Study finds those eating LF diets with high insulin levels most prone to weight gain

[Demi]

A great post from Dr Briffa in his blog today:


Study finds those eating low-fat diets with high insulin levels are most prone to weight gain

Posted By Dr John Briffa On 20th February 2008

It’s difficult to avoid the doom-laden statistics concerning rates of overweight and obesity. And at the same time we’ll no doubt be aware of the standard advice for those wanting to lose weight: ‘eat less and exercise more.’ The problem is, the evidence suggests that neither of these approaches is particularly effective for the purposes of weight loss in the long term.

Some researchers and scientists are in the process of thinking a little more creatively about the ‘obesity epidemic’. What, some are asking, if weight is not determined simply by the relative amounts of calories taken in and those that are metabolised by the body?

One important factor here concerns appetite. It makes sense for individuals who want to curb any tendency to overeat to consume foods that tend to be appetite-sating relative to other foods. The usual advice is geared toward getting individuals to eat a fibre-rich diet because, supposedly, ‘fibre fills us up’ and helps us ‘feel full for longer’. Actually, there is good evidence that, overall, protein (http://www.drbriffa.com/blog/2008/01/23/research-shows-that-protein-rich-low-carb-diets-are-most-effective-for-sating-the-appetite/) is the part of the diet that packs really appetite-sating power.

Another factor well worth considering concerns the tendency for food to predispose to fatty accumulation in the body. While it seems obvious that the major dietary spectre in this respect is fat, the reality is that the prime fat-producing hormone in the body is insulin. And insulin, as we know, is secreted chiefly in response to intake or carbohydrate.

Some have theorised that weight gain can be driven by a glut of insulin. Perhaps the most famous/infamous person to put forward this theory was the late Dr Robert Atkins. Others have come in his wake. Recently, new life has been breathed into this concept by Gary Taubes, author of ‘Good Calories Bad Calories: Challenging the conventional wisdom on diet, weight control, and disease’. I’ve not read this book, but know enough about it and Taubes’ previous work to recommend it to anyone who takes a keen interest in their (or other people’s) health.

While weight gain is unlikely to be solely about insulin, my belief is that it is likely a major factor here. Some support for this has come from a study published this month in the American Journal of Clinical Nutrition [1]. The researchers in this study basically assessed insulin levels (actually insulin levels 30 minutes after giving individuals 75 g of glucose) in 276 people and then followed them for an average of 6 years each. This insulin measurement can be taken as a proxy measure of an individual’s ability to handle carbohydrate (sugar) in the system.

The authors looked at the relationship between insulin levels and certain measurements including weight gain and waist circumference. They also, analysed whether there was any difference in results in those eating a low-fat diet compared to those eating a higher fat diet.

Here, essentially, is what they found:

In individuals eating a lower fat diet, higher levels of insulin were associated with an increased risk of weight gain and increase in waist circumference.

This association was not evident in individuals eating a higher-fat diet.

Overall, in the low-fat eating group, individuals with the highest insulin levels gained 4.5 kg (9.9 pounds) more than those with low insulin levels.

So, what are we to make of all of this? The most obvious thing to come out of this study is that higher insulin levels are associated with increased tendency to gain weight. This finding clearly lends support to the idea that insulin may have a key role to play in weight gain.

But why would this association be only evident in those eating a lower-fat diet? I don’t know for sure, but it’s likely to do less with fat, and more to do with carbohydrate: Because high insulin levels are generally a sign that individuals are not coping well with carbohydrate in the body, one might imagine that eating a carb-rich diet is more likely to land these people in trouble than those eating a lower carb diet. Those eating a low-fat diet tend to eat a diet rich in carb, and this may explain why these individuals were the ones most prone to weight gain.

Of course the corollary here is that individuals eating a higher-fat, and therefore lower carb, diet are likely to be less prone to weight gain induced by insulin, right? This finding doesn’t prove anything. But it does seem lend support to the concept of carbohydrate-control for weight loss.

