that easily convert to fat?

With regards to low carb & zero carb, does meat (or more precisely, does protein) NOT convert to fat just as fats, alcohols, & carbs (simple & complex)? Or do ALL excess calories convert to fat?

[lex_rooker]

Lex,

You SEEM to be saying that if one decreases their fat intake, then all other things being equal, they will lose body fat (with "other things being equal" meaning the same energy expenditure, the same food consumption, etc.).

Is this correct?

My experience and that of others seems to point to a tentative yes answer to this question.  There are a couple of issues.  The primary issue seems to be whether our bodies have adapted to the food.  In the case of carbs, the cellular metabolism is fermentive and all cells can use glucose without adapting, however, if the main fuel available suddenly becomes fatty acids, then the cells must create mitochondria to be able to use the fatty acids directly as fuel.  Until sufficient mitochondria and the associated enzymes have been built up in the cells, the cell’s ability to take up the available energy from fatty acids is impaired and the results are the same as if we just didn’t eat those fatty acids in the first place as the energy from them is mostly unavailable.  In other words, it appears that calories don’t count.  Once the cells adapt, then either form of energy source (glucose or fatty acids) will be efficiently metabolized and generally speaking, weight will be gained or lost depending on overall energy balance.   

So, if I need to increase my body fat percentage, I simply eat more fat, or more calories that easily convert to fat? But if I need to decrease my body fat percentage, I eat less fat, or fewer calories that easily convert to fat?

With regards to low carb & zero carb, does meat (or more precisely, does protein) NOT convert to fat just as fats, alcohols, & carbs (simple & complex)? Or do ALL excess calories convert to fat?

My experience is that, once adapted to fat as our primary food, then ALL excess calories, regardless of the source, will contribute to our overall energy balance.  However, the idea that to maintain weight, CALORIES IN must = CALORIES OUT is very simplistic and our bodies are very complex chaotic mechanisms.  There does seem to be a metabolic advantage to eating ZC or VLC as some research indicates that the alternate fat storage pathways (ASP/HSL etc) are not quite as efficient as insulin/AGP as described by Taubes in GCBC. 

My own experience has been that if I eat many carbs at all then weight gain is very rapid.   I would expect this as carbs cause BG to rapidly rise which the body sees as a threat and it deals with it by using insulin to remove the glucose, converting it to triglycerides, and storing it safely away in the fat cells where it can’t do any damage.

However, if I just overeat calories as fat and protein, then I do gain weight, but it is slower and I don’t seem to gain as much as I would from eating a similar calorie intake from carbs.  Eating fat does not cause a rapid rise in BG so there is no health threat driving the removal of excess fatty acids from the blood stream.  Since insulin levels are low, fat storage is now limited to the activity level of the enzymes (ASP/HSL) that allow direct fat storage at the cellular level.  This does seem to limit the rate and possibly the total amount of fat that can/will be stored based on any given calorie intake level.

We also know that when eating ZC or VLC some of the fatty acids are converted to ketones and excess ketones are eliminated from the body through urine, sweat, and breath.  This would be excess energy that was thrown away and therefore unavailable to be converted to fat, again providing a metabolic advantage to this dietary protocol.

Very complex subject and I certainly don’t claim to be an expert by any stretch of the imagination.  My postings are mainly an effort to dispel the myth that you can’t gain weight on a ZC or VLC diet.  You certainly can and generally speaking, once you’ve fully adapted to using fatty acids as your primary fuel at the cellular level, you will gain weight if you consistently consume more energy than you use regardless of the source of the energy (fat, protein, or carbs).  Many people on the ZIOH forum have been surprised when, after 18 months of continuous weight loss on ZC, they suddenly find they are putting on weight again.   Most have bought into the myth that you can only gain weight if you eat carbs and this just isn’t true.

Lex


 

[carnivore]

Lex,

Do you think that the symptoms associated with a switch to a high fat diet (increased heart rythm, etc.) can last the 18 months required to build up the enzymes/mitochondria to efficiently burn the fat ?

