Why Is Insulin Sensitivity Good? (From A Partitioning Point Of View)

[NU_nutrition_TS]

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For example, i was always a fat kid and teenager, and when i first started to get the notion that i needed to diet and exercise (not till very late - about 19 years old), the 1st book i read was Susan Kleiners Power Eating book, which advocates high carb low fat for the msot part. Being fat, and therefore probably insulin resistant, this diet just made me fatter. I also was not doing any resistance training (just lots of kickboxing). Being the late 90's i kept hearing how carbs were the devil, so i read diet books like Atkins, Anabolic Diet (older members here will remember me raving on about that one), and the NHE Diet, and because i was fat and insulin resistant these diets allowed me to shed quite alot of fat. Two of these books also strongly advocated resistance training, so i started doign that and that helped improve my insulin senstivity and enhance fat loss. But for about 3 years, i plateu'd on high fat diets. Eventually i came across the works of Lyle McDonald, Tom Venuto, Alan Aragon, Anthony Colpo, James Kreiger, Casey Butt, and others, and realised now that i was leaner and more muscular, in theory i should have much better insulin sensetivity to deal with carbs. I switched back to a higher carb, high protein, low-moderate fat diet, and hey presto i started to shed fat again, right down to about 9%. Also, my gym performacne was so much better on a higher carb diet. Ironically, the Power Eating plan by Susan Kleiner (the diet that originally made me fatter) is very close to the macro breakdown i eat now!

Interesting. You say you were a 'fat kid' - from what age did you become fat (I'm assuming you weren't born fat and remained that way through nursing and beyond weaning!)? Though there is some research to suggest that the diet of the mother can have effects on the way genes are expressed in her unborn baby leading to it being born a particular phenotype (possibly insulin resistant). Would you say your mother was on a typical high carb/low fat diet when she carried you? Also, if you think a particular diet led you to become fat as a kid, do you wonder whether your ability to eat that same diet now with apparent impunity will continue indefinitely or will it eventually drive you back to gaining fat?

Quite a few people who lose excess fat on a low carb/high fat diet seem to report a point where fat loss plateaus - My own experience would seem to confirm this - but I have no pressing desire to have single digit body fat levels and my current body fat percentage is well inside the ideal range for a man of my age anyway - however, I have noticed that I can eat at what would be considered a semi-starvation level in terms of calories and not lose the amount of weight such a deficit would predict.

Could it be that, once your metabolism has recovered to the point that any fat that is stored postprandially is also optimally released and oxidised during fasting periods (and you use predominantly fatty acids and ketones for energy production), you actually need fewer dietary calories to translate into cellular energy (ATP) because you get so much more ATP per molecule of fatty acid? This is just another reason why I find arbitrarily eating to a predetermined daily calorie allowance usually ends badly and would much prefer to eat to hunger/satiety!

[Donjman]

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Could it be that, once your metabolism has recovered to the point that any fat that is stored postprandially is also optimally released and oxidised during fasting periods (and you use predominantly fatty acids and ketones for energy production), you actually need fewer dietary calories to translate into cellular energy (ATP) because you get so much more ATP per molecule of fatty acid? This is just another reason why I find arbitrarily eating to a predetermined daily calorie allowance usually ends badly and would much prefer to eat to hunger/satiety!

Some great points. I must admit though if I let my appetite decide how much food I ate, I would probably be 20lbs lighter. Not really underweight but not muscular. It seems the body seeks an easy life. I'm yet to see a hunter gatherer tribe that looks very muscular. I fair amount seem lean and "light" in build. Humans seem geared towards throwing a rock to get the fruit down, rather than climbing the tree!

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So basically, lipogenesis from carbs occur when Total energy input exceeds Total Energy Expended (TEE) - i.e in a hypercaloric state.

That's not what I gathered from the study. Lipogenesis only occurs when total CARB intake overtakes expenditure, not just calories.

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Only when CHO energy intake exceeds TEE does DNL in liver or adipose tissue contribute significantly to the whole-body energy economy

So carbs to fat only happens when you pretty much consume enough carbohydrate that exceeds TEE.

