Energy balance

[mcsblues]

OK Gabe, just because you don't want your own thread, doesn't mean I can't pester you here!:p - (but if anyone else feels like jumping in, feel free).

BTW belated congratulations to you and Billie, and I hear you have a new job as well?

Anyway back to the question. In recent times there has been an at times heated debate amongst low carb supporters about the role of calories/energy balance in weight loss and maintenance. My friend Anthony Colpo has been the lightning rod for the temerity of his suggestion that weight loss, regardless of macronutrient ratios requires an energy deficit.

Just to be absolutely clear here, this is certainly not to suggest that 'calories are calories' or that there isn't a significant metabolic advantage in eating a higher protein, low carb diet. Anthony's position entirely recognises the importance of a favourable insulin:glucagon ratio to aid fat burning and the higher satiety of a low carb diet which for some, means energy restriction is automatic and effortless. He is simply talking about the balance between energy intake and expenditure (and part of that expenditure recognises the greater inefficiency of using protein as an energy source).

Phew! - I think that covers the background!;)

OK, I think it is common ground, even amongst opponents to this idea, that excessive energy intake will at the very least stall weight loss by the simple process of providing too many dietary calories for the body to be required to look elsewhere (eg. body fat) for energy needs. The much bigger question is whether maintaining weight loss can be compromised by excessive intake even while carbs are kept in the ketogenic range (say 50 or less). In simple terms, can excessive protein and/or fat intake lead to fat being deposited in this scenario?

My own position (and I'd have to say I have been dragged kicking and screaming to this conclusion!:o) is the answer is yes, and this is supported up by other people's experiences, including Anthony's who incorporates a 'bulking' phase in his body building routine whilst maintaining ketogenic carb intake.

So the question (finally) is firstly whether you agree, and if you do, perhaps you can have a stab at explaining the processes involved?

Would I be right in saying that even on a zero carb diet, glucagon is not dominant 24/7 and that it would not be healthy for us if it was? Does this mean that there are times even on a low carb diet that given sufficient (or excessive) protein and/or fat intake that fat storage will occur?

OK, one other brief question, did you get to the latest Nutrition and Metabolism conference, and if so what did you see as the highlights?

[Gabriel Guzman]

OK Gabe, just because you don't want your own thread, doesn't mean I can't pester you here!:p - (but if anyone else feels like jumping in, feel free).

BTW belated congratulations to you and Billie, and I hear you have a new job as well?


Thanks! Yes, I'll start in the new job next week. It's always a challenge to start from scratch but I hope it will lead to better opportunities down the road.


Anyway back to the question. In recent times there has been an at times heated debate amongst low carb supporters about the role of calories/energy balance in weight loss and maintenance. My friend Anthony Colpo has been the lightning rod for the temerity of his suggestion that weight loss, regardless of macronutrient ratios requires an energy deficit.


Your friend is partially right. Weight loss requires a caloric deficit but that doesn't necessarily has to happen the way most dietitians think. As research has shown, there are ways to create a caloric deficit without necessarily reducing caloric intake by just reducing the total amount of food.


Just to be absolutely clear here, this is certainly not to suggest that 'calories are calories' or that there isn't a significant metabolic advantage in eating a higher protein, low carb diet. Anthony's position entirely recognises the importance of a favourable insulin:glucagon ratio to aid fat burning and the higher satiety of a low carb diet which for some, means energy restriction is automatic and effortless. He is simply talking about the balance between energy intake and expenditure (and part of that expenditure recognises the greater inefficiency of using protein as an energy source).



Correct. This is what we like to call metabolic advantage.


OK, I think it is common ground, even amongst opponents to this idea, that excessive energy intake will at the very least stall weight loss by the simple process of providing too many dietary calories for the body to be required to look elsewhere (eg. body fat) for energy needs.


Here we need to be careful not to confuse terms. When dietitians and nutritionists (or anybody who likes to talk about energy balance and all that) talk about energy, they're not thinking about protein at all. They're tend to equate fat intake with energy intake. So, excessive energy intake is usually equated with a excessive fat intake, which in terms of the current dietary guidelines means anything about 30% of calories coming from fat. It's rare to hear that somebody would talk about excessive energy intake in the context of higher dietary protein.

To illustrate this, extreme examples are always good. What would be an excess of energy? 3000 calories? That's about 300+ gr of fat (if the diet is only fat), or 750 gr of effective carbohydrate (because effective carbohydrates are the ones that are metabolically important for energy, right?). Those same 3000 calories can come from 750 gr of net protein as well (which is roughly 100+ oz of meat, poultry or fish -let's just stick to those sources for a while to make things easier). If the carbohydrate source is, say butterhead lettuce, which contains ~11 gr ECC per kilo, we would need about 68 kilos of lettuce to get those 3000 calories. Whereas it's very easy to get 3000 calories from carbohydrate-rich foods, it's more difficult to get the same amount of calories from protein-rich foods or fat alone (have you seen people eating butter sticks with the same frequency they much on chips, bagels, candy or cookies?) and it would be virtually impossible to go through 68 kilos of lettuce to reach the 3000 calories of our example. The effect that protein has in the body, which include higher satiety and higher thermogenesis, is not the same as carbohydrates, even if the amount of energy is numerically equal. That has not been realized nor understood by those who like to tout the horn of the laws of thermodynamics applied to the human body.


The much bigger question is whether maintaining weight loss can be compromised by excessive intake even while carbs are kept in the ketogenic range (say 50 or less). In simple terms, can excessive protein and/or fat intake lead to fat being deposited in this scenario?


This part of the bigger question relates to my reply above. What constitutes an excessive intake of protein? Compared to what? When a minimum protein intake is set based on individual lean body mass and level of physical activity, it's impossible to over eat protein unless we do it on purpose and/or forcefully trying to override the satiety effect that protein has. How much fat is 'excessive'? The problem with those terms is that there is a set point above which everything seems excessive. But if we need to think of excess of protein and fat, let's assume 3 times our minimum protein intake. Why three times? Well, for the same reason fat intake should not be more than 30% of our caloric intake: no reason... Simply because 3 times sounds big enough. As much as many people like to think that just because certain amino acids can be converted into glucose when needed, this conversion doesn't occur automatically. It's hormonally regulated and there needs to be a stimulus to trigger that hormone response.

Also, as much as some people like to think that protein can be turned into fat becuase there is, indeed, a metabolically possible mechanism, this process doesn't take place without an excess carbohydrate present, which provides for necessary intermediates for protein to end up as fat. So, strictly speaking, protein can be converted to fat if the essential precursors for fat synthesis and biosynthetic reducing power are present. While I'll spare you the names of such precursors, I'll mention that one of the main generators of biosynthetic reducing power is a metabolic pathway that uses dietary glucose or fructose. So, provided that there is availability of glucose or fructose, proteins can potentially be used in the synthesis of fat.

Now, since context is everything, what happens when dietary carbohydrates are restricted in the diet, even in the event of 'excessive protein intake'? It is unlikely that the main fate of protein will be as fat. Part of the protein-to-fat argument also lies in the fact that after a period of starvation, glucagon is running the metabolic show and there are plenty of intermediates for fat synthesis that come from fat oxidation. In fact, such intermediates can be used for a lot of different processes, including fat synthesis. What's missing in this argument is that glucagon actually inhibits fat synthesis so no matter if the right intermediates are there, if the hormonal control is missing, the machinery for fat synthesis doesn't work. Indeed, insulin activates the machinery for fat synthesis but when somebody is on carbohydrate restriction, there is not enough insulin to keep fat synthesis on all the time, which is what happens in hyperinsulinemic states.

Also, we need to consider the actual feasibility of eating excessive amounts of protein and for that we have to consider the satiety effects that protein has. Therefore, it is unlikely that we can eat excessive amounts of protein unless we really force ourselves to do so. The beauty of Protein Power as a learning tool is that it helps you to estimate your protein intake tailored to your own needs, and the beauty of dietary protein as a nutrient is that it helps you set biological parameters to control food intake by increasing satiety more efficiently than any other nutrient.

You might remember one of Protein Power's recommendations about snacks... choose a snack that gives you half of your minimum protein intake (per meal) and with as little or no carbohdyrate at all... Now you know why.


My own position (and I'd have to say I have been dragged kicking and screaming to this conclusion!:o) is the answer is yes, and this is supported up by other people's experiences, including Anthony's who incorporates a 'bulking' phase in his body building routine whilst maintaining ketogenic carb intake.


It would be better if you could actually measure fat deposition to conclude that the increase in weight comes from that and not from fat-free mass. In 2003, Margriet Westertep published an illuminating review that highlighted the underexposed but important role of protein in food intake and body weight regulation. Several important points stand out from that review:


High-protein diets affect body weight loss positively only under ad-libitum energy intake conditions, implying also a decreased energy intake.

Body-composition and metabolic profile are improved.

Additional protein consumption results in a significantly lower body weight regain after weight-loss, due to body-composition, satiety, thermogenesis, and energy inefficiency, while the metabolic profile improves.


Note that in the studies mentioned in that review, as well as more recent ones, after weight loss there is a lower body weight regain (if at all) and the weight comes from fat-free mass, i.e. lean body mass. More important is that the weight gain is within 1-3 kg range and does not constitute a 'rebound' to initial, pre-weight loss conditions. Although this discussion is revolving to protein an weight gain, it's important to mention that those studies also report a general improvement in metabolic profile.

The implications from these findings are profound and can find a place in various scenarios. For dietitians and nutritionists because recommendations for increasing the percentage of energy from protein while reducing energy intake represents an alternative for weight loss. For clinical researchers because they can assess the effect of increasing the percentage energy from a highly satiating macronutrient, and the potential roles of protein in a negative and positive energy balance. And finally, to guide policy makers and those with the responsibility of suggesting dietary guidelines aimed to keep and improve people's health.

So, is it really that those in the maintenance phase of their rehabilitation (of course achieved by increasing protein in their diets while controlling dietary carbohydrate) regain all the lost weight from eating extra protein during their maintenance period?


So the question (finally) is firstly whether you agree, and if you do, perhaps you can have a stab at explaining the processes involved?


I guess after my long response the answer is no. Based on current research, there is no support to the notion that people eating more protein will end up gaining weight from fat, unless other circumstances come into play. And that is my safe button because more than once, when you look deep enough, the increase in protein came with an increase of other things that may affect how the body responds.


Would I be right in saying that even on a zero carb diet, glucagon is not dominant 24/7 and that it would not be healthy for us if it was?


You don't need a zero-carb diet to have glucagon running the metabolic show. However, as you well know, there are grups of humans that have no access to dietary carbohydrates at all, which would suggest that their insulin:glucagon ratio is very low, yet they are healthy by current standards. Having a zero-carb diet doesn't mean that the body doesn't get the glucose it needs to function. The liver is quite capable of providing for that. Mike Eades actually ellaborates more on this in his post Vampire Myths (http://72.32.36.211/drmike/archives/2006/03/vampire_myths.html) available in his blog.

There are situations, again, when we need to look at the context. In uncontrolled diabetes, for example, there is an abnormal secretion of glucagon which drives uncontrolled production of ketones resulting in ketoacidosis (not ketosis!), a condition that as you know could be fatal. But as I said, that is a pathological condition, and not the result of eating little dietary carbohydrate.