After 10 months on such a diet, I still have a high pulse (correlated to the amount of fat I eat), and I have a very high LDL, high VLDL and triglycerides. I wonder if my body is still not adapted or if a high fat diet is simply not appropriate for me. I am also anxious because hyperlipidemia is not particularly healthy on the long term.

[Hannibal]

Excerpt from Harper's Illustrated Biochemistry, 28e
Chapter 16. Overview of Metabolism & the Provision of Metabolic Fuels

Lipids in the diet (Figure 16–6) are mainly triacylglycerol, and are hydrolyzed to monoacylglycerols and fatty acids in the gut, then re-esterified in the intestinal mucosa.
Here they are packaged with protein and secreted into the lymphatic system and thence into the bloodstream as chylomicrons, the largest of the plasma lipoproteins. Chylomicrons also contain other lipid-soluble nutrients. Unlike glucose and amino acids, chylomicron triacylglycerol is not taken up directly by the liver.
It is first metabolized by tissues that have lipoprotein lipase, which hydrolyzes the triacylglycerol, releasing fatty acids that are incorporated into tissue lipids or oxidized as fuel.

[lex_rooker]

Lex,

Do you think that the symptoms associated with a switch to a high fat diet (increased heart rhythm, etc.) can last the 18 months required to build up the enzymes/mitochondria to efficiently burn the fat ?

After 10 months on such a diet, I still have a high pulse (correlated to the amount of fat I eat), and I have a very high LDL, high VLDL and triglycerides. I wonder if my body is still not adapted or if a high fat diet is simply not appropriate for me. I am also anxious because hyperlipidemia is not particularly healthy on the long term.

Frederic,
As I remember it took quite awhile for the heart palpitations and night time leg cramps to completely go away.  Rapid pulse rate and palpitations (feeling my heart pounding in my chest) would often be very evident in the morning when I woke up.  Leg cramps would wake me up in the middle of the night and I'd have to get out of bed and stretch to make the cramp go away.  I think I suffered these two problems in varying degrees for 18 months to 2 years (I thought they’d never go away). Then they just went away on their own. Their disappearance seemed to coincide with the drop in ketone levels in my urine as my body started to use more of the ketones as fuel. 

The problems resurfaced for a short time when I did my high fat experiment.  The experiment forced me to lower protein and raise fat intake which caused ketones to return to high levels even though my body was clearly burning them as fuel.  The occurance of night time leg cramps and rapid heart rate did start to decline noticeably during the 5 months I did the experiment and they totally stopped when I again lowered intake fat back down below 80% of calories.

As I’ve stated in my Journal, I’ve recently raised fat intake to 80% of calories again in an effort to lower HbA1c levels.  However, this time the palpitations and cramps haven’t returned even though ketones have risen again.

It appears to be a hormonal issue related to deep ketosis and the adrenal system and not an issue with cellular level metabolism.  My guess is that when you say that your high pulse is correlated to the amount of fat you eat, you experience a higher pulse rate (and possibly palpitations) when eating higher fat.  The higher percentage of fat in your diet (especially when there are no carbs present) the more ketones are produced and the greater the effect on the adrenal hormones which can cause your heart to race.  You can either add a small amount of carbs to your diet to reduce ketone levels, or reduce fat and increase protein which will also reduce ketone levels as excess protein will be converted to glucose thus moderate ketones as well - or you can just wait it out like I did.


I think Peter's Hyperlipid Blog discusses this issue here:

http://high-fat-nutrition.blogspot.com/2009/11/brief-discussion-of-ketosis.html
 

The belief that all body systems become keto-adapted within a few weeks is a myth.  It is true that not everyone suffers from every problem related to adaptation, but it is clear that total adaptation takes many months.

Lex

[carnivore]

Frederic,
As I remember it took quite awhile for the heart palpitations and night time leg cramps to completely go away.  Rapid pulse rate and palpitations (feeling my heart pounding in my chest) would often be very evident in the morning when I woke up.  Leg cramps would wake me up in the middle of the night and I'd have to get out of bed and stretch to make the cramp go away.  I think I suffered these two problems in varying degrees for 18 months to 2 years (I thought they’d never go away). Then they just went away on their own. Their disappearance seemed to coincide with the drop in ketone levels in my urine as my body started to use more of the ketones as fuel.  