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With the hypercaloric state in mind, comes what you mentioned above from Lyles articles - that the degree of lipogenesis is affected by muscle insulin sensitivity. I.e if your muscles have good insulin sensitivity, less insulin is output in relation to the food / drink because less is needed for nutrient storage in the muscles, and therefore the excess calories from carbs above maintenance can be driven into muscles and not adipose tissue

^^ exactly. But what I'm trying to say is, if you take 2 people, 1 resistant and 1 sensitive, and they both have say 50% glycogen levels in muscle tissue, the first few "loads" of carbohydrate you can argue that the sensitive guy is going to store them as glycogen faster and get back to lipogenesis.

But what when glycogen is full in both? Is insulin sensitivity of any benefit to him then? It seems truley just a calorie game after that. That's what I keep trying to understand in my head. Once you take away the fact that the muscle tissue is just shoving calories into glyogen stores, and you get 2 guys with full glyogen, but one sensitive and one resistant then what are the benefits of sensitivity (surplus deficit or maintenance)?

It seems paradoxical that someone would even have high insulin sensitivity with full glycogen. Is it even possible??? So perhaps the real benefit isn't just "insulin sensitivity" but what CAUSED it in the first place. IE exercise lowered glycogen increased amino acid uptake.

What I'm trying to say is, just flicking a switch (if you could) and making someone insulin sensitive, without changing calories, glyocgen levels or making them exercise, shouldn't impact body composition for those reasons above. Now if there is a glyocgen debt, a PLACE for the calories to go, then it makes total sense that he will tap into lypolysis quicker. I don't think "insulin sensitivity" on it's own is relevant without something that caused it because of calories!

It's the reason that caused the sensitivity (along with the sensitivity that follows) that causes calories to be redirected. Not just flicking a switch.

Is my line of thinking making any sense, or have I got this totally backwards?

[NU_nutrition_TS]

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Some great points. I must admit though if I let my appetite decide how much food I ate, I would probably be 20lbs lighter. Not really underweight but not muscular. It seems the body seeks an easy life. I'm yet to see a hunter gatherer tribe that looks very muscular. I fair amount seem lean and "light" in build. Humans seem geared towards throwing a rock to get the fruit down, rather than climbing the tree!

I have noticed this. Many indigenous peoples tend to be reasonably lean but not hugely muscular (some don't even have a particularly athletic physique). There was a TV programme not so long ago that sent a group of fitness buffs and amateur athletes (from various disciplines) to different tribes around the world and a put them into traditional sport/competition with them. In almost all cases the natives beat the western fitness buffs even though they appeared beefier. Body-building is peculiar in that success is judged almost exclusively on appearance (aesthetic/cosmetic considerations) not physical performance - though a certain amount of strength increase is inherent in body-building exercise. People who have to exert themselves physically everyday in a variety of situations just to survive need strength and endurance for the least amount of bulk (to maintain agility and also to keep energy needs within the limits of what food is available). So appearance (in terms of muscle size and symmetry) is not a consideration.

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But what I'm trying to say is, if you take 2 people, 1 resistant and 1 sensitive, and they both have say 50% glycogen levels in muscle tissue, the first few "loads" of carbohydrate you can argue that the sensitive guy is going to store them as glycogen faster and get back to lipogenesis.

But what when glycogen is full in both? Is insulin sensitivity of any benefit to him then? It seems truley just a calorie game after that. That's what I keep trying to understand in my head. Once you take away the fact that the muscle tissue is just shoving calories into glyogen stores, and you get 2 guys with full glyogen, but one sensitive and one resistant then what are the benefits of sensitivity (surplus deficit or maintenance)?

It seems paradoxical that someone would even have high insulin sensitivity with full glycogen. Is it even possible??? So perhaps the real benefit isn't just "insulin sensitivity" but what CAUSED it in the first place. IE exercise lowered glycogen increased amino acid uptake.

What I'm trying to say is, just flicking a switch (if you could) and making someone insulin sensitive, without changing calories, glyocgen levels or making them exercise, shouldn't impact body composition for those reasons above. Now if there is a glyocgen debt, a PLACE for the calories to go, then it makes total sense that he will tap into lypolysis quicker. I don't think "insulin sensitivity" on it's own is relevant without something that caused it because of calories!

It's the reason that caused the sensitivity (along with the sensitivity that follows) that causes calories to be redirected. Not just flicking a switch.

Is my line of thinking making any sense, or have I got this totally backwards?