Does this mean that there are times even on a low carb diet that given sufficient (or excessive) protein and/or fat intake that fat storage will occur?


With respect to protein, I frankly doubt it. With respect to fat, the worse case scenario is a stall in weight loss. Gaining weight from fat means accumulating it somewhere, and that process is not favored by glucagon. Again, if we talk about excess fat, let's make sure is not excess fat with a fair amount of carbohydrate because the scenario is completely different.


OK, one other brief question, did you get to the latest Nutrition and Metabolism conference, and if so what did you see as the highlights?

Unfortunately I didn't attend. I was in the process of ending my previous work and moving to another state. I checked the program online, though, and I saw that there was a lot of new information. Some of the results are not surprising but it's great that they are now published so they can be discussed!!! I really hope I'll be able to attend next time.

[realruth]

Question...
OK normally we lose weight on the 30=40ecc levels.....

But when other things come into play like hormones ie:menopause there *could * be weight gain at the very same levels?

This is relevant to so many of us who are at that stage and seem to have experienced that particular effect despite being 100% on plan.
For myself I have found that to NOT gain weight my ecc levels have to be 30 or less.
To lose weight I have to do more than drop the ecc levels.
I eat between 80-100 P each day without major exercise..walking/biking etc
I did not watch my fat levels but the online food measure indicates I get around 45-50% Fats on a daily basis.

Now I ask this because when I was getting to goal just over a year ago I could eat exactly the same food (have journals) and lose 3=4 lbs per month. This does not happen now and over the last year I gained weight as hormone levels changed ( have lost some of it now but not all of it).

So did I lose the Metabolic advantage some where ;) ?
Or have hormones mor eof a role to play than we know at the moment?

Ruth

[Gaelen]

Ruth, I think it's nearly impossible to discount the role hormones play or their effect on metabolic advantage. As someone who's hormone levels were placed into a tailspin by cancer treatment nearly two years ago, and who's experienced ups and downs in weight loss and weight maintenance throughout, I know that when I'm on treatment (and my hormones are thrown far out of whack) I can NOT lose, whether or not I exercise and even if I eat completely on plan. When I'm off treatment (like now) and my hormone levels return to some semblance of normal, I can lose a little bit, as long as I both exercise and stay carefully under 45g ECC. But at the moment I've been off treatment since Jan. 18, and I feel more 'normal' as far as my eating habits than I have felt in months--but getting to feeling normal took a few weeks of metabolic/hormonal normalization, and I'm not sure how much more of these kinds of challenges my endocrine system can handle. In a couple weeks, when I start the last four or five cycles of chemo and my hormones are knocked out of their natural rhythms again, all bets will be off.

[mcsblues]

Thanks so much for you detailed answer, and good luck with the new job - what does it involve?

As for my question, I think to an extent we are talking at cross purposes, so I will (if you can stand it!:p) go through it again, but first it might help to explain my own experience, as I think it is far from unique, and might help explain my interest in this topic.

I am well into my 3rd year of a PP lifestyle. I have been 'maintaining' after an initial 60 pound weight loss for nearly 2 years. My carb intake apart from very occasional deviations has essentially remained the same on maintenance as it was during the weight loss phase. I don't 'count' carbs (or calories) - but apart from a few weeks in the early stages of weight loss when I educated myself about the carb content of my regular foods, I never have. I am never the less confident, even with those occasional indulgences (mostly for fruit) that there has been no 'carb creep', and that my intake remains in the 20 - 50cg range, BUT - I find that in order to keep the fluctuations in my weight within a reasonable range I now need to check not just my carb intake (which I find easy) but also my total intake of low carb food - which I find more difficult.

If there is one criticism I have for the Eades (and in the general scheme of things it is pretty minor) it is that they do not attempt to address the issue of emotional eating. Yes I recognise and have experienced the higher satiety of a higher protein, low carb diet. But I think it is important to recognise that the alleviation of true hunger is only one of the reasons why we eat, and even when you have cured the unstable blood sugar fuelled hunger, there are those of us who will still overeat in response to other factors – and it is this behaviour which is at least partially responsible for our initial weight gain.

Your friend is partially right. Weight loss requires a caloric deficit but that doesn't necessarily has to happen the way most dietitians think. As research has shown, there are ways to create a caloric deficit without necessarily reducing caloric intake by just reducing the total amount of food.
Yes, I understand this (and so does he) and this is the reason he uses the term energy deficit rather than calorie deficit (which doesn’t recognise metabolic advantage).

Correct. This is what we like to call metabolic advantage.
Yes, I referred to it as metabolic advantage too!

Here we need to be careful not to confuse terms. When dietitians and nutritionists (or anybody who likes to talk about energy balance and all that) talk about energy, they're not thinking about protein at all. They're tend to equate fat intake with energy intake. So, excessive energy intake is usually equated with a excessive fat intake, which in terms of the current dietary guidelines means anything about 30% of calories coming from fat. It's rare to hear that somebody would talk about excessive energy intake in the context of higher dietary protein.
Well since we are talking about this issue within the context of a low carb diet, forget what nutritionists say, the excess will come from protein and fat.

To illustrate this, extreme examples are always good. What would be an excess of energy? 3000 calories? That's about 300+ gr of fat (if the diet is only fat), or 750 gr of effective carbohydrate (because effective carbohydrates are the ones that are metabolically important for energy, right?). Those same 3000 calories can come from 750 gr of net protein as well (which is roughly 100+ oz of meat, poultry or fish -let's just stick to those sources for a while to make things easier). If the carbohydrate source is, say butterhead lettuce, which contains ~11 gr ECC per kilo, we would need about 68 kilos of lettuce to get those 3000 calories. Whereas it's very easy to get 3000 calories from carbohydrate-rich foods, it's more difficult to get the same amount of calories from protein-rich foods or fat alone (have you seen people eating butter sticks with the same frequency they much on chips, bagels, candy or cookies?) and it would be virtually impossible to go through 68 kilos of lettuce to reach the 3000 calories of our example. The effect that protein has in the body, which include higher satiety and higher thermogenesis, is not the same as carbohydrates, even if the amount of energy is numerically equal. That has not been realized nor understood by those who like to tout the horn of the laws of thermodynamics applied to the human body.
Yes, I understand all this, but believe me I can very easily overeat low carb foods – for this reason I really have to limit how much cheese I keep in the house!

This part of the bigger question relates to my reply above. What constitutes an excessive intake of protein? Compared to what? When a minimum protein intake is set based on individual lean body mass and level of physical activity, it's impossible to over eat protein unless we do it on purpose and/or forcefully trying to override the satiety effect that protein has. How much fat is 'excessive'? The problem with those terms is that there is a set point above which everything seems excessive. But if we need to think of excess of protein and fat, let's assume 3 times our minimum protein intake. Why three times? Well, for the same reason fat intake should not be more than 30% of our caloric intake: no reason... Simply because 3 times sounds big enough.
Whoa! I can’t imagine how hard it would be to get fat down below 30% on low carb, and I take it you are not suggesting we should try. And I’m sorry but for me at least (and I’m sure I am not alone!), overeating fat and protein is all too easy.

As much as many people like to think that just because certain amino acids can be converted into glucose when needed, this conversion doesn't occur automatically. It's hormonally regulated and there needs to be a stimulus to trigger that hormone response.
Yes I understand, and I quote Gannon and Nuttall at people who don’t frequently!
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=524031

Also, as much as some people like to think that protein can be turned into fat becuase there is, indeed, a metabolically possible mechanism, this process doesn't take place without an excess carbohydrate present, which provides for necessary intermediates for protein to end up as fat. So, strictly speaking, protein can be converted to fat if the essential precursors for fat synthesis and biosynthetic reducing power are present. While I'll spare you the names of such precursors, I'll mention that one of the main generators of biosynthetic reducing power is a metabolic pathway that uses dietary glucose or fructose. So, provided that there is availability of glucose or fructose, proteins can potentially be used in the synthesis of fat.
Well now we are getting down to the area I do want you to address. If we accept that gluconeogenesis only occurs on demand, that doesn’t cover the fate of metabolised amino acids not required for this purpose. As I understand it (please correct me if I am wrong!) any amino acids not used for muscle repair or building will result (after deanimation) in the same building blocks for de novo synthesis of fatty acids that glucose/carbs can supply (pyruvate and acetyl CoA) - if those are not used for ATP or glucose production, what does happen to them? Likewise, any dietary fat not used for current energy demands will presumably be available for other purposes.

Now, since context is everything, what happens when dietary carbohydrates are restricted in the diet, even in the event of 'excessive protein intake'? It is unlikely that the main fate of protein will be as fat. Part of the protein-to-fat argument also lies in the fact that after a period of starvation, glucagon is running the metabolic show and there are plenty of intermediates for fat synthesis that come from fat oxidation. In fact, such intermediates can be used for a lot of different processes, including fat synthesis. What's missing in this argument is that glucagon actually inhibits fat synthesis so no matter if the right intermediates are there, if the hormonal control is missing, the machinery for fat synthesis doesn't work. Indeed, insulin activates the machinery for fat synthesis but when somebody is on carbohydrate restriction, there is not enough insulin to keep fat synthesis on all the time, which is what happens in hyperinsulinemic states.
Yes, but does glucagon inhibit fat synthesis 24/7? – or does the normal amount of insulin in a low carb fuelled person allow for some fat to be deposited. If not, what happens to these intermediates from fat as well as protein, that are excess to current demands for energy or lean tissue repair?

Also, we need to consider the actual feasibility of eating excessive amounts of protein and for that we have to consider the satiety effects that protein has. Therefore, it is unlikely that we can eat excessive amounts of protein unless we really force ourselves to do so. The beauty of Protein Power as a learning tool is that it helps you to estimate your protein intake tailored to your own needs, and the beauty of dietary protein as a nutrient is that it helps you set biological parameters to control food intake by increasing satiety more efficiently than any other nutrient.

You might remember one of Protein Power's recommendations about snacks... choose a snack that gives you half of your minimum protein intake (per meal) and with as little or no carbohdyrate at all... Now you know why.
Yes, I appreciate the theory of calorie restriction through the satiety of protein. In practice I think that it is stable blood sugar itself which will offers an even higher likelihood of lower calorie intake, but be that as it may, as I have said before, the actual amount we eat is not driven solely by hormones or macronutrient ratios.

It would be better if you could actually measure fat deposition to conclude that the increase in weight comes from that and not from fat-free mass. In 2003, Margriet Westertep published an illuminating review that highlighted the underexposed but important role of protein in food intake and body weight regulation. Several important points stand out from that review:
High-protein diets affect body weight loss positively only under ad-libitum energy intake conditions, implying also a decreased energy intake.
Body-composition and metabolic profile are improved.
Additional protein consumption results in a significantly lower body weight regain after weight-loss, due to body-composition, satiety, thermogenesis, and energy inefficiency, while the metabolic profile improves.Note that in the studies mentioned in that review, as well as more recent ones, after weight loss there is a lower body weight regain (if at all) and the weight comes from fat-free mass, i.e. lean body mass. More important is that the weight gain is within 1-3 kg range and does not constitute a 'rebound' to initial, pre-weight loss conditions. Although this discussion is revolving to protein an weight gain, it's important to mention that those studies also report a general improvement in metabolic profile.