The problems resurfaced for a short time when I did my high fat experiment.  The experiment forced me to lower protein and raise fat intake which caused ketones to return to high levels even though my body was clearly burning them as fuel.  The occurance of night time leg cramps and rapid heart rate did start to decline noticeably during the 5 months I did the experiment and they totally stopped when I again lowered intake fat back down below 80% of calories.

As I’ve stated in my Journal, I’ve recently raised fat intake to 80% of calories again in an effort to lower HbA1c levels.  However, this time the palpitations and cramps haven’t returned even though ketones have risen again.

It appears to be a hormonal issue related to deep ketosis and the adrenal system and not an issue with cellular level metabolism.  My guess is that when you say that your high pulse is correlated to the amount of fat you eat, you experience a higher pulse rate (and possibly palpitations) when eating higher fat.  The higher percentage of fat in your diet (especially when there are no carbs present) the more ketones are produced and the greater the effect on the adrenal hormones which can cause your heart to race.  You can either add a small amount of carbs to your diet to reduce ketone levels, or reduce fat and increase protein which will also reduce ketone levels as excess protein will be converted to glucose thus moderate ketones as well - or you can just wait it out like I did.


I think Peter's Hyperlipid Blog discusses this issue here:

http://high-fat-nutrition.blogspot.com/2009/11/brief-discussion-of-ketosis.html
 

The belief that all body systems become keto-adapted within a few weeks is a myth.  It is true that not everyone suffers from every problem related to adaptation, but it is clear that total adaptation takes many months.

Lex

Thank's Lex. The only solution I have found so far is to reduce my fat intake, as carbs seems to do nothing to alleviate the symptoms. However, I may not eat enough, because fruits alone gives me hypoglycemia and I don't see how I can eat 50g of carbs a day on a raw food diet without BG swings...
As for cramps, seafood does the trick.

My pulse is always higher in the night/morning than in the evening, perhaps because I burn less calories during the night, increasing ketones production.
My pulse increases and is disturbed after a high fat meal.
My teeth are also too much sensitive when I eat lots of fat. And my vision is blurred...

Did you check your cholesterols/triglycerides during you high fat diet adaptation when you had these heart/cramp symptoms ?
I must say that I am afraid of my poor blood results, and I would not want my hyperlipidemia to last for too long...(no to mention possible adrenal burn out)

[lex_rooker]

Frederic,
Yes, I had blood work done during the time I was eating high fat.  The PDF files of all my lab work is posted in the first entry of my Jorunal.  You'll see that Triglycerides, Cholesterol, and just about everything else improved.  My Doctor warned me that cholesterol and triglycerides would sky rocket, but just the opposite happened.

Lex

[SkinnyDevil]

...reduce fat and increase protein which will also reduce ketone levels as excess protein will be converted to glucose thus moderate ketones as well...

I must have a fundamental misunderstanding of physiology. I was under the impression protein does not convert to glucose. If protein converts to glucose & excess glucose coverts easily to fat, then why do VLC & ZC diets like Atkins work so well in achieving weight loss....especially for those who do no exercise?

EDIT: Re-word...not that protein does NOT convert, but that it does not easily convert...and so doesn;t so long as there is body fat available to burn.

[lex_rooker]

I must have a fundamental misunderstanding of physiology. I was under the impression protein does not convert to glucose. If protein converts to glucose & excess glucose coverts easily to fat, then why do VLC & ZC diets like Atkins work so well in achieving weight loss....especially for those who do no exercise?

EDIT: Re-word...not that protein does NOT convert, but that it does not easily convert...and so doesn;t so long as there is body fat available to burn.

I must have a fundamental misunderstanding of physiology. I was under the impression protein does not convert to glucose. If protein converts to glucose & excess glucose coverts easily to fat, then why do VLC & ZC diets like Atkins work so well in achieving weight loss....especially for those who do no exercise?