I would say that makes the most sense. You have to have somewhere for all this glucose to go - if glycogen stores are full then I can't see the body stuffing any more into them just to clear the excess glucose. There is oxidation - but again there has to be demand; if you are not particularly active when you have excess glucose to clear then I can't see the muscles suddenly springing into intense action just to clear it. Of course there are other avenues like NEAT and thermogenesis (plus futile cycling) but they do not usually make up a huge contribution to TDEE. However, adipose cells are able to be stuffed and you will even make more adipose cells if the ones you already have are filled to capacity.

It would seem that is the main mechanism by which exercise (particularly intense resistance exercise) improves carbohydrate metabolism - by constantly taking glycogen out of storage to make room for excess glucose coming in. But as I have often asked before - which is the chicken and which is the egg? Are we exercising to allow us to eat the excess dietary carbs or are we eating the excess dietary carbs to support the exercise? It seems you could tackle the problem from either direction.

[Donjman]

This is what (for the moment at least) I can't seem to get my head around.

Fair enough intense exercise will deplete glycogen, which means muscle "wants" more carbohydrate, and in the next carb load it will refill (as will liver glyco probably) . Also someone insulin sensitive will have lower fasting insulin and (lower insulin + less time under a carb/protein load).

I don't really see how this partitions calories away from fat as it were. Since all dietary fat is GOING to adipose tissue anyway and be released when insulin is low, and in a normal person lipogenesis isn't really going to happen. It does allow for fat to be oxidised effortlessly (since insulin inhibits lipolysis and insulin levels are lower in a sensitive person). But I come back to the same point again.

If you take away the fact that the exercise burns calories, then you take away the calories for the glycogen debt, then what's the benefit for "calorie partitioning" and body composition. Isn't the same number of calories just going to do the same thing once this "debt" for glycogen and exercise is made up for?

I come back to the same point I seem to be stuck at Nu. Can oxidation exceed fat storage (ie can NET fat loss be achieved) in a calorie surplus or indeed maintenance. I don't at the moment see how it can be, since fat is always the LAST to be dealt with. Am I wrong there?

Fat can only be oxidised when insulin is lowish (unless FAT cells are resistant and that's a whole other issue).

[NU_nutrition_TS]

Nutritional science is often presented as if it is a fairly settled science, with most of the metabolic pathways and permutations pretty much elucidated, but the truth is that little is known for certain and much remains to be pinned down. For example, most 'honest' researchers will say that they know very little about lipogenesis in humans because the methods they currently have at their disposal for determining it are not very accurate or revealing. So the questions surrounding how people get fat are really still wide open and the simple 'too many calories in and not enough out' is not really helpful as a mechanistic explanation.

Some comments I have read recently have gone so far as to say we should really abandon the idea of 'calorie balance' in favour of 'substrate balance'. That is to say, the body has a certain level of each major substrate that it holds onto and so changes occur based on how, when and why these levels fluctuate. Taking the three main macronutrients as an example, there is little to no storage capacity for amino acids (aside for a little general whole body protein synthesis and subsequent breakdown, which together constitutes the 'amino acid pool') - so they will be preferentially oxidised when there is an excess of them to clear (this may also include conversion to glucose>glycogen via gluconeogenesis). Next in line is glucose - there are two limited storage depots: liver and muscle glycogen. Beyond those is adipose tissue storage via glucose synthesis into fatty acids and glycerol (needed to make triglycerides - the storage form of fat). Finally we have fatty acids which are either oxidised for energy (plus structural/hormonal uses) or stored in adipose tissue.

Since this also constitutes a hierarchy - with amino acids always taking priority over glucose and both amino acids and glucose taking priority over fatty acids (alcohol actually comes before all of these as there is zero storage capacity for alcohol!) - you can see that a surplus of both protein and carbs will limit the oxidation of fatty acids.

Because insulin is considered the major 'storage' hormone, this is often invoked as the major player in storing these substrates when present in the blood in excess quantities after a meal. However, there is research to show that insulin has a much more prominent role in preventing various metabolic actions than it does in permitting them. Most cells can and will take up glucose without much help from insulin, for example, and it seems more likely that insulin helps with blood sugar control by signalling the liver to shut down release/production of endogenous glucose - AND blunting the release of fatty acids from adipose tissue - while exogenous glucose is cleared.