References:

1. Chaput JP, et al. A novel interaction between dietary composition and insulin secretion: effects on weight gain in the Quebec Family Study. Am J Clin Nutr 2008;87:303-309


http://www.drbriffa.com/blog/2008/02/20/study-finds-those-eating-low-fat-diets-with-high-insulin-levels-most-prone-to-weight-gain/

[kneebrace]

Great find Demi. More evidence that insulin resistance is the real 'disease' of fat accumulation. People with no insulin resistance whatsoever can get fat by eating a lot of fatty/carby food. Eventually a lot of them will develop insulin resistance anyway and then losing the accumulated bodyfat will be even more difficult.

Low carb clinicians have been demonstrating for decades that restricting carbohydrate tends to restore insulin sensitivity.

Stuart

[mike_d]

... higher insulin levels are associated with increased tendency to gain weight. This finding clearly lends support to the idea that insulin may have a key role to play in weight gain.Unfortunately excess insulin can cause more serious problems than a secondary weight increase.

[ttlaitin]

the same study was discussed also in the thread:

Differences in Insulin Secretion Explain Differences in Weight Gain (http://forum.lowcarber.org/showthread.php?p=7270667)

[M Levac]

People with no insulin resistance whatsoever can get fat by eating a lot of fatty/carby food.


That is incorrect.

[LessLiz]

How is that incorrect? Or do you believe that being overweight in and of itself is proof of insulin resistance?

I'd argue that most overweight people in the US who are not insulin resistant put on the weight eating a high carb/high fat diet. That is the American diet.

[rightnow]

Actually, in the overfeeding studies, it was pretty much not workable to make anybody fat by eating too much--they promptly lost weight to 'norm' state the moment the forced-study was over. It does seem to appear that the overweight condition may be a reflection of the existence of some degree of insulin resistance. If that were the case, then a "complete lack of IR" would make it unlikely that anybody in that state would be overweight.

Or I guess another way of thinking about it is that one wouldn't look at an overweight person and say, "Are they insulin-resistant, to some degree?" since if they weren't, they wouldn't be overweight in the first place.

PJ

[M Levac]

How is that incorrect? Or do you believe that being overweight in and of itself is proof of insulin resistance?

I'd argue that most overweight people in the US who are not insulin resistant put on the weight eating a high carb/high fat diet. That is the American diet.

It is incorrect in two respects. Low insulin resistance is not the cause of obesity. And, fatty food is not the cause of obesity either. Instead, fatty food makes us lean. The combination of carbs and fat is actually a mitigating factor because of the fat. It's entirely the carbs that make us fat. Without fat, carbs will still make us fat, only faster than if we ate fat as well.

Being overweight leads to insulin resistance. It's not proof of it. Still what leads to being overweight is too much insulin in the first place so I guess it is a sort of proof in that fashion. But I wouldn't argue it that way anyway.

High insulin resistance means glucose is not readily used but still readily stored as fat. Thus, we grow fatter while remaining hungry so we eat more, grow fatter still until we just can't deal with all the glucose and become diabetic. I don't explain it so well but that's basically the Syndrome X or Metabolic Syndrome that we've read about.


Actually, the American diet is high carb low fat just as recommended by the food pyramid. At least in comparison to the diet prior to the late '70s. Which was lower carb and higher fat than it is now.

[M Levac]

Just synthesized more info on the subject. I felt it more appropriate to make a new post rather than to add to the previous one.


The combination of carbs and fat we eat has no bearing on how much fat we store.

It has to do with the alpha glycerol phosphate molecule. This molecule is the bond that binds three fatty acids to form triglycerides. Glycerol is obtained either from dietary fats or from glucose oxidation (when glucose is used as fuel).

Adipose tissue is where fat is stored. Fat is stored in fat cells as triglycerides. Fat enters adipose tissue, fat cells, as fatty acids and exits fat cells as fatty acids. It cannot enter fat cells as triglycerides because trigs are too big. So, when trigs are brought to fat cells for storage, it must be disassembled into fatty acids and a glycerol molecule. Only the fatty acids enter the fat cells. The glycerol molecule stays out. This leaves us one glycerol molecule short to recombine the fatty acids into triglycerides. The glycerol molecule that is needed can only be obtained by burning glucose inside the fat cell.