The implications from these findings are profound and can find a place in various scenarios. For dietitians and nutritionists because recommendations for increasing the percentage of energy from protein while reducing energy intake represents an alternative for weight loss. For clinical researchers because they can assess the effect of increasing the percentage energy from a highly satiating macronutrient, and the potential roles of protein in a negative and positive energy balance. And finally, to guide policy makers and those with the responsibility of suggesting dietary guidelines aimed to keep and improve people's health.

So, is it really that those in the maintenance phase of their rehabilitation (of course achieved by increasing protein in their diets while controlling dietary carbohydrate) regain all the lost weight from eating extra protein during their maintenance period?

I guess after my long response the answer is no. Based on current research, there is no support to the notion that people eating more protein will end up gaining weight from fat, unless other circumstances come into play. And that is my safe button because more than once, when you look deep enough, the increase in protein came with an increase of other things that may affect how the body responds.
I know this is a PP forum, but you seem to consider protein in isolation rather a lot;) and in the real low carb world additional protein comes packaged with fat. Lets take my danger food cheese as an example. I think I could just about live on cheese given half a chance! Now it obviously varies with variety but let us say that a ‘typical’ cheese has roughly equivalent amounts of protein and fat in grams – so very roughly twice as many fat calories as protein with minimal carbohydrate. My own experience tells me that on a low carb diet I have to be careful of my intake of cheese or I will gain weight, and as much as I would like to say this is all LBM, it isn’t, and as much as I would like to tell you this weight gain is limited to 1 – 3 kg … it isn’t. Now the only explanation I can see is that there is either some mechanism that allows for weight (fat) gain from excessive fat and protein calories on a low carb diet (and granted it is much slower and harder to achieve than if carbs are also high) OR there is some other process at play … perhaps my insulin resistance has worsened over the last 2 years?

The last time I checked I was not menopausal, and while I really feel for the terrible ordeal that Gaelen is enduring, my hormones are not being messed around by chemotherapy (or any other drugs) – so I was rather hoping there was a simple metabolic process which would explain why portion control, particularly of high fat foods is still necessary for me to maintain my weight loss successfully.

Don’t get me wrong, I am truly thankful for the freedom that a low carb diet offers me, in addition to its many health benefits. I will never eat any other way. It just seems that freedom does come with some limitations, even within the low carb framework.

You don't need a zero-carb diet to have glucagon running the metabolic show. However, as you well know, there are grups of humans that have no access to dietary carbohydrates at all, which would suggest that their insulin:glucagon ratio is very low, yet they are healthy by current standards. Having a zero-carb diet doesn't mean that the body doesn't get the glucose it needs to function. The liver is quite capable of providing for that. Mike Eades actually ellaborates more on this in his post Vampire Myths (http://72.32.36.211/drmike/archives/2006/03/vampire_myths.html) available in his blog.

There are situations, again, when we need to look at the context. In uncontrolled diabetes, for example, there is an abnormal secretion of glucagon which drives uncontrolled production of ketones resulting in ketoacidosis (not ketosis!), a condition that as you know could be fatal. But as I said, that is a pathological condition, and not the result of eating little dietary carbohydrate.
Yes I understand all that – my zero carb scenario was just an extreme example ("always good"!:)) – but the question remains, does a low carb diet mean glucagon is dominant all the time? Surely if it was no anabolic processes could take place and this would include muscle building as well as fat deposition?

With respect to protein, I frankly doubt it. With respect to fat, the worse case scenario is a stall in weight loss. Gaining weight from fat means accumulating it somewhere, and that process is not favored by glucagon. Again, if we talk about excess fat, let's make sure is not excess fat with a fair amount of carbohydrate because the scenario is completely different.
Hmmm, well my experience, and those of many others such as Ruth seems to paint a different picture.

[hawk]

I eat 160 gms protien a day and salad ,3 carb protien shakes,cottage cheese I eat has 3 grams per half cup. I do not lose without vigorous excersize. If I stop excersize I stop losing.Every pound lost is hard won.
I tried to go lo fat and finially began to lose. I lost 9 pounds but after 5weeks I was dragging around feeling anemic. So now I upped the fat and am staying the same again. I'm 5'5" 162 pounds 25% body fat.(if my body fat testing was accurate.) I feel better. Even sick I feel better.
The only carbs I eat now are raw salad vegetables,tomatoes,spinach,cukes,peppers,cottage cheese,ranch dressing(hate to waste it on that tho) 1/4 cup organic yogurt and a few strawberries or blueberries and green beans.

[hawk]

Gaelen, I don't know how you do it. You are a strong woman. An incredibly strong woman. It's unbelievable what you have gone through. When is your next treatment? Does this diet help you? My best freind has just gone through chemo. She's begun to ask my advise on diet. I feel like I know nothing compared to others on this board.

[Gaelen]

Gaelen, I don't know how you do it. You are a strong woman. An incredibly strong woman. It's unbelievable what you have gone through. When is your next treatment? Does this diet help you? My best freind has just gone through chemo. She's begun to ask my advise on diet. I feel like I know nothing compared to others on this board.

Hawk, yes, I do think this diet helps--and the nutritionist at the oncology center where I get my local treatments agrees. Eating this way for two years prior to diagnosis defnitely made my body stronger going into chemo, it helped me be and stay stronger throughout chemo and it helped me be and stay stronger through two really intense surgeries. My personal experience is anecdotal, but some scientists are beginning to research the effect of dietary sugars on both fast and slow growing cancers, and the current consensus (among scientists) is that in the case of fast growing tumors, you have got to limit sugars, especially simple sugars.

Now, does that mean I don't eat sugar, or haven't at any time during the last two years...no. I'm human, and on bad days, I eat what I can stand to eat. But it does give me the resolve to keep trying to keep carb intake under control, even when they're the only food that looks even remotely palatable. Luckily, on the second chemo regimen, it was a lot easier to eat and I wanted proteins. On the first regimen, I didn't want food at all, much less protein.

My next treatment is maybe next Wednesday; we have to see to what extent my liver has regenerated, and if the hepatic infusion pump is capable of perfusing the liver adequately.

[Gabriel Guzman]

Question...
OK normally we lose weight on the 30=40ecc levels.....

But when other things come into play like hormones ie:menopause there *could * be weight gain at the very same levels?

This is from the Q&A on Protein Power that the Eades have written before:

From Protein Power Q&A:
How will the diet affect women's menstrual cycles or someone on estrogen replacement therapy?

Insulin is a powerful hormone with many responsibilities, one of them being a storage hormone. Higher insulin levels from eating a high carbohydrate diet will promote the storage of estrogen in the fat cells and tissues. When levels of insulin are lowered due to a decrease in carbohydrates, excess estrogen is released, possibly causing a disruption in menstrual cycles. Some women may notice spotting or break through bleeding mid cycle or their flow may become lighter or heavier. We recommend being patient, continuing on the plan and within 2-3 cycles, the hormone levels will become balanced.

During menopause, levels of reproductive hormones begin to decline, with a shift toward catabolism (body, bone, and muscle wasting). Estrogen replacement alone or with Provera can promote fluid retention and fat gain. In women who have under gone hysterectomy and ovarian removal, some estrogen may be necessary, but in women who still have ovaries, natural progesterone by itself may be a better option. Eating the Protein Power Plan diet will promote higher levels of the "mother" hormones from which reproductive hormones must be made after the ovaries begin to slow down or cease production. The diet also provides a better magnesium-to-calcium balance to keep bones strong and ward off osteoporosis.


This is relevant to so many of us who are at that stage and seem to have experienced that particular effect despite being 100% on plan.
For myself I have found that to NOT gain weight my ecc levels have to be 30 or less.
To lose weight I have to do more than drop the ecc levels.


I'm curious to know what else do you know. Some other people may benefit from your experience.


I eat between 80-100 P each day without major exercise..walking/biking etc
I did not watch my fat levels but the online food measure indicates I get around 45-50% Fats on a daily basis.


Is this 45-50% of your total caloric intake or 45-50 "gr" per day? (just curious)


So did I lose the Metabolic advantage some where ;) ?
Or have hormones more of a role to play than we know at the moment?


I think that the metabolic advantage can be lost but I don't think that happens as a result of us aging. It's interesting that in some cultures, there isn't even a word for menopause or hot flashes. The body goes through several, sometimes dramatic changes during a person's life and more adjustments need to be done. Maybe that's the stage now, to find the right tweak that will get things moving again :)

[mcsblues]

Getting back to the original question Gabe ... ;)

Let me see if I can simplify it.

Lets take the extreme example of a high fat high protein zero carb diet. On that regime is it possible to gain weight (and here I mean fat) if fat and/or protein calories are high enough?

If so, what are the processes involved given that insulin levels will presumably be quite low for all or most(?) of the time?

If not, what happens to the excess calories?

If not, setting aside for a moment unusual hormonal conditions and/or confounding medication, .... does that mean that if anyone finds they regain any weight on maintenance, they are simply eating too many grams of carbs - end of story?.

[dvdmon]

Malcolm, I'm not a scientist like Gabe, but my non-scietist opinion is that many things can effect insulin levels in the body. I believe I've heard of evidense that states exercise level has an effect on it, and I would guess that it's possible that stress (psychological) does as well. I can't imagine it being a stretch to postulate levels of other hormones in the body like estrogen and progesterone could affect insulin levels as well. Whether this has been demonstrated in a study I don't know, but it would be interesting to understand all the potential factors in insulin production. Obviously diet is a major one, but if one can't explain increased weight from fat by diet (ie you are not consuming excess caloric consumption and you are eating a low-carb diet) and lack of exercise/activity, then why not look for other factors that might influence insulin and thus effect fat production in the body? One other dietary issue occurs to me though, and that is the matter of the so-called "starvation mode." Not that we've seen clinical proof of this either, although it's often sited as fact. Finally, there's the whole issue of general metabolism. Muscle mass plays into this. Muscle mass does decrease with age unless you are pretty vigilent about keeping it built up. I imagine this is even harder for women whose physiology, I believe, is on average not condusive to as much muscle mass as their male counterparts. In any case, it's a very interesting topic you raise and I think it helps us to think more "3-dimensionally" about body fat, diet, and exercise.

[Gabriel Guzman]

Getting back to the original question Gabe ... ;)

Let me see if I can simplify it.

Lets take the extreme example of a high fat high protein zero carb diet. On that regime is it possible to gain weight (and here I mean fat) if fat and/or protein calories are high enough?


The example may not be that extreme. In fact, traditional Inuit food could be considered high in fat. The traditional diets of sub-Arctic living peoples such as the Dene and the Métis contained so little fat, that foods high in fat became highly-prized. These foods are still appreciated today. Some of them are:


whitefish eggs (15% fat)
caribou tongue (17% fat)
loche liver, harvested in late fall (40% fat)
beaver tail (43% fat)


To this list you can also add Arctic Char, seal, walrus and whale, all of them rich in fat, Omega-3 fats in this case. Thus, strictly speaking, the traditional, non-Westernized Inuit diet can be considered high in fat. Interestingly enough, you don't find much carbohydrate-rich foods in their traditional diet. In fact, contrary to what many people think that only carbohydrate-containing foods also contain vitamines and the like, the traditional Inuit diet provides Vitamin A and iron from seal liver, Maktaaq, caribou, rabbit, Ptarmigan, mussels, goose, and duck; Zinc and B-Vitamins from arctic Char, seal, walrus and whale; calcium from fish heads, skin and bones. So, truly a 'high' fat, virtually zero carb diet.