The latter makes sense in that insulin is an ubiquitous hormone in most living things on earth and probably developed before there were many concentrated food sources of glucose and was more likely (IMO) useful in controlling endogenous production, along with glucagon and other related hormones, at much lower concentrations than is typically seen today in humans eating a typical industrialised diet.

I think the other mistake people make is in equating excess insulin with the immediate post-prandial release in response to a high carbohydrate load. What is much more pertinent is fasting insulin levels and there are plenty of studies that can show both associations and correlations between high fasting insulin levels and diseases like obesity, diabetes, etc. There are also intervention studies that demonstrate a high carbohydrate diet often leads to increased fasting insulin levels and a low carbohydrate diet will, in turn, reduce those fasting levels. It is the fasting insulin level that is most likely to impact on increased body fat accrual as it is the between-meal and fasting periods when the cells rely on the release of fatty acids from adipose tissue for their energy needs. Elevated fasting insulin levels are more likely to blunt lipolysis during these times. This is when cells begin to starve for energy and hunger can be increased, driving the individual to eat (especially carby snacks) in order to meet that energy demand. In this instance it is lack of cellular energy (due to adipose cells not releasing stored fatty acids) that drives hunger that drives increased food intake and not increased food intake, due to simple gluttony, that creates an excess of calories that get stored as fat.

That's not really answering your question directly (other than to say substrate storage levels in combination with various hormonal signals activated by dietary intake will have a bearing on partitioning) but suggesting nothing is as simple as the current scientific consensus would have you believe!

[hailtotheking]

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Interesting. You say you were a 'fat kid' - from what age did you become fat (I'm assuming you weren't born fat and remained that way through nursing and beyond weaning!)? Though there is some research to suggest that the diet of the mother can have effects on the way genes are expressed in her unborn baby leading to it being born a particular phenotype (possibly insulin resistant). Would you say your mother was on a typical high carb/low fat diet when she carried you? Also, if you think a particular diet led you to become fat as a kid, do you wonder whether your ability to eat that same diet now with apparent impunity will continue indefinitely or will it eventually drive you back to gaining fat?

Quite a few people who lose excess fat on a low carb/high fat diet seem to report a point where fat loss plateaus - My own experience would seem to confirm this - but I have no pressing desire to have single digit body fat levels and my current body fat percentage is well inside the ideal range for a man of my age anyway - however, I have noticed that I can eat at what would be considered a semi-starvation level in terms of calories and not lose the amount of weight such a deficit would predict.

Could it be that, once your metabolism has recovered to the point that any fat that is stored postprandially is also optimally released and oxidised during fasting periods (and you use predominantly fatty acids and ketones for energy production), you actually need fewer dietary calories to translate into cellular energy (ATP) because you get so much more ATP per molecule of fatty acid? This is just another reason why I find arbitrarily eating to a predetermined daily calorie allowance usually ends badly and would much prefer to eat to hunger/satiety!

Hey nu sorry it took me so long to reply to this. I have had food poisoning for a few days from eating some bad mussels

I think i started to get fat when i hit puberty. My mums cooking was generally pretty good (she used to make casseroles and good quality pies from fresh, and we always had veg), but she was always very 'generous' with portions. My dad used to be a fishmonger so, unlike alot of my friends, we ate oily fish quite frequently. We did get treated to Mc D's or fish and chips once a week. I was never really into sport or outdoor pursuits as a kid, and liked playing computer games and watching TV too much, so my hunch was it was as a result of too many calories and not enough activity.

I personally think the calorie requirement estimators you see around overestimate how many calories people need anyway, so i'm not surprised you can eat 'under maintenance' calories and not gain weight.

with regards to your theories on more efficient use of fats for energy, i honestly dont know. The effects of fasting specifically on how nutrients are metabolised doesnt appear to have been looked into that much so far

[NU_nutrition_TS]

Thanks for the response HTTK and sorry to hear about the food poisoning - I hope you have recovered now.

Again - interesting that this happened around puberty; when most kids have a growth spurt (usually upwards rather than outwards) and often have increased appetites because they have a hormonally driven increase in metabolism, due to the extra growth, that demands extra intake. This is what Gary Taubes cites as an example of where hormonally driven growth drives food intake rather than food intake drives growth - or, as he says, pubescent kids don't grow/develop into adults because they suddenly eat more food - they eat more food because the hormonally driven growth spurt (from child to adolescent - or adolescent to adult) drives up their hunger and, as a consequence of that, they eat more.