At least, that's how I understand it. I haven't read anything to the effect that glycerol outside fat cells can get inside fat cells. All I've read is that glycerol is obtained through glucose oxidation inside fat cells. It is this one that is used to recombine fatty acids into trigs for storage. Glycerol, if I remember correctly, is also a form of fuel. If that's how it works, then it can be used by fat cells eventually. I don't know what happens after that, I'm not there yet in my comprehension of the subject.

Insulin is what controls adipose tissue. It's also what brings glucose to fat tissue. If I understand it properly, glycerol will not be used as long as glucose is present. Thus, even if it was possible for glycerol to enter fat cells, there is strictly no need for it to enter when there's glucose being brought by insulin. I think that's why the glycerol from dietary fats can't be used for fat storage.

Actually, I think that's why fat cells get bigger and bigger. Glucose is constantly being brought to them so they never use the glycerol by-product of glucose oxidation so it can always be used to recombine fatty acids into trigs for storage.

Summary:

Carbs are the sole food responsible for fat accumulation.

So, this is another reason why Kneebrace's statement is incorrect.

[Beth1708]

Carbs are the sole food responsible for fat accumulation.

So, this is another reason why Kneebrace's statement is incorrect.

Hi Marc,

The research that Taubes reported suggests that there may be some truth to what you have said. However, if I'm understanding all that has been said, by Taubes and on this forum, I don't think that we actually know enough to be certain that carbs are the sole culprit.

The smoking gun may be lying near the demon wheat, but we haven't seen the fingerprints on the handle. :)

Beth

[LessLiz]

The issue is the extrapolation from the impact of fat in the absence of carbs to the impact of fat in the presence of carbs. The American diet -- not the diet espoused by the FDA and its food pyramid but what American's truly eat -- is high in carbs and relatively high in fat as well as definitely high in total calories. With high levels of carbs creating high levels of insulin it isn't reasonable, in my opinion, to assume that consumed fats have no impact on fat storage.

The reason fat is a net neutral is the lack of insulin response. I can't think of any reason to assume that fat remains a net neutral in the presence of high concentrations of insulin.

[kneebrace]

It is incorrect in two respects. Low insulin resistance is not the cause of obesity. And, fatty food is not the cause of obesity either. Instead, fatty food makes us lean. The combination of carbs and fat is actually a mitigating factor because of the fat. It's entirely the carbs that make us fat. Without fat, carbs will still make us fat, only faster than if we ate fat as well.

Being overweight leads to insulin resistance. It's not proof of it. Still what leads to being overweight is too much insulin in the first place so I guess it is a sort of proof in that fashion. But I wouldn't argue it that way anyway.

High insulin resistance means glucose is not readily used but still readily stored as fat. Thus, we grow fatter while remaining hungry so we eat more, grow fatter still until we just can't deal with all the glucose and become diabetic. I don't explain it so well but that's basically the Syndrome X or Metabolic Syndrome that we've read about.


Actually, the American diet is high carb low fat just as recommended by the food pyramid. At least in comparison to the diet prior to the late '70s. Which was lower carb and higher fat than it is now.

Martin, aren't you forgetting that dietary fat is happily stored (and far more efficiently than carbs are converted to fat too) in the presence of insulin. You don't have to be insulin resistant to have insulin in your bloodstream. Even someone who has never eaten carby food in their lives will have baseline levels of insulin. It is a very important hormone.

Insulin resistance just means a lot more insulin and much faster weight gain if excess calories are consumed, either fat protein or carbs, but particularly fat.

Restricting carbohydrate will tend to restore insulin sensitivity in time. Some people who have done a lot of damage with a lifetime of excess carbs will probably never recover full insulin sensitivity, and will tend to store any excess calories. Restricting carb will help with this because it is much more difficult to consume excess calories. So cutting carbs is a triple whammy: more insulin sensitivity ; less insulin for a given level of insulin resistance; and less appetite.

Restricting carbs is a very good idea. But low carbers do indulge in a lot of wishful thinking IMHO, when trying to understand the metabolic pathways involved.