The problem in the 'extreme example' is that there is no distinction between the types of fat in the diet. In an Inuit-type of diet, which I chose because it closely resembles your example, most of the fat is not saturated fat (no that saturated fat is bad in any way) and it's known that Omega-3 fats are 'burnt' rather than 'stored'.

Are the Inuit obese or overweight? The simple answer is no. The problem, as discussed by Stig Andersen an co-workers in their article "Gender diversity in developing overweight over 35 years of Westernization in an Inuit hunter cohort and ethno-specific body mass index for evaluation of body-weight abnormalities" (European Journal of Endocrinology (2004) 151: 735–740), the measuring stick to decide if a population is obese or overweight is not globally applicable. For the Inuit, which have a different body build (larger torse and shorter limbs), the WHO standard to measure overweight/obesity (the all mighty BMI) simply doesn't apply because the BMI standard was developed based on caucasian populations. In 1963, and Inuit BMI standard was generated specific for that population and by that standard, Inuit back then had a very low incidence of obesity.

It makes sense for many reasons. First their diet. Second, Also, obesity was a severe drawback when hunting. Thus, obesity was not feasible among male hunters. These people lived from what they caught or hunt and the records from 1963 seemed to support a very low incidence of oveweight and/or obese individuals. Excessive food intake was limited to short periods after successful hunting followed by periods of food shortage. In fact, in the extreme example you propose, maintaining a diet high in fat, which would come with a fair amount of protein as well if the sources are like those of the Inuit, would likely result in self limitation of food intake, time during which the body would have to tap into its own sources for energy.

So, instead of just answering 'no' to your question above, in a highly unlikely scenario, I think an argument to that is more productive.


If so, what are the processes involved given that insulin levels will presumably be quite low for all or most(?) of the time?


Again, you're assuming that in the extreme example you propose, food intake is unlimited as well, which is highly unlikely. A diet like that, which would include protein sources as well (unless is done in a very unnatural way) would likely result in reduced food intake due to higher and longer satiety. By the same token, the thermic effect of food would also affect the energy expenditure, thus affecting the whole energy balance towards more expenditure.

But since you're talking about extremes, then with insulin levels low, say just enough to keep blood sugar levels constant but not enough to drive fat synthesis all the time and not enough to drive fat intenalization into the fat cells, the scenario of gaining weight from fat is really unlikely.


If not, what happens to the excess calories?


Which ones? If the seemingly excess of fat coms from fats that are more burned that stored, then heat (thermogenesis) would be the likely result.


If not, setting aside for a moment unusual hormonal conditions and/or confounding medication, .... does that mean that if anyone finds they regain any weight on maintenance, they are simply eating too many grams of carbs - end of story?.

That could be one reason but that individual could also make sure that the amount of protein is where it should be and not below that. The problem is that it's almost impossible to set aside the effect of hormones in the regulation of energy balance. If we don't consider their effect, then we can only speculate and talk about extreme examples.

[mcsblues]

Yes, the only reason I proposed an extreme example is to take the possibility of eating too many carbs out of the equation. If we assume that most of us are not likely to consume a great deal of caribou toungue or beaver tail then we need to look at more commonly available food sources and the fat that comes with them. I am at work so I don't have sources to hand but from memory beef fat is something like 40% saturated, about the same in MUFAs and the rest PUFAs (largely omega 6 with modern farming).

So lets look at an example where an individual is getting plenty of protein (ie above the minimum intake the Eades prescribe) minimal amounts of carbohydrates and the rest fat in something like the ratios above - and that total calorie intake exceeds expenditure. Is it possible to store fat in that scenario? (my own experience suggests that it is!) If fat storage occurs does this indicate that carbs and therefore insulin is not restricted enough, or are there other pathways which allow for fat storage while insulin is kept in check? - or are there other factors which may be raising insulin in the absence of carbs? (I know protein is supposed to promote insulin release, but I think the Eades tell us in PP that this is countered by a similar rise in glucagon so that protein will not affect the hormonal balance).

I raise these questions, not just because I seem to have an issue with portion/calorie control since I have been maintaining, but also as someone pointed out to me a while back (hi Stuart:)), the Eades are fairly definitive about this subject, saying in effect that fat storage cannot occur if carbs are kept low enough;

They say in PPLP - page 58

" Opening the Door of the Fat Cell"
If insulin levels are low enough, then fat storage pretty much shuts down. It almost doesn't matter how much you eat- it's not going to get into the fat cells without the assistance of insulin......
..... The remarkable , even stunning, realization is not that while she (the weight loss warrior glutton) was eating all this food she lost only 4 pounds but that she didn't gain 30 pounds!. The point is that she kept her insulin low by keeping her carbohydrates restricted and wasn't able to store the fat that she ate...... The good news is that if you are trying to lose weight , the minute you do reach your goal you can increase your calories substantially without the fear of gaining weight, as long as you keep your carbohydrates restricted enough to keep your insulin low..."

and then on page 321, in the chapter entitled 'Lifeplan Nutrition' they add:
"Once you've gotten to your weight goal, you won't have to worry about limiting your intake of good quality fats anymore as long as you keep your insulin controlled. YOU SIMPLY CANNOT STORE FAT--- AND ADD ON FAT POUNDS---UNLESS YOU TURN YOUR INSULIN LOOSE. (my emphasis) But to keep a rein on insulin output , most people will have to limit carbohydrate intake , at least to some extent, most of the time....."

[Gabriel Guzman]

Yes, the only reason I proposed an extreme example is to take the possibility of eating too many carbs out of the equation. If we assume that most of us are not likely to consume a great deal of caribou toungue or beaver tail then we need to look at more commonly available food sources and the fat that comes with them. I am at work so I don't have sources to hand but from memory beef fat is something like 40% saturated, about the same in MUFAs and the rest PUFAs (largely omega 6 with modern farming).

The example of the Inuit food was intended to show that there may be possible to consume higher amounts of fat and protein while having no access to carbohydrates. Having said that, we don't need to eat caribou tongue but we can make better choices as to the source of our own food; grass fed vrs. grain feed for example, in the case of beef. Free ranged poultry and wild salmon as opposed of farmed fish. All these sources are naturally 'balanced' in the type of fats they come with, and that makes a lot of difference.


So lets look at an example where an individual is getting plenty of protein (ie above the minimum intake the Eades prescribe) minimal amounts of carbohydrates and the rest fat in something like the ratios above - and that total calorie intake exceeds expenditure. Is it possible to store fat in that scenario? (my own experience suggests that it is!) If fat storage occurs does this indicate that carbs and therefore insulin is not restricted enough, or are there other pathways which allow for fat storage while insulin is kept in check?


Not to my knowledge.


...or are there other factors which may be raising insulin in the absence of carbs? (I know protein is supposed to promote insulin release, but I think the Eades tell us in PP that this is countered by a similar rise in glucagon so that protein will not affect the hormonal balance).


I know many like to suggest that protein will necessarily rise insulin levels to levels comparable with hyperinsulinemia. Indeed there may be a very small effect but never comparable to the effect of glucose and not enough to take over and drive fat synthesis in a constitutive way (all the time), mainly because is likely that glucagon would be counteracting insulin action in tha regard. In uncontrolled diabetes there may be increase catabolism of protein and it's also known that there is equally uncontrolled production of glucose by the liver (gluconeogenesis) for which the main substrate is glycerol coming from fat oxidation.


I raise these questions, not just because I seem to have an issue with portion/calorie control since I have been maintaining, but also as someone pointed out to me a while back (hi Stuart:)), the Eades are fairly definitive about this subject, saying in effect that fat storage cannot occur if carbs are kept low enough;

They say in PPLP - page 58

" Opening the Door of the Fat Cell"
If insulin levels are low enough, then fat storage pretty much shuts down. It almost doesn't matter how much you eat- it's not going to get into the fat cells without the assistance of insulin......
..... The remarkable , even stunning, realization is not that while she (the weight loss warrior glutton) was eating all this food she lost only 4 pounds but that she didn't gain 30 pounds!. The point is that she kept her insulin low by keeping her carbohydrates restricted and wasn't able to store the fat that she ate...... The good news is that if you are trying to lose weight , the minute you do reach your goal you can increase your calories substantially without the fear of gaining weight, as long as you keep your carbohydrates restricted enough to keep your insulin low..."

and then on page 321, in the chapter entitled 'Lifeplan Nutrition' they add:
"Once you've gotten to your weight goal, you won't have to worry about limiting your intake of good quality fats anymore as long as you keep your insulin controlled. YOU SIMPLY CANNOT STORE FAT--- AND ADD ON FAT POUNDS---UNLESS YOU TURN YOUR INSULIN LOOSE. (my emphasis) But to keep a rein on insulin output , most people will have to limit carbohydrate intake , at least to some extent, most of the time....."

And they're pretty much on the money. However, certain pathological conditions really wreck the way the body controls glucose output. For example, insulin resistant states are seen by the cells as 'glucose starvation' regardless the commonly seen hyperglycemia that accompanies hyperinsulinemia. This 'perceived' starvation by the cells triggers a response from the liver which starts making more glucose regardless of how much is already in circulation. The newly made glucose only worsens the already hyperglycemic state. Maintenance, however, is not likely to be a pathological state.

As it turns out, liver and adipose cells both have a common type of protein in their membrane called 'aquaporins'. They're not identical but they function in the same way; they're glycerol channels. When fat is oxidized, glycerol is produced. Glycerol, after following a series of chemical reactions, can be used by the liver if needed to make glucose (gluconeogenesis). Beautifully enough, when that happens, both types of aquaporins, those in the liver and those in the fat cells work together so the aquaporin in the fat cells helps glycerol leave and the aquaporins in the liver help glycerol to come in to be used for gluconeogenesis. In the normal (non-pathological state), insulin inhibits the expression of both types of aquaporins. If insulin levels decrease and glucose is needed, say during an overnight fast, when glucagon levels would likely increase as a result, the expression of these proteins is increase so glycerol can be used as described above. A drop in insulin levels doesn't necessarily mean that glucose is needed.

In a pathological state such as insulin resistance, aquaporins are highly expressed in fat and liver cells. For cells that are insulin resistant, it doesn't matter that there is glucose available, they just don't 'see it' and as far as those tissues are concerned, they're 'starving'. The response is to try to supply them, thus triggering the making of more glucose by the liver which only worsens any existent hyperglycemia.

These findings come mostly from studing diabetic mice that display profound insulin resistance, hyperinsulinemia and are also obese (this particular type of mouse is referred as db+/db+). Humans also have aquaporins but if this is what happens I don't know, I haven't look into that yet).

(Note: most of these concepts have been generated from mouse studies and even though mice and humans have aquaporins that are very similar in DNA sequence, thus making it tempting to extrapolate from mice to humans, mice are not humans. I have not looked into studies in humans comparing lean and obese so I can't comment more on that).