EDIT: Re-word...not that protein does NOT convert, but that it does not easily convert...and so doesn;t so long as there is body fat available to burn.

This is one of those religious arguments.  There are those that say protein only converts to glucose when needed, and there are others that believe that some portion of all the protein we eat is converted to glucose.  I'm in the second camp as my personal experience supports that some portion of all protein eaten is converted to glucose.

Example:  I eat a mixture of meat and fat that provides 80+% of calories from fat and about 90g protein per day while supplying around 2,000 calories of total energy.  My average blood glucose will hover right around 85 mg/dl.  If my body needed more then it would start sacrificing lean muscle mass or something to create a higher BG level.  But it doesn't do this so it appears that 85 mg/dl is sufficient to meet my body’s need for glucose.  My lean body mass remains stable (based on caliper measurements) as does my weight.  I can eat this high level of fat for months at a time and BG continues to average 85 mg/dl, and lean body mass as well as weight stay stable.  Everything seems to be in balance and happy.

Now, if I reduce the fat level to 65% of calories and raise the amount of protein that I’m consuming to 150g /day, while eating an amount of food that keeps total energy the same at around 2,000 calories, the spikes in BG reach higher peaks after eating, and average BG rises to 100 mg/dl.  If I continue this regimen for several months, everything remains in balance as well, its just that average BG, and the BG spikes after eating are at higher levels.  I don’t seem to gain weight so my assumption is that total energy consumed vs total energy expended is again in balance.

Continuing on with this same line of reasoning, if my body already has a relatively high BG level of 100 mg/dl, then why would BG spike even higher after eating a protein rich meal?  It certainly doesn’t need more glucose.  This could only happen if some portion of all the protein eaten is converted to glucose.

Now I have to ask the question:  If protein is only converted to glucose when the body needs it, and, if my body is happy for months at a time with a BG of 85 mg/dl, then what would cause the rise in BG when more protein is consumed and BG to fall when less protein is consumed?  The only answer that I can come up with is that some portion of all dietary protein is converted to glucose independent of the body’s immediate need.

I also have found that if I increase protein consumption even more (above 150g/day), the glucose spike after eating rises even higher, but average BG tends to stabilize right around 100 mg/dl. This makes me believe that enough glucose is being created to cause insulin to kick in and hold it right at the threshold.  When we eat carbs the glucose spike is huge and rapid, often within minutes of eating.  This causes the body to overestimate the insulin requirement and dump more insulin than is needed.  This causes BG to fall rapidly after the high carb meal and it may fall to such an extent that we start craving something sweet to bring the levels back up.  This is the normal see-saw most high carb eaters experience.  When the body creates glucose from protein, the rise is much slower but for a longer duration, often several hours.  The very slow rise allows the pancreas time to react with the proper amount of insulin and BG is much more stable.  It would also keep BG close to the threshold where the body starts to release insulin.  For me this seems to be right at 100 mg/dl.

It is also interesting that when eating a higher level of protein, BG stays in a very tight range right around 100 mg/dl for about 20 hours per day. The other 4 hours is directly after eating where BG slowly rises then gently falls back to the 95-100 range.  When eating less protein and higher fat, BG averages right around 85 mg/dl but swings up and down much more.  It may drop into the mid 70’s a couple of hours before eating, and rise to 110 for an hour or so after eating and then gently falling back to 80-85 where it stays until a few hours before my next meal.  This makes me believe that 85 mg/dl is below the threshold where insulin is released as it is not being held constant, but swings in gentle curves peaking after eating and dipping before the meal. 

BG also swings much more in response to exercise when protein intake is lower.  If I’m eating the low protein protocol and BG is 85 and I then run a couple of miles, BG will fall during the run by maybe 10 points, and it will stay near this lower level until I eat my next meal.  This makes me believe that there is no excess glucose hanging around and if it gets consumed, then it will stay low, with the body only sacrificing tissue to create more if it is necessary.  This would tend to keep BG at the lower threshold.  If I’m eating a large amount of protein and BG is 100 when I start my run, it is usually still between 95 and 100 after the run.  Again, supporting the idea that there may be an overall excess of glucose when eating the higher protein diet and insulin is moderating it at the higher threshold level.