Whether you overeat low carb food is usually a matter of how delicious it is. Plainer 'more boring' low carb food is much less likely to lead to overeating. But low carb can be pretty damn yummy, and if it is some degree of self discipline is usually needed as well. Which makes overeating in paleolithic times a lot less likely I suppose. Raw meat without condiments, sauces etc. or the fairly bland pre - fructose selectively bred fruits, was the only thing on the menu, and it was probably hard to eat too much of it.

Stuart

[M Levac]

Martin, aren't you forgetting that dietary fat is happily stored (and far more efficiently than carbs are converted to fat too) in the presence of insulin. You don't have to be insulin resistant to have insulin in your bloodstream. Even someone who has never eaten carby food in their lives will have baseline levels of insulin. It is a very important hormone.

Insulin resistance just means a lot more insulin and much faster weight gain if excess calories are consumed, either fat protein or carbs, but particularly fat.

Restricting carbohydrate will tend to restore insulin sensitivity in time. Some people who have done a lot of damage with a lifetime of excess carbs will probably never recover full insulin sensitivity, and will tend to store any excess calories. Restricting carb will help with this because it is much more difficult to consume excess calories. So cutting carbs is a triple whammy: more insulin sensitivity ; less insulin for a given level of insulin resistance; and less appetite.

Restricting carbs is a very good idea. But low carbers do indulge in a lot of wishful thinking IMHO, when trying to understand the metabolic pathways involved.

Whether you overeat low carb food is usually a matter of how delicious it is. Plainer 'more boring' low carb food is much less likely to lead to overeating. But low carb can be pretty damn yummy, and if it is some degree of self discipline is usually needed as well. Which makes overeating in paleolithic times a lot less likely I suppose. Raw meat without condiments, sauces etc. or the fairly bland pre - fructose selectively bred fruits, was the only thing on the menu, and it was probably hard to eat too much of it.

Stuart

Forgive me, Kneebrace, but if there's somebody forgetting something, it must surely be you.

In the post immediately following the one you quoted from me, I explain further why your statement is incorrect. You will see that indeed you forget the detail I speak of in that post. The detail is the alpha glycerol molecule. Without it, there can be no fat accumulation. Then there's this little blurb of yours right here:

You wrote and I quote:

"But low carbers do indulge in a lot of wishful thinking IMHO, when trying to understand the metabolic pathways involved."

Who do you think you are, telling us what to think? We should suddenly forget we have a brain and take your word for it? We should stop thinking for ourselves? With this little blurb, you've lost your entire credibility that wasn't so hot to begin with. We think for ourselves even if you want us to stop. Because that's what that bit tells us: Don't use your brains, don't think, let me do the thinking for you, I'm better than you are, all of you.

"Wishful thinking"?!?

If there's anybody wishing for something, it's surely you, Kneebrace. But what you wish for is yet a mystery. At least, you haven't fully disclosed your intentions. Oh you've run around the subject a few times with arguments for positive caloric balance but this is the first time you say we are wishing for things we can't have and imply we should not. Do you insinuate that we will never learn anything by using our brains? How preposterous. At this time, I must say that your words tell me more than you intend. Your words appear to confuse the subject rather than to simplify it. Perhaps it's due to a misunderstanding on your part but I don't think so in view of the eloquence you've demonstrated all throughout your frequent posts in this forum. You do appear to fully grasp the subject yet persist with the positive caloric balance hypothesis. You persist with this theorem because of your argument that to lose fat, we must eat fewer calories. To eat fewer calories as a requirement of losing fat is precisely the application of the positive caloric balance hypothesis.

I have serious doubts as to your honesty. Especially because you persist and perpetuate a hypothesis that has clearly been demonstrated as flawed and without value. Still, you may be completely honest here and just don't get it. Either way, make up your mind on which basis you wish to continue to argue the subject but bear in mind that we now know how to discuss it with you, Kneebrace. If I were you, I'd go with the "I don't get it" reason. The alternative is rather sad.

Am I attacking the person instead of addressing the subject? You bet I am. Bear in mind, that is precisely what you did too so it's all good to me:

You wrote and I quote:

"Martin, aren't you forgetting..."

That is so presumptuous on your part, isn't it?


Your statement is incorrect and will remain so from now to the end of time. But you can make a different statement. It's not all lost.