The point is that is highly unlikely that people in maintenance, which we can safely say are not in a pathological state can suddenly behave as if they werein one unless something else is going on. Moreover, without exhausting all possibilities I think the easiest conclusion to make, though not necessarily correct would that an increase of protein over our individual minimum necessarily results in weight gain despite the fact that when we reach maintenance we are more insulin sensitive, more efficient in fat utilization for energy, and are likely to be less sedentary. Otherwise, we might need to re-think what maintenance is. Studies like those conducted by M. Westertep on dietary protein and body weight regulation certainly don't suggest that. Those studies, by the way, were conducted not using protein in isolation but actually meals that included more protein from both animal and plant sources. I think you weren't clear or I probably didn't make that clear in a previous post.

[Mitra]

Dr Mike's recent blog (http://www.proteinpower.com/drmike/archives/2006/03/post.html) mentions insulin in relation to managing ketone production:

As the level of ketone bodies rises in the blood, it stimulates the release of insulin from the pancreas. The spurt of insulin then shuts down the process that makes ketones.

Is this a mechanism by which excess fat consumption would lead to excess fat storage even in the absence of carbohydrates?

If insulin is required to control ketone production, why do low-carb diets work so well in people who are insulin-resistant?

[Gabriel Guzman]

Dr Mike's recent blog (http://www.proteinpower.com/drmike/archives/2006/03/post.html) mentions insulin in relation to managing ketone production:

Is this a mechanism by which excess fat consumption would lead to excess fat storage even in the absence of carbohydrates?


I seriously doubt it because it would need insulin high enough to keep fat internalization going all the time, which doens't happen under carbohydrate restriction. So the phrase "As the level of ketone bodies rises in the blood, it stimulates the release of insulin from the pancreas. The spurt of insulin then shuts down the process that makes ketones... needs to be taken into the right context. Even during carbohydrate restriction, after a meal, there is a spurt of insulin as a normal response so nutrients can be taken care of, but doesn't mean that insulin stays around in high concentrations all day to not only take care of nutrients but also drive fat synthesis and/or accumulation. In fact, studies comparing post-prandial insulinemic responses show that those on a carbohydrate-restricted diet have a smaller insulin response after a meal than those on a high-carbohydrate diet.


If insulin is required to control ketone production, why do low-carb diets work so well in people who are insulin-resistant?

What insulin controls is actually fat oxidation, not directly the production of ketones. I admit that I have not yet read any studies in humans that directly show the dynamics of insulin appearance in plasma as ketones increase. I did a preliminary search but I came out with a few recent studies on isolated rat cells, which need to be taken with a pinch of salt precisely because the system is isolated and things can be very different in vivo.

Having said that, since the 80s and probably earlier than that, it's been known that ketones stimulate insulin secretion, at least in experiments with isolated rat islet cells. In those experiments insulin release was, however, potentiated by ketone bodies in the presence of sub-stimulatory concentrations of glucose. In simpler terms, in those experiments the ketone-stimulated insulin released needed some glucose as well in concentrations equal or less than 5 mM (this concentration is considered stimulatory). Also the concentration of ketones has to be considered. In those old experiments, ketones in concentrations of 5mM were required (+ 5mM glucose) to have an observable insulin release. Without that little glucose, ketones didn't stimulate insulin release even at concentrations around 20 mM. It was also noted that maximum insulin release occurred at ketone concentrations of 10 mM and and returned to minimal at ketone concentrations of 15 mM. Remember that these experiments were done with isolated cells after either feeding rats or fasting them for 48 hours and in all cases, a little glucose was needed to see any effect on insulin release.

Now, those numbers don't mean much unless we put then into the right perspective, so we can have an idea on how much ketosis is induced under different conditions.


Mixed, regular diet: 0.01 mM
ketosis: 0.02 mM
fasting 2-3 days: 1 mM
after exercise: up to 2 mM
fasting 1 week: 5 mM
ketogenic diet: 5-6 mM
fasting 3-4 weeks: 6-8 mM
ketoacidosis: 8+ mM
diabetic ketoacidosis: up to 25 mM


In the experiments mentioned above, concentrations above 15 mM (with stimularory concentrations of glucose) did not increase insulin release so even if there were a slight similarity with what happens in humans, a ketogenic diet would not produce ketones above that level. In fact, ketosis due to a ketogenic diet are lower than true long-term fasting levels because ketogenic diets do not lower insulin levels to zero and ther is always insulin around to keep fatty acids around or below 1 mM. In other words, there is always some insulin around to keep fat breakdown (lipolysis) under control.

I still have problems envisaging the actual pathway or pathways involved in a direct action of ketons on insulin release. The first thing that comes to my mind is how good are the pacreatic cells in using ketones. I seem to remember reading somewhere that oxidaton of ketones in the pancreatic cells is not as efficient as oxidation of glucose, which make sense because the primary tigger for insulin release is, after all, glucose. Another possibility would be that ketones in fact regulate insulin secretion by acting on glucagon secretion instead.

We have to remember that there is always some insulin around, even in a true ketogenic diet (which is truly a very low carbohydrate diet). Absolute lack of insulin occurs only in Type 1 diabetes. That means that glucagon can be release even in the presence of simultaneous release of insulin. We need to remember that we normally talk about the insulin:glucagon ratio, which means that even if the ratio is 'low' there is always some insulin around.

It's also known that Most substrates glucose, free fatty acids and ketone bodies suppress glucagon secretion. This is supported in the observation that inhibition of the metabolism of these substrates prevents the inhibition of glucagon release. Thus, it's plausible that ketone bodies also function as a negative feedback to regulate glucagon production, which in turn regulates fatty acid oxidation that produces ketones. In this way, when ketones reach certain concentration, instead of directly boosting insulin release, they in fact inhibit glucagon release, which in turn limits fat oxidation and ketone production.

[Mitra]

Thank you, Gabe - I do appreciate the time and effort you put into providing these explanations.

[mcsblues]

Gabe, like Janet, I really appreciate the time you put into this, and soory its been a few days since you had more questions from me!

So lets look at an example where an individual is getting plenty of protein (ie above the minimum intake the Eades prescribe) minimal amounts of carbohydrates and the rest fat in something like the ratios above - and that total calorie intake exceeds expenditure. Is it possible to store fat in that scenario? (my own experience suggests that it is!) If fat storage occurs does this indicate that carbs and therefore insulin is not restricted enough, or are there other pathways which allow for fat storage while insulin is kept in check?

Not to my knowledge.

So what happens to fat and protein calories that are excess to current energy/muscle repair requirements then? If they are excreted in this scenario surely this would be simple to measure in a controlled experiment. Has anyone done this?

The only other possibility would seem to be a concurrent increase in BMR, Again one would imagine this would be easily detectable - even back in Stefansson's time they were measuring this sort of thing weren’t they? (I seem to recall he spoke of having to lie in a 'glass coffin' (or something like that) and think neutral thoughts!:) Is there experimental evidence that shows this?

I know many like to suggest that protein will necessarily rise insulin levels to levels comparable with hyperinsulinemia. Indeed there may be a very small effect but never comparable to the effect of glucose and not enough to take over and drive fat synthesis in a constitutive way (all the time), mainly because is likely that glucagon would be counteracting insulin action in tha regard.

There are some nice graphs in the latest Gannon and Nuttall paper - http://www.nutritionandmetabolism.com/content/pdf/1743-7075-3-16.pdf
- the second figure shows the effect on BS and insulin from the ingestion of 50g protein on 'normal' and type 2 diabetic subjects. As you would expect there if there is gluconeogenesis it is only sufficient to maintain BS in normal subjects while the high insulin of type 2s (and exaggerated insulin response) prevents gluconeogenesis - so BS falls. But both seem to have a significant insulin response, and in the type 2 instance, clearly those hormones which act to raise/stabilise BS (like glucagon) have not kicked in.

I'd like to know how they determine a subject is "normal" - if that means not significantly insulin resistant, then wouldn't 'our' response to protein lie somewhere between the two curves?

I'm not sure what you mean by "fat synthesis in a constitutive way (all the time)" - does this mean fat synthesis can occur some of the time - and wouldn't this be the case even on a high carb diet (eg during an overnight fast ketosis might occur so that fat synthesis wouldn't be occuring 24/7)?

[Gabriel Guzman]

Gabe, like Janet, I really appreciate the time you put into this, and soory its been a few days since you had more questions from me!

So what happens to fat and protein calories that are excess to current energy/muscle repair requirements then? If they are excreted in this scenario surely this would be simple to measure in a controlled experiment. Has anyone done this?


The problem I see is to define what is 'excess' calories from protein or fat. You're assuming that there is, indeed, an amount considered excess. Perhaps part of the problem is that an individual's caloric needs are calculated based on basal metabolic rate, which in turn is a reflection of the diet itself. Somebody that has completely switched to burning more fat than carbohydrate for energy may come with very different 'caloric needs' than someboy who's not an efficient fat burner. After all, the estimation of caloric need (or the standard calorie rule) is based on using basal metabolic rate but it that is already increased, as it happens with diets higher in protein and fat, then what exactly is that individual's caloric need?

The experiments of Gannon and Nutall, for example, are not mesuring an 'excess' but an increase in the amount of protein. So, from that angle, I don't think that there are studies measuring diets based on say 80% of calories coming from protein, which sounds like a large amount.


The only other possibility would seem to be a concurrent increase in BMR, Again one would imagine this would be easily detectable - even back in Stefansson's time they were measuring this sort of thing weren’t they? (I seem to recall he spoke of having to lie in a 'glass coffin' (or something like that) and think neutral thoughts!:) Is there experimental evidence that shows this?


Indeed, an increase of dietary protein has shown an increase in thermogenesis which is another way of looking at an increase in basal metabolic rate and that has been measured several times, especially during the past few years when the research on carbohydrate control got more momentum. Donald Layman, among others, reported an increase in thermogenesis after changing the ratio protein:carbohydrate in the diet towards more protein. His sutides are not necessarily in the 'low-carb' mark and yet show that even slighly decrease in their intake in favor of more protein can significantly impact post-prandial thermogenesis and insulin homeostasis (i.e. better insulin response after a meal).


There are some nice graphs in the latest Gannon and Nuttall paper - http://www.nutritionandmetabolism.com/content/pdf/1743-7075-3-16.pdf
- the second figure shows the effect on BS and insulin from the ingestion of 50g protein on 'normal' and type 2 diabetic subjects. As you would expect there if there is gluconeogenesis it is only sufficient to maintain BS in normal subjects while the high insulin of type 2s (and exaggerated insulin response) prevents gluconeogenesis - so BS falls. But both seem to have a significant insulin response, and in the type 2 instance, clearly those hormones which act to raise/stabilise BS (like glucagon) have not kicked in.


First of all, that graph refers to subjects that have not yet adapted to an increase in protein in their diet (i.e. single meal studies). A few more graphs into the paper you see that after 5 weeks of dietary change, glucose levels decrease dramatically while insulin levels don't change significantly (more about that in the following paragraphs).

Okay, let's look at the graph in figure 2 closely, which happens to be the same figure presented in a previous paper from 2003 (Frank Q Nuttall, and Mary C Gannon. Metabolic response of people with type 2 diabetes to a high protein diet. Nutrition & Metabolism 2004, 1:6). The authors wrote this about those particular experiemnts:

Nuttal and Gannon, 2003 (emphasis is mine)
We also determined the serum insulin response to the ingested protein and in confirmation of the studies of Berger, Fajans and others, we observed a modest increase in the insulin concentration in the non-diabetic subjects.