Here is an entry from my journal where I do some mathematical gymnastics that seem to support that about 58% of all the protein eaten is converted glucose.

http://www.rawpaleoforum.com/journals/lex's-journal/msg3720/#msg3720

This was probably more than you wanted to know, but I wanted to give you as complete and answer as possible.

Lex

[SkinnyDevil]

This causes BG to fall rapidly after the high carb meal and it may fall to such an extent that we start craving something sweet to bring the levels back up.  This is the normal see-saw most high carb eaters experience.

As an aside, perhaps this is why traditional meals have for so long included DESSERT.

This was probably more than you wanted to know, but I wanted to give you as complete and answer as possible.

No, actually - it was a fabulous and very informative answer. Thanx!

[lex_rooker]

The post above is rather long and a key point may have been lost in the forrest of words.  What I don't think I made clear is that I believe that there is a distinct difference between dietary protein and protein released through sacrificing internal healthy tissue.

My experience as discussed above is that some percentage of all dietary protein is probably converted to glucose and the conversion rate is probably somewhere around 58% if the source of the protein is meat.

However, my experiments have shown that if the body runs low on glucose and must sacrifice healthy tissue to create it, then it will only do so when necessary, and will only sacrifice the minimum tissue necessary to meet the immediate requirement. 

So, in effect both sides of the argument may have some truth to them.  On the side supporting the theory that protein is only converted to glucose when needed, I think it can be shown that this is probably true if healthy tissue must be sacrificed in the process.  On the side supporting the theory that some percentage of all protein is always being converted to glucose, I think it can be shown that this is probably true for protein consumed as food.

By extension it is also probably true that even when tissue is being sacrificed, the resulting protein is probably converted to glucose at the same percentage (about 58%) as dietary protein.  It's just that healthy tissue won't be sacrificed at all unless there is a critical need.

I also have a theory that the conversion rate is dependent on the amino acid profile of the protein.  Some amino acids can be converted to glucose and others can’t.  For animal protein (meat), it seems that about 58% of the amino acids are available for conversion.  However, protein from plant sources have a completely different amino acid profile and therefore would likely have a totally different rate of conversion.

As dietary protein from meat, and muscle tissue sacrificed to meet a critical glucose requirement are both from animal sources, their amino acid profile would be similar and therefore their conversion rate should be about the same.

I have no idea what the rate of conversion might be for plant based proteins. These always occur in the presence of large amounts of carbohydrate and there is no easy way for a layman to isolate them or determine their amino acid profile.  Without lab facilities capable of doing such an analysis, I have no way to prove or disprove the above theory.

If anyone can confirm (or wishes to shoot holes in) my reasoning, feel free.  I’m very good as sticking my foot in my mouth – to the point that now I just change feet!

Lex

[carnivore]

This is one of those religious arguments.  There are those that say protein only converts to glucose when needed, and there are others that believe that some portion of all the protein we eat is converted to glucose.  I'm in the second camp as my personal experience supports that some portion of all protein eaten is converted to glucose.

Example:  I eat a mixture of meat and fat that provides 80+% of calories from fat and about 90g protein per day while supplying around 2,000 calories of total energy.  My average blood glucose will hover right around 85 mg/dl.  If my body needed more then it would start sacrificing lean muscle mass or something to create a higher BG level.  But it doesn't do this so it appears that 85 mg/dl is sufficient to meet my body’s need for glucose.  My lean body mass remains stable (based on caliper measurements) as does my weight.  I can eat this high level of fat for months at a time and BG continues to average 85 mg/dl, and lean body mass as well as weight stay stable.  Everything seems to be in balance and happy.

Now, if I reduce the fat level to 65% of calories and raise the amount of protein that I’m consuming to 150g /day, while eating an amount of food that keeps total energy the same at around 2,000 calories, the spikes in BG reach higher peaks after eating, and average BG rises to 100 mg/dl.  If I continue this regimen for several months, everything remains in balance as well, its just that average BG, and the BG spikes after eating are at higher levels.  I don’t seem to gain weight so my assumption is that total energy consumed vs total energy expended is again in balance.