[M Levac]

The issue is the extrapolation from the impact of fat in the absence of carbs to the impact of fat in the presence of carbs. The American diet -- not the diet espoused by the FDA and its food pyramid but what American's truly eat -- is high in carbs and relatively high in fat as well as definitely high in total calories. With high levels of carbs creating high levels of insulin it isn't reasonable, in my opinion, to assume that consumed fats have no impact on fat storage.

The reason fat is a net neutral is the lack of insulin response. I can't think of any reason to assume that fat remains a net neutral in the presence of high concentrations of insulin.

There are three possible combinations with appropriate results:

Fat + carbs = half good, half bad
Fat - carbs = all good
Carbs - fat = all bad

The presence of fat in any diet is a mitigating factor, not an exacerbating factor. This means, it makes it better, not worse. Take out the fat and the situation grows worse by the minute. Put fat back in and the situation goes back to normal. Take out the carbs and the situation quickly gets better in all regards. Put carbs back in and the situation goes to hell in a minute.

[M Levac]

Hi Marc,

The research that Taubes reported suggests that there may be some truth to what you have said. However, if I'm understanding all that has been said, by Taubes and on this forum, I don't think that we actually know enough to be certain that carbs are the sole culprit.

The smoking gun may be lying near the demon wheat, but we haven't seen the fingerprints on the handle. :)

Beth

We know enough, but not all the information is contained in the same place. We must hunt down the elements before we can put them together for a complete understanding. Wheat as the sole culprit? No, it doesn't fit the facts. Wheat is not the only food that stimulates an insulin response and insulin is what controls fat accumulation.

In order to understand nutrition, we must understand endocrinology. The two are directly related yet are distinctly separated in their respective professions. This is in part why we can't get all the information from the same place. The other reason is because we learn in blips one bit at a time.

[M Levac]

Glycerol, as I've said, is a product of burning glucose. But, contrary to what I've said, it is released in the bloodstream with the free fatty acids by adipose tissue in lipolysis. It is not kept inside the fat cells as I thought.

Glycerol can be used to recombine into glucose by the liver. But it can't be used to create new glucose. This means that no matter how much fat we eat, we can't create glucose out of that fat. For glucose to exist, it must be eaten or produced through gluconeogenesis. And the only time gluconeogenesis produces glucose is when there is not enough in our blood. Our body will never produce too much glucose when all is well.

In conclusion, it's impossible to get fat by eating fat. It's the carbs that make us fat and only the carbs.

[kneebrace]

There are three possible combinations with appropriate results:

Fat + carbs = half good, half bad
Fat - carbs = all good
Carbs - fat = all bad

The presence of fat in any diet is a mitigating factor, not an exacerbating factor. This means, it makes it better, not worse. Take out the fat and the situation grows worse by the minute. Put fat back in and the situation goes back to normal. Take out the carbs and the situation quickly gets better in all regards. Put carbs back in and the situation goes to hell in a minute.

Martin, IMHO this is simplistic nonsense. If you eat fatty carby food, you burn the carbohydrate and store the fat. It doesn't matter how indignant you get, you can't change human metabolism. I'm sorry you are getting so offended. Some biochemistry reading will surely help?

If there is carbohydrate to burn, the human body would much rather burn that than fat, and the baseline insulin and whatever insulin is released to deal with the carbohydrate will happily usher the fat into adipocytes. Any insulin resistance will just make this process even more rapid because there is so much more insulin floating around.

Also, you said:

Glycerol, as I've said, is a product of burning glucose. But, contrary to what I've said, it is released in the bloodstream with the free fatty acids by adipose tissue in lipolysis. It is not kept inside the fat cells as I thought.

Glycerol can be used to recombine into glucose by the liver. But it can't be used to create new glucose. This means that no matter how much fat we eat, we can't create glucose out of that fat. For glucose to exist, it must be eaten or produced through gluconeogenesis. And the only time gluconeogenesis produces glucose is when there is not enough in our blood. Our body will never produce too much glucose when all is well.

In conclusion, it's impossible to get fat by eating fat. It's the carbs that make us fat and only the carbs.