In the case of non-diabetic, even though the graph shows an increase, you have to look to also look at the time axis as well. It is not so much how high the increase in insulin is but how long does it stay high so insulin not only lowers blood glucose but also has the chance to act on other metabolic pathways that depend on it. Layman has also showed such an increase in postprandial insulin after a meal that has more protein but it returns to basal rather quickly and doesn't stay high all day. Another aspect is that the seemingly dramatic change in insulin occurs in the subjects with Type 2 Diabetes, not the normal controls which show not only less insulin than diabetics but also, like they wrote, a modest increase. Although they didn't design the study to measure it, that modest increase is not likely to drive fat synthesis in the way it happens when insulin levels remain high all the time.

The graph in figure 2 also shows what happens after ingesting 50 gr protein without adaptation. Perhaps the graph in figure 4 (which was also presented in the article from 2003) shows better what happens after the subjects, in this case diabetics have been on diet that gives them twice the dietary protein (30%). This graph is important because it applies to the subjects with the diease.

Nuttal and Gannon, 2006
The plasma glucose concentrations during the 24-hour period at the end of the 5 weeks on the control diet, or 5 weeks on the high protein diet, are shown in Figure 3. The blood sampling was started at 8 am. Breakfast, lunch, dinner and snack are shown on the X-axis. The differences appear modest. However, when these data are integrated over 24 hours, using the fasting glucose concentration as baseline, the integrated glucose area actually was reduced by 38% on the high protein diet (Figure 4).


The emphasis is on fasting glucose concentration and they didn't mention much about insulin (which is what shows in figure 4). What they wrote back in 2003 is a better explanation of what they observed:

Nuttal and Gannon, 2003 (emphasis mine)
Although the differences in postprandial glucose values were not very large, when integrated over the 24-hour period, there was a 38% decrease in postprandial glucose area response. If the 24-hour integrated area is considered to be 100% when the subjects ingested the 15% protein diet, when they ingested the 30% protein diet it was 62%. Even though the postprandial glucose concentration was decreased on the 30% protein diet, the insulin area response was modestly increased.


When you see the bar graph for insulin (Figure 4 of the 2006 paper), note the error bars. When looking at figures like this, to conclude that something is significantly different the error bars should be so that if you were to put them together, they wouldn't overlap (this is a useful rule of thumb in the absence of the actual statistics). The error bars in the insulin graph clearly overlap if you put them side by side, which means the differences measured are not significant, in this case meaning that the apparent increase in insulin levels after 5 weeks on a 30% protein in the diet are not significantly different to the same time on a 15% protein in the diet.

There are no bars for normal individuals but the graph you pointed out in figure 2 shows even better that in the normal case, and if we talk about your original question regarding people in maintenance, the increase in insulin is modest if anything.

All this is useful to make the point that even when you see an increase in insulin, it doesn't mean that significant fat synthesis/internalization will necessarily follow, particularly when the increase is 'modest'.

You're assuming that gluconeogenesis immediately follows after protein intake. Insulin can also be made from a particular amino acid; arginine, which makes it what we call it a 'secretagoge' (sometimes equated to 'surrogate') for insulin production. Single meal experiements can also show that protein is as powerful as glucose to induce insulin secretion. In fact, Nuttal and Gannon have observed that in the past. But what happens after adaptation to dietary changes is what I think really matters and what it has been shown is that there is better postprandial insulin homeostasis. Once could plausible think that the little insulin secreted, rather than acting on fat synthesis actually acts to modulate gluconeogenesis by inhibiting the pathway. The decrease in blood glucose reported by Nuttal and Gannon seem to support that in type 2 diabetics. Thus, even though there is more protein coming in, gluconeogenesis remains in check by the little insulin secreted as a result. That is, at least, one interpretation.

But the other part of your question, once again, assumes that somehow certain metabolic pathways occur in isolation, such as gluconeogenesis. In fact, they don't and sicne we as 'open systems' comply pretty well with the laws of thermodynamics (not just the first one), there is one thing that's not cosidered in your reasoning: metabolic cost.

Let's assume for a moment that gluconeogenesis follows immediately after protein intake. Of course, 'immediately' here means in the post absorptive state becasue protein from beef, for example, is not immediately dismantled to provide the amino acids required for gluconeogenesis. Some people believe that but it's a misconception.

For gluconeogenesis to take place, the necessary amino acids are required and to have them available, some proteins that supply branched chain amino acids need to be synthesized first. The need to meet the obligate demand for glucose means that a low carbohydrate diet can lead to increased gluconeogenesis from protein. Left like that, that analysis is incomplete as it greatly underestimates the real costs (energy costs). The major loss of energy, including that lost through thermogenesis, is the need to re-synthesize the proteins that supply branch chain amino acid. Some have calculated that such cost is between 18% (synthesis) and 27% (the cycle being: synthesis + breakdown through ubiquitin-proteasome pathway -this is a specific and important pathway to degrade proteins). Such calculations are also probably low as other researchers have summarized estimates of the costs of protein synthesis and suggests that as much as 4–5 cal/g are required. Therefore, increased gluconeogenesis will, in turn, lead to increased protein turnover, which in turn leads to even greater energy costs, which is one of the possible reasons why increasing protein in the diet, while reducing carbohydrates creates a desireable metabolic advantage without affecting the integrity of the body as a whole (i.e. while becoming and/or remaining healthy) during the process. We've left out other important adaptations that occur when a person is in 'maintenance' but that would make this post even longer!


I'd like to know how they determine a subject is "normal" - if that means not significantly insulin resistant, then wouldn't 'our' response to protein lie somewhere between the two curves?


If you're referring to Nuttal and Gannon's studies, normal means 'non-type 2 diabetics', which is sometimes equated to not being insulin resistant.


I'm not sure what you mean by "fat synthesis in a constitutive way (all the time)" - does this mean fat synthesis can occur some of the time - and wouldn't this be the case even on a high carb diet (eg during an overnight fast ketosis might occur so that fat synthesis wouldn't be occuring 24/7)?

No, I by constitutive I mean fat synthesis significantly all the time in order to accumulate a significant amount and gain significant weight from it. However, fat synthesis can be shut down, for example if not enough insulin is available to drive that pathway and it normally happens when there is more glucagon around, in which case it is fat oxidation (which includes fat mobilization from its stores). It would be metabolically ineficient for the body to have fat synthesis and fat oxidation on at the same time in the same tissue. There is no net energy production, which is ultimately the goal and is what we call a futile cycle.

[mcsblues]

The problem I see is to define what is 'excess' calories from protein or fat. You're assuming that there is, indeed, an amount considered excess. Perhaps part of the problem is that an individual's caloric needs are calculated based on basal metabolic rate, which in turn is a reflection of the diet itself. Somebody that has completely switched to burning more fat than carbohydrate for energy may come with very different 'caloric needs' than someboy who's not an efficient fat burner. After all, the estimation of caloric need (or the standard calorie rule) is based on using basal metabolic rate but it that is already increased, as it happens with diets higher in protein and fat, then what exactly is that individual's caloric need?

The experiments of Gannon and Nutall, for example, are not mesuring an 'excess' but an increase in the amount of protein. So, from that angle, I don't think that there are studies measuring diets based on say 80% of calories coming from protein, which sounds like a large amount.

Indeed, an increase of dietary protein has shown an increase in thermogenesis which is another way of looking at an increase in basal metabolic rate and that has been measured several times, especially during the past few years when the research on carbohydrate control got more momentum. Donald Layman, among others, reported an increase in thermogenesis after changing the ratio protein:carbohydrate in the diet towards more protein. His sutides are not necessarily in the 'low-carb' mark and yet show that even slighly decrease in their intake in favor of more protein can significantly impact post-prandial thermogenesis and insulin homeostasis (i.e. better insulin response after a meal).
OK, I have read Layman as well as Fineman and Fine and I think I understand inefficiency of digesting protein particularly when it comes to using it as an energy source - from a dietary POV this is obviously a good thing, but what are we talking about here? - a few hundred calories a day? Lets go to one of those extreme examples again.:) Lets say you BMR calculated the 'normal' way - ie for a SAD diet is 2000 kcal. OK on a low carb diet - say 10/30/60 (% carbs/protein/fat) the inefficiencies in effect raise your BMR to 2500kcal (the difference is probably less but this is just an example) Now what happens if you raise calories to 4000 (maintaining the low carb macronutrient ratios) What happens at 6000? This is what I mean by excess calories ... so what happens to them? Surely they can't all be accounted for through thermogenesis? I think the Feinman paper suggests that carbs and fat are similarly efficient (or inefficient) energy sources - but most low carb writers suggest that after a period of adaptation we become more efficient in utilising fat - in which case some of favourable effects of the higher protein will be balanced out. Either way there must come a point when dietary intake of fat and protein will exceed even an enhanced demand for energy ... and if as you say there are no mechanisms which would permit this excess (sorry I can't think of another word!) to be deposited as fat, then surely whatever does happen to it should be easily measurable. But I haven't seen any papers which explore this scenario.

First of all, that graph refers to subjects that have not yet adapted to an increase in protein in their diet (i.e. single meal studies). A few more graphs into the paper you see that after 5 weeks of dietary change, glucose levels decrease dramatically while insulin levels don't change significantly (more about that in the following paragraphs).
So what caused the glucose levels to fall dramatically if it wasn't insulin?

We've left out other important adaptations that occur when a person is in 'maintenance' but that would make this post even longer!
When you have the time I am listening!:p

If you're referring to Nuttal and Gannon's studies, normal means 'non-type 2 diabetics', which is sometimes equated to not being insulin resistant.
I think the Eades quote Reaven's statistics and interpret them to say 75% of the population would be insulin resistant to some degree - it would seem rather sloppy science if some standardised measure of what is 'normal' has not been developed. If these controls are truly part of the 25%, then the rest of 'us' must surely have some degree of the sort of response the type 2s demonstrate. After all the diagnosis of what is and isn't diabetes is just numbers - if your insulin response falls just short of the definition you are still going to have most of the problems.


No, I by constitutive I mean fat synthesis significantly all the time in order to accumulate a significant amount and gain significant weight from it. However, fat synthesis can be shut down, for example if not enough insulin is available to drive that pathway and it normally happens when there is more glucagon around, in which case it is fat oxidation (which includes fat mobilization from its stores). It would be metabolically ineficient for the body to have fat synthesis and fat oxidation on at the same time in the same tissue. There is no net energy production, which is ultimately the goal and is what we call a futile cycle.
I wasn't suggesting that synthesis and oxidation would happen at the same time, or that synthesis would occur all the time. My suggestion was that glucagon would not be dominant 24/7 (and it would surely be unhealthy if it was??) and if that is the case, wouldn't that leave open the possiblility of fat synthesis some of the time?

[Gabriel Guzman]

OK, I have read Layman as well as Fineman and Fine and I think I understand inefficiency of digesting protein particularly when it comes to using it as an energy source - from a dietary POV this is obviously a good thing, but what are we talking about here? - a few hundred calories a day?


It may not seem like a lot to you but if you think of that very small amount every day, regardless of how much you move, in the end it does account to a significant amount. And that is only accounted by the effect of protein. Add the more efficient utilization of fat to that and you've got an even more favorable scenario for weight loss.