Continuing on with this same line of reasoning, if my body already has a relatively high BG level of 100 mg/dl, then why would BG spike even higher after eating a protein rich meal?  It certainly doesn’t need more glucose.  This could only happen if some portion of all the protein eaten is converted to glucose.

Now I have to ask the question:  If protein is only converted to glucose when the body needs it, and, if my body is happy for months at a time with a BG of 85 mg/dl, then what would cause the rise in BG when more protein is consumed and BG to fall when less protein is consumed?  The only answer that I can come up with is that some portion of all dietary protein is converted to glucose independent of the body’s immediate need.

I also have found that if I increase protein consumption even more (above 150g/day), the glucose spike after eating rises even higher, but average BG tends to stabilize right around 100 mg/dl. This makes me believe that enough glucose is being created to cause insulin to kick in and hold it right at the threshold.  When we eat carbs the glucose spike is huge and rapid, often within minutes of eating.  This causes the body to overestimate the insulin requirement and dump more insulin than is needed.  This causes BG to fall rapidly after the high carb meal and it may fall to such an extent that we start craving something sweet to bring the levels back up.  This is the normal see-saw most high carb eaters experience.  When the body creates glucose from protein, the rise is much slower but for a longer duration, often several hours.  The very slow rise allows the pancreas time to react with the proper amount of insulin and BG is much more stable.  It would also keep BG close to the threshold where the body starts to release insulin.  For me this seems to be right at 100 mg/dl.

It is also interesting that when eating a higher level of protein, BG stays in a very tight range right around 100 mg/dl for about 20 hours per day. The other 4 hours is directly after eating where BG slowly rises then gently falls back to the 95-100 range.  When eating less protein and higher fat, BG averages right around 85 mg/dl but swings up and down much more.  It may drop into the mid 70’s a couple of hours before eating, and rise to 110 for an hour or so after eating and then gently falling back to 80-85 where it stays until a few hours before my next meal.  This makes me believe that 85 mg/dl is below the threshold where insulin is released as it is not being held constant, but swings in gentle curves peaking after eating and dipping before the meal. 

BG also swings much more in response to exercise when protein intake is lower.  If I’m eating the low protein protocol and BG is 85 and I then run a couple of miles, BG will fall during the run by maybe 10 points, and it will stay near this lower level until I eat my next meal.  This makes me believe that there is no excess glucose hanging around and if it gets consumed, then it will stay low, with the body only sacrificing tissue to create more if it is necessary.  This would tend to keep BG at the lower threshold.  If I’m eating a large amount of protein and BG is 100 when I start my run, it is usually still between 95 and 100 after the run.  Again, supporting the idea that there may be an overall excess of glucose when eating the higher protein diet and insulin is moderating it at the higher threshold level.

Here is an entry from my journal where I do some mathematical gymnastics that seem to support that about 58% of all the protein eaten is converted glucose.

http://www.rawpaleoforum.com/journals/lex's-journal/msg3720/#msg3720

This was probably more than you wanted to know, but I wanted to give you as complete and answer as possible.

Lex

And what about glycogen stored in the liver ?
Eating meat triggers glucagon which raises BG.

[lex_rooker]

And what about glycogen stored in the liver ?

I give up, what about it? 

Eating meat triggers glucagon which raises BG.

I've found nothing that states that eating meat itself triggers the release of glucagon.  Do you have a resource?

Lex   

[carnivore]

I give up, what about it?  

I've found nothing that states that eating meat itself triggers the release of glucagon.  Do you have a resource?

Lex    

Here for instance : http://www.vivo.colostate.edu/hbooks/pathphys/endocrine/pancreas/glucagon.html

"Elevated blood levels of amino acids, as would be seen after consumption of a protein-rich meal: In this situation, glucagon would foster conversion of excess amino acids to glucose by enhancing gluconeogenesis."

In your explanation, you ignore glycogen stores and how it can impact BG.
After a protein-rich meat, glucagon will stimulate the breakdown of glycogen stored in the liver, thus increasing your BG.