Well, for a start, glycerol isn't 'a product of burning glucose' at all. And the glycerol backbone of triacyl glycerols (the form fat is stored in adipocytes) can be stripped away from the fatty acids (about 10% of the energy in triglycerides) and indeed is used to create new glucose, but like glluconeogenesis from dietary protein or muscle will only occur on an 'as needed' basis. So eating an excess of protein or fat won't produce new glucose unless glucose dependent tissues actually need it.

But you still seem to be forgetting that fat can easily be stored in adipocytes with the help of insulin, and everyone except insulin dependent diabetics produces a constant supply of insulin.

I'm really not trying to distress you Martin. If this stuff offends you, don't blame me, blame evolution. I'm afraid you can't change human metabolism to suit your low carb sacred cows, much as you seem to want to.

Stuart

[M Levac]

Martin, IMHO this is simplistic nonsense. If you eat fatty carby food, you burn the carbohydrate and store the fat. It doesn't matter how indignant you get, you can't change human metabolism. I'm sorry you are getting so offended. Some biochemistry reading will surely help?

If there is carbohydrate to burn, the human body would much rather burn that than fat, and the baseline insulin and whatever insulin is released to deal with the carbohydrate will happily usher the fat into adipocytes. Any insulin resistance will just make this process even more rapid because there is so much more insulin floating around.


Stuart


Don't be so arrogant. With a statement like this "..., you burn the carbohydrate and store the fat." It's clear you're the one who needs to read about the subject. But since you're so arrogant, you wouldn't even consider it for a second.


If there is carbohydrates to burn, it's because it was eaten. It's not because the body would rather burn it. It will burn it before any fat because insulin is present. When insulin is present, lipolysis stops and ketosis stops as well and glycolysis starts. If carbohydrates was indeed the preferred fuel, the body would store energy as such. Instead, the body stores energy as triglycerides, saturated fat. If no carbohydrates are eaten, there is no surplus glucose, there is no surplus insulin, there is no fat accumulation. This, regardless of the amount of fat eaten. Also regardless of the amount of fat eaten, the amount of energy stored is solely determined by the amount of carbohydrates eaten.


If there is a preference to use glucose as fuel when it is present in overabundance, it's because it is toxic in greater quantity than what the body needs. Burning it for fuel is one way to get rid of it. The other way is to store it. But once we reach a point where we can't burn it and can't store it, we excrete it through our urine as is. But for us to reach that point, we first have to go through a whole lot of sickness and pain.

When in lipolysis and when carbohydrates are eaten, lipolysis stops immediately and glycolysis starts just as fast. This is not because our body prefers to use glucose but because it must deal with it immediately to prevent it from poisoning us.

Don't you want to write about glycerol? Try it and see if you can make this molecule go away.

[kneebrace]

When in lipolysis and when carbohydrates are eaten, lipolysis stops immediately and glycolysis starts just as fast. This is not because our body prefers to use glucose but because it must deal with it immediately to prevent it from poisoning us.



OK, I'm done, anybody else want to have a crack at this? :).
Oh shucks, I just couldn't resist it. Martin, aren't you forgetting about the other energy storage medium, glycogen? Too 'toxic' to even think about perhaps?

Stuart.

[Wifezilla]

zzzzzzzzzzzzzzzz

[M Levac]

OK, I'm done, anybody else want to have a crack at this? :).
Oh shucks, I just couldn't resist it. Martin, aren't you forgetting about the other energy storage medium, glycogen? Too 'toxic' to even think about perhaps?

Stuart.

Hit the wall of truth, did we? Can't cope with it, can we?

Glycogen is inconsequential in terms of quantity. We can only store so much and when that's full, it's back to adipose stuffing.

I didn't even start on lipogenesis and you're copping out. But I will allow you to retire without further damage to your ego as it were.

[DrH]

I wish this were the case for me ... I was diagnosed as IR this past January - a year and a half after starting a strict LC plan (started Atkins 6/06). I can only imagine how bad my numbers would have been had I not eaten a LC diet! Jill



Great find Demi. More evidence that insulin resistance is the real 'disease' of fat accumulation. People with no insulin resistance whatsoever can get fat by eating a lot of fatty/carby food. Eventually a lot of them will develop insulin resistance anyway and then losing the accumulated bodyfat will be even more difficult.