Lets go to one of those extreme examples again.:) Lets say you BMR calculated the 'normal' way - ie for a SAD diet is 2000 kcal. OK on a low carb diet - say 10/30/60 (% carbs/protein/fat) the inefficiencies in effect raise your BMR to 2500kcal (the difference is probably less but this is just an example) Now what happens if you raise calories to 4000 (maintaining the low carb macronutrient ratios) What happens at 6000? This is what I mean by excess calories ... so what happens to them? Surely they can't all be accounted for through thermogenesis?


First of all, on a low carb diet, which produces adaptation to fat as the preferred source of fuel, the standard calorie rule doesn't apply unless you correct for the respiratory quoficient to estimate BMR. That alone changes the amount of calories needed as 'basal'. The 'normal' way to estimate BMR considers only body weight and could either underestimate or overestimate thea mount of calories if a person is very muscular of very overweight, respectively. A far more accurate way to estimate BMR is to account for the caloric equivalent of the nutrients, and it is here where it matters a great deal if a person's diet includes more fat, protein or carbohydrate. Even then, standard methods to estimate metabolic rate assume that the portion of protein in the diet is fairly constant, which may not be the case. Nonetheless, and keeping that in mind, it is possible to estimate metabolic rate by multiplying the caloric equivalent times the respiratory quotient (RQ). RQ, which is an indication of how much oxygen is being used is largely influenced by the composition of macronutrients and is higher when more fat is used for energy. Hence, the RQ when the substrate for energy is mainly fat, as it happens on a low carbohdyrate diet, is significantly smaller compared to the RQ when energy is produced mostly by using carbohdyrates.

In the article by Phinney about ketogenic diets and physical performance, he makes the observation that when the subjects adapted to a ketogenic diet had a mean respiratory quotient of 0.72 (the theoretical is 0.75), which indicates that their substrate for energy is mainly fat. The RQ when the substrate for energy is mainly carbohydrate is 1.00, hence the importance of considering that when talking about estimations of BMR.

Therefore, without that consideration, the BMR could be overestimated up to 25% and you can carry that overestimation all the way to the estimation of basal caloric needs since to do that, according to the standard calorie rule, you multiply your BMR times an appropriate activity factor.

The standard method to estimate BMR, the Harris-Benedict formula, which by the way was published in 1919 when there were fewer people in the world, accounts for gender, age, height and weight appears to be reasonably accurate for normal people with normal body fat. Given that there were far fewer obese people around back in the early 1900s than there are today, we should always be aware of this weakness. If we used lean instead of total body weight, we could presumably compensate for the weakness of the formula. The actual BMR would thus be related to fat-free mass and then to estimate caloric needs, we would multiply that lean body mass-related BMR times the appropriate activity factor. On a low carbohydrate diet, most of the energy comes from fat utilization and since the aim of weight loss or maintenance is not to sacrifize muslce protein, then it makes perfect sense to estimate calories in terms of lean body mass, which in other words means estimate the amount of protein needed to maintain such mass, which in turn strongly suggest where those calories should come from. Now that sounds awfully similar to the way the 'minimum protein intake' is calculated in Protein Power.

All this round-about of calories and extreme examples of calories is just to emphasize that increasing caloires in the way you suggest, without any need for it is most likely to offset any acquired balance, and that's assuming that is actually possible to consciously do so for extended periods.



I think the Feinman paper suggests that carbs and fat are similarly efficient (or inefficient) energy sources...


On the contrary. Fat and carbohydrates are very efficient energy sources because the body doesn't need to invest much to extract every from them. Protein, on the other hand, needs a high energy cost to extract the little energy they can provide.


- but most low carb writers suggest that after a period of adaptation we become more efficient in utilising fat - in which case some of favourable effects of the higher protein will be balanced out.


This is a little difficult to understand... Do you mean thermogenesis and increased satiety when you say "favorable effects of higher protein"? How does this 'balance' play out in your view (or the view of the low carb writers you refer to)? Adaptation or rather becoming more efficient in utilizing fat actually spares protein from being used to produce energy to be used to keep glucose levels constant when and if needed.


Either way there must come a point when dietary intake of fat and protein will exceed even an enhanced demand for energy ... and if as you say there are no mechanisms which would permit this excess (sorry I can't think of another word!) to be deposited as fat, then surely whatever does happen to it should be easily measurable. But I haven't seen any papers which explore this scenario.


I think it helps to think of how all this is regulated. It's not just about the amounts of nutrients, hormones that act behind the metabolic pathways, redundant mechanisms that act together to regulate energy utilization, or even the neurotransmitters that help regulate food intake, and other probably yet unknown factors , it's not about either of these alone but how they work in concert. So far you've been thinking not only on extreme examples but also isolated mechanisms, which are fine to understand each piece of the puzzle we call 'metabolism'. Perhaps the reason why you haven't seen papers working on the extremes, at least in humans, is because it would be quite difficult to work on those extreme cases unless there is a disease related to it. For example, you can read examples of diets that rely almost exclusively on fat (80+ percent of the caloric intake as fat) for treating epilepsia, but very few studies would attempt that in normal people, most likely because it wouldn't pass the ethical hurdles. After all, it's still incorrect to feed people large amounts of fat and see what happens...

What I'm trying to say is that once energy demands are met, it's quite hard to override the body's multiples mechanisms that act to control energy homeostasis. That is of couse, talking about protein and fat because such override happens quite frequently with carbohydrates. In other words, the extreme example of 4000 calories keeping the same nutrient ratio (I assume you meant same 'low-carb-adequate protein' scenario), in my opinion, is qutie difficult to achieve and maintain unless the energy demands are set that high.



So what caused the glucose levels to fall dramatically if it wasn't insulin?


Better glucose uptake.


I think the Eades quote Reaven's statistics and interpret them to say 75% of the population would be insulin resistant to some degree - it would seem rather sloppy science if some standardised measure of what is 'normal' has not been developed.


I don't have an answer to that and as we've said before, the most challenging part of this is to unlearn what we have in the past. If you think that's sloppy science, think about the decision-making factor that leads to prescription of statis;total cholesterol and the calculation of LDL. As we know, that means nothing unless that number is put into the context of particle size, triglycerides and HDL. That important decisions are made on outdated formulas that may not apply any more is more scary than sloppy. I think we could write counltess threads with examples of sloppy science.


If these controls are truly part of the 25%, then the rest of 'us' must surely have some degree of the sort of response the type 2s demonstrate. After all the diagnosis of what is and isn't diabetes is just numbers - if your insulin response falls just short of the definition you are still going to have most of the problems.


More and more, it would seem that many conditions should now be re-defined not in terms of specific factors but in a more operational way as a set of markers that respond to some kind of intervention. For example, Volek and Feinman wrote a review (http://www.nutritionandmetabolism.com/content/2/1/31)precisely on these kinds of consideration. In my opinion, an excelent review to keep around.


I wasn't suggesting that synthesis and oxidation would happen at the same time, or that synthesis would occur all the time. My suggestion was that glucagon would not be dominant 24/7 (and it would surely be unhealthy if it was??) and if that is the case, wouldn't that leave open the possiblility of fat synthesis some of the time?

Indeed, glucaon is not dominant 24/7. As noted on another thread, glucagon secretion seems to also be regulated by ketones and fatty acids precisely to prevent modulate hepatic glucose output. But just because glucagon can be regulated doesn't meant that fat synthesis should necessarily follow, particularly if you're talking about sustained fat synthesis so weight gain can ensue.

[mcsblues]

It may not seem like a lot to you but if you think of that very small amount every day, regardless of how much you move, in the end it does account to a significant amount. And that is only accounted by the effect of protein. Add the more efficient utilization of fat to that and you've got an even more favorable scenario for weight loss.
I agree even a few hundred calories is significant long term, but that is not to say you can take that principle and eat whatever you like as long as the carbs are kept low - or am I wrong?



On the contrary. Fat and carbohydrates are very efficient energy sources because the body doesn't need to invest much to extract every from them. Protein, on the other hand, needs a high energy cost to extract the little energy they can provide.

My point was they seem similarly efficient (about 40% from memory) it is protein which is the odd man out so to speak, particularly if used for energy production when (again from memory efficiency could drop from 33% to 27% or less?).


This is a little difficult to understand... Do you mean thermogenesis and increased satiety when you say "favorable effects of higher protein"? How does this 'balance' play out in your view (or the view of the low carb writers you refer to)? Adaptation or rather becoming more efficient in utilizing fat actually spares protein from being used to produce energy to be used to keep glucose levels constant when and if needed.
My point was that increasing the % of protein in the diet confers the so called metabolic advantage that low carb writers refer to - ie you can eat more calories and still lose the same amount (or more) compared to a lower protein high carb diet - precisely because of the thermogenisis associated with protein metabolism (especially if gluconeogenisis is required to replace glucose for dependant cell formerly supplied by carbs). The inefficiency of protein is therfore good news from a weight loss POV.

OTOH if after a period of adaptation we become more efficient in using fat as an energy source through ramping up of ketone production or more cells 'acquiring' the ability to use FFAs directly - than while this is great from an exercise performance POV as Phinney and others suggest, it surely has the opposite impact on how much we can eat to lose or maintain? - if we need less to meet energy demands.



I think it helps to think of how all this is regulated. It's not just about the amounts of nutrients, hormones that act behind the metabolic pathways, redundant mechanisms that act together to regulate energy utilization, or even the neurotransmitters that help regulate food intake, and other probably yet unknown factors , it's not about either of these alone but how they work in concert. So far you've been thinking not only on extreme examples but also isolated mechanisms, which are fine to understand each piece of the puzzle we call 'metabolism'. Perhaps the reason why you haven't seen papers working on the extremes, at least in humans, is because it would be quite difficult to work on those extreme cases unless there is a disease related to it. For example, you can read examples of diets that rely almost exclusively on fat (80+ percent of the caloric intake as fat) for treating epilepsia, but very few studies would attempt that in normal people, most likely because it wouldn't pass the ethical hurdles. After all, it's still incorrect to feed people large amounts of fat and see what happens...
Well true, but there are plenty of people who eat this way without being told to!:)

What I'm trying to say is that once energy demands are met, it's quite hard to override the body's multiples mechanisms that act to control energy homeostasis. That is of couse, talking about protein and fat because such override happens quite frequently with carbohydrates. In other words, the extreme example of 4000 calories keeping the same nutrient ratio (I assume you meant same 'low-carb-adequate protein' scenario), in my opinion, is qutie difficult to achieve and maintain unless the energy demands are set that high.
Well again I guess its annecdotal but there seem to be no shortage of people like me who find it is possible (to overeat on low carb) if some control is not exercised. Janet found this in Staying Power and while it seems slightly at odds with the PPLP quotes earlier in this thread, I must admit I couldn't agree more!

"Weight control over the long haul is like a three-legged stool: one leg is carb intake, one leg is calorie intake, and one leg is calorie output. As long as all three legs are stable the stool will balance, but if one of them breaks, the stool will fall. So it is with the balance you'll find in maintenance. Even after you've advanced through to your carbohydrate maximum, your game plan must remain flexible."

Michael R Eades, MD & Mary Dan Eades, MD
Staying Power


Better glucose uptake.
There had been a dramatic improvement in insulin resistance in five weeks??