[lex_rooker]

"Elevated blood levels of amino acids, as would be seen after consumption of a protein-rich meal: In this situation, glucagon would foster conversion of excess amino acids to glucose by enhancing gluconeogenesis."

In your explanation, you ignore glycogen stores and how it can impact BG.
After a protein-rich meat, glucagon will stimulate the breakdown of glycogen stored in the liver, thus increasing your BG.

Frederic,
Most of what I write about is my observations on things I can measure.  I've certainly written about how BG rises after a protein rich meal.  In fact, that was the major thesis of my previous posts on this thread.  I think it is also well known that there are very large glycogen stores in the liver which can be released when necessary.  This is one of the body's major reserves used to regulate glucose levels in the dynamic and chaotic conditions of every day living.

The link you provided seems to validate my direct experience – BG rises after eating a high protein meal.  I never discounted that BG can be affected by liver glycogen stores.  I just have no evidence that it is a significant factor in the conversion of dietary protein to glucose. I have applied simple math to the measurements and observations that I’m able to make, and the results seem to support that about 58% of the protein eaten adds additional glucose or glycogen to the body.  This is demonstrated by the fact that temporary weight gain caused by eating the high protein meal is consistent with the necessary additional water retention required to keep the proper tissue fluid balance if 58% of the protein was converted to glucose or glycogen. This is based on a research document that I read several years ago stating that for every gram of glucose and/or glycogen added (or removed) from blood and tissue, the body must store or release about 6g of water for the body to stay in proper fluid balance.  Glucose or glycogen released from the liver – even if it caused a rise in BG, would not contribute additional glucose to the body and therefore would not require additional water storage for the body to remain in proper fluid balance as newly added glucose derived from a meal would.  Is my reasoning simplistic?  Yup.  Are there a host of variables that could account for the body taking on additional water? Certainly.  However, I’ve done this experiment many times and it always comes out with similar results supporting (not proving) the idea that new glucose is created from dietary protein at some fairly consistant percentage.

 If you are convinced that a significant percentage of the rise in BG after eating a protein rich meal is directly caused by the release of stored liver glycogen, can you demonstrate this either by direct measurement or by inference through a calculation showing how some parameter we can measure tracks closely with the release of liver glycogen stores (or glucagon levels) but would not be affected by the conversion of the dietary protein itself?  In other words, can you disprove the validity of my observations or how I arrived at my conclusions? 

I’ve never claimed to know everything and several of my ideas posted on this form and elsewhere have been proven to be flat out wrong.  I’m not at all bothered by being wrong.  Putting my ideas out in public allows for comment and feedback and provides a learning opportunity.

Lex

[alphagruis]

 If you are convinced that a significant percentage of the rise in BG after eating a protein rich meal is directly caused by the release of stored liver glycogen, can you demonstrate this either by direct measurement or by inference through a calculation showing how some parameter we can measure tracks closely with the release of liver glycogen stores (or glucagon levels) but would not be affected by the conversion of the dietary protein itself?  In other words, can you disprove the validity of my observations or how I arrived at my conclusions?  
Lex

Lex

Your reasoning makes sense to me and I think it might well be essentially correct. By the way your observations are really of high interest from a scientific point of view.

After a look at the biochemistry involved the reason I see for the objection of Frederic to be irrelevant or not hold seems to be the following:

Glucagon is released in case of a protein rich meal that results in a high concentration of amino acids in blood.

 Yet if BG is normal (not too low), there is at any rate a level of glucose in the liver quite high enough to prevent breakdown of glycogen. Glycogenolysis then cannot occur because an enzyme involved in its pathway is merely inactive. This enzyme is the phosphorylase which is inhibited by binding to glucose when its concentration is normal. By the way this is actually a necessary condition since there is no reason to break down glycogen if there is enough glucose in the blood.

In other words this means that if glucagon is released because of elevated levels of amino acids in blood it will trigger the conversion of a fraction of them into glucose but it cannot trigger glycogenolysis if simultaneously BG is normal. For glyconenolysis to take place glucose levels in blood and liver must be low and glucagon released for that specific reason.