Low carb clinicians have been demonstrating for decades that restricting carbohydrate tends to restore insulin sensitivity.

Stuart

[LC FP]

Originally Posted by M Levac
If there is carbohydrates to burn, it's because it was eaten. It's not because the body would rather burn it. It will burn it before any fat because insulin is present. When insulin is present, lipolysis stops and ketosis stops as well and glycolysis starts.
Nicely put.

But I have a question. Does this mechanism only hold in someone with a normal metabolism? Insulin resistant states really confuse me when it comes to this stuff. And unfortunately most adult humans are now at least somewhat insulin resistant.

In an inulin resistant person with visceral fat, which I've read is naturally insulin resistant, does your statement about lipolysis, ketosis and glycolysis still hold? Thanks--

[M Levac]

Nicely put.

But I have a question. Does this mechanism only hold in someone with a normal metabolism? Insulin resistant states really confuse me when it comes to this stuff. And unfortunately most adult humans are now at least somewhat insulin resistant.

In an inulin resistant person with visceral fat, which I've read is naturally insulin resistant, does your statement about lipolysis, ketosis and glycolysis still hold? Thanks--

The correct answer, I think, is that the normal metabolism leads to insulin resistance because of too high carbs intake. After a while, metabolism becomes abnormal because of insulin resistance. Normal functions are disrupted and all kinds of bad things start to happen. If I understand it correctly, when the cell shuts down its insulin receptors, other hormones that need insulin to work are also shut out this way so they can't do their job.

I think it holds true even with high insulin resistance. Cutting out all carbs will allow glucose and insulin level to drop, cells will slowly adapt to that "new" state and open up their receptors once insulin is at a safer level. As that happens, lipolysis, ketosis and gluconeogenesis somewhat resume normally. At least as normally as possible.

A person who is less resistant will use glucose more readily than one who is highly resistant. Resistance doesn't happen everywhere at the same time. The liver is the first, then the muscles, then the fat cells. So when the liver and the muscles are resistant, the fat cells can still accept insulin and glucose so the person gets fatter but remains hungry because he can't use glucose anywhere else. So he eats more and more until fat cells become resistant, he can't deal with the glucose anymore and becomes diabetic. This is the normal metabolic progress of somebody who continues to eat carbs.

If we didn't become resistant to insulin, we'd probably get poisoned by glucose and go into a coma. I don't know what would happen really. Insulin does many things, one of which is to stimulate cellular division. Maybe we'd age so fast that it wouldn't make much difference in the end. Maybe we'd grow cancerous all over.

In the end, what is not normal is to eat carbs.

[Beth1708]

Resistance doesn't happen everywhere at the same time. The liver is the first, then the muscles, then the fat cells. So when the liver and the muscles are resistant, the fat cells can still accept insulin and glucose so the person gets fatter but remains hungry because he can't use glucose anywhere else. So he eats more and more until fat cells become resistant, he can't deal with the glucose anymore and becomes diabetic.

Where did you get this?

Beth

[M Levac]

Where did you get this?

Beth

First in the link below, then elsewhere as I kept on reading about the subject:

http://www.lowcarb.ca/articles/article149.html

Quote from the article:

" How else does insulin affect cardiovascular disease? We've only just touched upon it. Insulin is a so-called mytogenic hormone. It stimulates cell proliferation. It stimulates cells to divide. If all of the cells were to become resistant to insulin we wouldn't have that much of a problem. The problem is that all of the cells don't become resistant. Some cells are incapable of becoming very resistant. The liver becomes resistant first, then the muscle tissue, then the fat. When the liver becomes resistant, what is the effect of insulin on the liver, it is to suppress the production of sugar. The sugar floating around in your body at any one time is the result of two things, the sugar that you have eaten and how much sugar your liver has made. When you wake up in the morning it is more of a reflection of how much sugar your liver has made. If your liver is listening to insulin properly it won't make much sugar in the middle of the night. If your liver is resistant, those brakes are lifted and your liver starts making a bunch of sugar so you wake up with a bunch of sugar."

[JL53563]

Where did you get this?

Beth
Taubes also talks about this in GCBC.