I don't have an answer to that and as we've said before, the most challenging part of this is to unlearn what we have in the past. If you think that's sloppy science, think about the decision-making factor that leads to prescription of statis;total cholesterol and the calculation of LDL. As we know, that means nothing unless that number is put into the context of particle size, triglycerides and HDL. That important decisions are made on outdated formulas that may not apply any more is more scary than sloppy. I think we could write counltess threads with examples of sloppy science.

Well true, ther is no shortage of bad science when you start looking into what has been written about diet - Keys would be a prime example! But surely the assessment of pre existing insulin sensitivity is central to any exploration of the metabolic response to changing macronutrient ratios? - and good scientists (such as we now have in the LC field) should examine this or the nature of their control subjects and the responses of study groups will be questionable without some baseline being established.


More and more, it would seem that many conditions should now be re-defined not in terms of specific factors but in a more operational way as a set of markers that respond to some kind of intervention. For example, Volek and Feinman wrote a review (http://www.nutritionandmetabolism.com/content/2/1/31)precisely on these kinds of consideration. In my opinion, an excelent review to keep around. Damn, work calls - I will get back to reading this later!

Indeed, glucaon is not dominant 24/7. As noted on another thread, glucagon secretion seems to also be regulated by ketones and fatty acids precisely to prevent modulate hepatic glucose output. But just because glucagon can be regulated doesn't meant that fat synthesis should necessarily follow, particularly if you're talking about sustained fat synthesis so weight gain can ensue. But why does weight gain rely on "sustained fat synthesis"? Wouldn't a little bit here and there seperated by periods when synthesis did not occur but all energy requirements where easily met from dietary sources result in long term weight gain?

[Gabriel Guzman]

I agree even a few hundred calories is significant long term, but that is not to say you can take that principle and eat whatever you like as long as the carbs are kept low - or am I wrong?


No, it doesn't. I suppose if somebody wants to do it, then they do it but a lot of signals are triggered in order to exert control. For example, the time of start for feeding may be somewhat voluntary but once the appropriate signals to stop feeding are triggered, then stopping food intake is pretty much biological (i.e. satiety). Perhaps some people just like to get pass that. With carbohydrate, however, that doesn't seem to work as well and maybe, and combined with an insulin roller coaster, the actual time for stop feeding may not even be set. You've probably noticed that when we say 'I can't eat another piece of steak...' we really mean it... but we can always have an extra piece of cake even though we've said we're full! ;)


My point was they seem similarly efficient (about 40% from memory) it is protein which is the odd man out so to speak, particularly if used for energy production when (again from memory efficiency could drop from 33% to 27% or less?).


Actually the dynamic action of carbs and fats are ~1 and ~9%, respectively whereas that of protein is ~25-30%. So, protein is quite ineficient as energy source. That is not to say that the body won't use it in extreme conditions such as true starvation, defined as a long fasting period, which is not an overight fast.



My point was that increasing the % of protein in the diet confers the so called metabolic advantage that low carb writers refer to - ie you can eat more calories and still lose the same amount (or more) compared to a lower protein high carb diet - precisely because of the thermogenisis associated with protein metabolism (especially if gluconeogenisis is required to replace glucose for dependant cell formerly supplied by carbs). The inefficiency of protein is therfore good news from a weight loss POV.


Actually, those who actually talk and/or write about protein are not the majority of 'low-carb writers'. In fact, some of them may not even consider protein as important as we, or at least I do. Thermogenesis is only part of the equation; longer and higher satiety is another important part. In my opinion, the combination of increased thermogenesis (which is a reflextion of increased metabolic rate) and a higher, longer satiety is one of the factos why protein conferes metabolic advantage. However, the link between thermogenesis and increased satiety, to my knowledge, hasn't been fully established. A link between thermogenesis and gluconeogenesis is not that obivious either, but gluconeogenesis is certainly a costly process that requires energy. Metabolic advantage by increased gluconeogenesis may not necessarily reflect on increased thermogenesis.


OTOH if after a period of adaptation we become more efficient in using fat as an energy source through ramping up of ketone production or more cells 'acquiring' the ability to use FFAs directly - than while this is great from an exercise performance POV as Phinney and others suggest, it surely has the opposite impact on how much we can eat to lose or maintain? - if we need less to meet energy demands.


Depending on utilization of ketones for energy is not advantageous only within the context of exercise. Phinney's work only make the point that carbohydrates are not the exclusive source of energy as it has been preached for decades. It's because ketones are used that protein is spared from being used as energy source. And perhaps that's why we can always make ketones (whether or not people detect them in their urine). From an evolutionary point of view, the ability to use ketones may have just given another added advantage to our species in times of scarcity. After a period of adaptation, the use of fat (through ketones) we become more efficient, not stalled, just as after a period of adaptation to carbohydrate control, we become more insulin sensitive, which also means less insulin to do the job.


Well again I guess its annecdotal but there seem to be no shortage of people like me who find it is possible (to overeat on low carb) if some control is not exercised. Janet found this in Staying Power and while it seems slightly at odds with the PPLP quotes earlier in this thread, I must admit I couldn't agree more!

"Weight control over the long haul is like a three-legged stool: one leg is carb intake, one leg is calorie intake, and one leg is calorie output. As long as all three legs are stable the stool will balance, but if one of them breaks, the stool will fall. So it is with the balance you'll find in maintenance. Even after you've advanced through to your carbohydrate maximum, your game plan must remain flexible."

Michael R Eades, MD & Mary Dan Eades, MD
Staying Power




And I agree, carb intake (on the low side) provides the optimal metabolic scenario; calorie intake (especially from nutrients that are absolutely essentia and nurture the body; protein and fat, not just overall calories) and calorie output (which may include more physical activity or higher metabolic rate taking advantage of the dynamic action of food) is what provides the dynamics to maintain. Should that dynamics shifts towards less caloric output, particularly when we've become more sensitive, then weight gain may ensue. Should that dynamics shifts towards excessive caloire output, say through vigorous exercise without proper protein intake and weight loss may even occur by losing fat-free mass. And we don't even have to talk about the dynamics shifting towards an increase of carb intake to levels we all know because that wrecks the metabolic scenario. Nonetheless, I think we can see where it's easier to lose such balance and is not calorie intake if we really understand that the source of calories matter.


There had been a dramatic improvement in insulin resistance in five weeks??


If there is something dramatic about carbohydrate control is the rather short time that it takes to stabilize glucose and insulin homeostasis. So, it is possible to see changes like this in short periods.


Well true, ther is no shortage of bad science when you start looking into what has been written about diet - Keys would be a prime example! But surely the assessment of pre existing insulin sensitivity is central to any exploration of the metabolic response to changing macronutrient ratios? - and good scientists (such as we now have in the LC field) should examine this or the nature of their control subjects and the responses of study groups will be questionable without some baseline being established.


I will comment on an article I just read about a meta-analysis of 'low carb vrs low fat' studies, which of course concludes that low carb diets are not to be recommended because of their adverse effect on total cholesterol and LDL levels. Of course, we know that total cholesterol and LDL levels calculated from the Friedewald formula are meaningless without any information about the LDL profile itself. The meta-analysis, however, does recognize that low carb diets did increase HDL and decrease triglycerides more than low-fat diets... so, go figure. Of the very few positive aspects I found on that meta-analysis is the identification of flaws and errors in the experimental design that make most nutrition studies hard to compare, if not impossible, to other equally flawed studies. So, I think that researchers in the low carbohydrate field should take note of those errors in order to design high quality studies that can leave no doubt of their methodology.


But why does weight gain rely on "sustained fat synthesis"? Wouldn't a little bit here and there seperated by periods when synthesis did not occur but all energy requirements where easily met from dietary sources result in long term weight gain?

Weight gain from fat can be due to either fat synthesis (which then stays stored) or fat accumulation. Of course, there is also weight from fluid retention. Weight gain from fat-free mass is actually a desireable outcome. Which other mechanism do you envisage for sustained weight gain that is not from fat synthesis/accumulation, water retention or fat-free mass increase?

[mcsblues]

...and another thing!;)

Don't panic! just a few things I need cleared up.:)

1. We were talking about the relative efficiency of carbs, fats and protein when used for energy. I said;"My point was they (carbs and fats) seem similarly efficient (about 40% from memory) it is protein which is the odd man out so to speak, particularly if used for energy production when (again from memory efficiency could drop from 33% to 27% or less?)."

You said;
Actually the dynamic action of carbs and fats are ~1 and ~9%, respectively whereas that of protein is ~25-30%. So, protein is quite ineficient as energy source.
Fine and Feinman say;
The effect of metabolic path on the energetics of oxidation is illustrated in Table 1 (http://www.nutritionandmetabolism.com/content/1/1/15/table/T1) which summarizes the analysis from our earlier paper [2 (http://www.nutritionandmetabolism.com/content/1/1/15#B2)]. In this example, a mole of glucose directly oxidized to CO2 and water generates 38 moles of ATP with an overall efficiency of about 38.5%. On the other hand, if glucose is first incorporated into glycogen, followed by hydrolysis of the glucose and subsequent oxidation, 2 moles of ATP are lost per mole in this cycle with overall efficiency reduced to 35%. Similarly an amino acid from an "average" protein, when directly oxidized to CO2, produces ATP with an efficiency of about 33%. If the amino acid is first incorporated into a protein and later hydrolyzed and oxidized, four ATP's per molecule are used for synthesis of the peptide bond. This reduces the efficiency to 27%. Smaller degrees of inefficiency are seen for lipid cycles (Table 1 (http://www.nutritionandmetabolism.com/content/1/1/15/table/T1)) but multiple cycles may have a cumulative effect. It is estimated, for example, that half of depot fatty acids in triacylglycerol have been through at least one cycle [14 (http://www.nutritionandmetabolism.com/content/1/1/15#B14)]. It should be apparent that variation in efficiency is not a thermodynamic issue but an empiric question to be determined by the requirements of metabolism. http://www.nutritionandmetabolism.com/content/1/1/15 (paper)
http://www.nutritionandmetabolism.com/content/1/1/15/table/T1 (table 1)

Can you explain the difference between "dynamic action" and the efficiency measures they describe?

2.You say (in response to the Eades three legged stool quote from Staying Power);
I agree, carb intake (on the low side) provides the optimal metabolic scenario; calorie intake (especially from nutrients that are absolutely essentia and nurture the body; protein and fat, not just overall calories) and calorie output (which may include more physical activity or higher metabolic rate taking advantage of the dynamic action of food) is what provides the dynamics to maintain. Should that dynamics shifts towards less caloric output, particularly when we've become more sensitive, then weight gain may ensue.
The question remains ... how? In your scenario carb intake and calorie intake remain the same, but calorie output drops - perhaps due to lower exercise, but surely the result (weight gain) would be the same if calorie output and carb intake remained constant but calorie intake increased. And in what way have we become more "sensitive"?

In this example I assume the weight gain we are both talking about is fat gain not LBM (or perhaps a combination of the two) - but that raises (yet) another question. If fat gain is theoretically impossible if carbs are kept low enough, wouldn't (anabolic) muscle building be similarly restricted if insulin is kept low enough to ensure the (catabolic) hormone glucagon dictates that fat cannot be deposited? And I assume you are not saying that LBM cannot be increased on a ketogenic diet so long as adequate dietary protein is available.