  

 

[carnivore]

If you are convinced that a significant percentage of the rise in BG after eating a protein rich meal is directly caused by the release of stored liver glycogen, can you demonstrate this either by direct measurement or by inference through a calculation showing how some parameter we can measure tracks closely with the release of liver glycogen stores (or glucagon levels) but would not be affected by the conversion of the dietary protein itself?  In other words, can you disprove the validity of my observations or how I arrived at my conclusions?  

I’ve never claimed to know everything and several of my ideas posted on this form and elsewhere have been proven to be flat out wrong.  I’m not at all bothered by being wrong.  Putting my ideas out in public allows for comment and feedback and provides a learning opportunity.

Lex

Lex,

I am convinced of...nothing. Just asking questions and trying to understand.

As glucagon and insulin are both in the blood, especially after several hours of fasting and a protein rich meal, how can one be sure that no break down of glycogen from the liver occurs?
After all, amino acids are systematically converted to glucose after a protein rich meal, at approximately always the same rate, even when BG is not too low.

[lex_rooker]

Lex,

I am convinced of...nothing. Just asking questions and trying to understand.

As glucagon and insulin are both in the blood, especially after several hours of fasting and a protein rich meal, how can one be sure that no break down of glycogen from the liver occurs?
After all, amino acids are systematically converted to glucose after a protein rich meal, at approximately always the same rate, even when BG is not too low.

I'm in pretty much the same boat.  There is very little I know for sure and I too have far more questions than answers.   

And, of course I'm not sure that there is no breakdown of glycogen from the liver, and I never said there wasn't. Since I don't have a way to measure the contribution of glucose from liver reserves, not sure what, if anything, meaningful I could add to the subject.  My calculations seem to indicate that most of the BG created from a high protein meal is "new" glucose, but again, this is just speculation from simplistic calculations based on rather shaky assumptions derived from experiments with poor (or non existent) controls.  It's a good thing that none of it matters and our bodies will do the right thing regardless of what nonsense our brains invent.

Lex 

[PaleoPhil]

I'm in pretty much the same boat.  There is very little I know for sure and I too have far more questions than answers.  
....

Then you are no fool, for Tyl Eulenspiegel the trickster of Germanic folklore said: "There is no greater fool than someone who thinks himself clever." I came across that just a couple days ago.

Tricksters are a seemingly universal feature of "primitive" societies. In the most "primitive" of societies--band societies, such as that of the San Bushmen--even the gods make mistakes and are sometimes the butt of jokes. Seems to me that this is the most realistic outlook.

The trickster outlook was echoed by Socrates, who whenever questioned about his judgment on a matter of debate, apparently used to say that he knew nothing for certain, and instead would ask questions of the questioner which eventually resulted in the questioner answering his own question. Plato's writes in his Republic: "Behold...the wisdom of Socrates; he refuses to teach himself, and goes about learning of others...."

My understanding is that Karl Popper added a corollary to this (or perhaps borrowed it form someone else) to the effect of "I only know what I don't know," or "I only know what the existing evidence does NOT support." (These are rough inklings from my memory that could be off).

I am also a great fan of the outlook and work of Nassim Taleb, in part because he is a fellow fan of Socrates and Popper. Taleb further builds on the insights of Socrates and Popper with his "causal opacity" in which "we are limited  in our ability to ferret out causes or in confirming our error rate in causal inference," as evidenced by the terrible track record of "experts" who try to do so.

It seems to me that the trickster spirit of hunter-gatherer mythology, Socrates, Plato, and Taleb all recognize that seeking final, absolute answers is a futile quest. Instead, we use the tools at our disposal to question, investigate and experiment. The end result of our questions is more questions.

[Addendum: And wouldn't you know it, in re-acquainting myself with Popper, I quickly find someone who attempts to shoot Popper's falsification approach to ribbons:

Martin Sewell, "Popper's Falsification," http://science.martinsewell.com/falsification.html

I'd be interested in people's opinions on Sewell's points.]