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Thread: Is Stephan Guyenet suggesting Gary Taubes is wrong re insulin resistance? page 2

  1. #11
    sting's Avatar
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    Quote Originally Posted by loafingcactus View Post
    Sigh, people think I'm trying to pick a fight when I'm not even trying.

    I'm not trying to pick a fight- I was addressing the topic. Someone = this Guyenet dude.
    OK oops sorry as i said my English is not my first language, sry my bad

  2. #12
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    Quote Originally Posted by Neckhammer View Post
    Yup he should move on....Its an old pissing contest between those two.
    Sting, Neckhammer is right on this. Those two "experts" have been so busy running each other down that it is getting a little silly (on both sides).

    Stephan has this theory about what he calls "food reward" that he thinks is The Answer To Everything. Taubes may be a bit too narrowly focused on insulin while not giving enough time to the effects of leptin, ghrelin, etc.

    But all the two can do is run each other down. Personally, I think there is room for them both to be right.

  3. #13
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    This is a shorter version

    Stephan Guyenet replies to a comment...
    Hi Todd,

    Let me try to explain it a different way. The idea, as stated by Taubes, is that 1) insulin goes up, 2) lean tissues become insulin resistant, 3) fat tissue remains insulin sensitive, therefore 4) insulin action on fat cells is increased, and this leads to 5) fat accumulation.

    The scientific literature shows that fat tissue progressively becomes insulin resistant as it expands. In fact, the insulin resistance of fat cells if anything outpaces the increase in fasting and post-meal insulin. Therefore, insulin action on fat cells if anything is gradually reduced as fat accumulates. This is the opposite of what the hypothesis would predict.

    Couple this with the fact that insulin is not rate-limiting for fat oxidation, and I don't see the theoretical basis for this hypothesis.

  4. #14
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    Quote Originally Posted by sting View Post
    This is a shorter version

    Stephan Guyenet replies to a comment...
    Hi Todd,

    Let me try to explain it a different way. The idea, as stated by Taubes, is that 1) insulin goes up, 2) lean tissues become insulin resistant, 3) fat tissue remains insulin sensitive, therefore 4) insulin action on fat cells is increased, and this leads to 5) fat accumulation.

    The scientific literature shows that fat tissue progressively becomes insulin resistant as it expands. In fact, the insulin resistance of fat cells if anything outpaces the increase in fasting and post-meal insulin. Therefore, insulin action on fat cells if anything is gradually reduced as fat accumulates. This is the opposite of what the hypothesis would predict.

    Couple this with the fact that insulin is not rate-limiting for fat oxidation, and I don't see the theoretical basis for this hypothesis.

    ^ Call me when you've caught up with 2013. You've still got lots of comments to run through.

  5. #15
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    Quote Originally Posted by sting View Post
    This is a shorter version

    Stephan Guyenet replies to a comment...
    Hi Todd,

    Let me try to explain it a different way. The idea, as stated by Taubes, is that 1) insulin goes up, 2) lean tissues become insulin resistant, 3) fat tissue remains insulin sensitive, therefore 4) insulin action on fat cells is increased, and this leads to 5) fat accumulation.

    The scientific literature shows that fat tissue progressively becomes insulin resistant as it expands. In fact, the insulin resistance of fat cells if anything outpaces the increase in fasting and post-meal insulin. Therefore, insulin action on fat cells if anything is gradually reduced as fat accumulates. This is the opposite of what the hypothesis would predict.

    Couple this with the fact that insulin is not rate-limiting for fat oxidation, and I don't see the theoretical basis for this hypothesis.
    As the action of insulin is reduced, the pancreas may respond by producing more insulin. Having more and more insulin with less and less response is what insulin resistance is.

    When a person gets to this state they have so much insulin in their systems that it never comes down enough. This makes their bodies less able to use their own fat reserves for fuel. They become hungry even with abundant fat stores, so they eat. It becomes a vicious circle. I have been there. It is not fun.

    The question is, what causes this and what is the proper solution. And I think what causes the most arguing is that too many people think that just because you gained some fat it means the same action is happening in your body that happens in someone with insulin resistance, and also that if cutting carbs helps people with insulin resistance recover their ability to lose weight it ought to help every person who wants to drop a few pounds.
    Female, 5'3", 49, Starting weight: 163lbs. Current weight: 135 (more or less).
    Starting squat: 45lbs. Current squat: 180 x 2. Current Deadlift: 230 x 2

  6. #16
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    Reading more of Stephan work and I'm not sure i agree with what he says here..

    Stephan Guyenet said: So basically, there are these interconnections between the circuits that regulate body fat levels and regulate the response to rewarding food. That is, food that you find tasty, palatable―in certain ways. Those systems are interconnected and they actually influence one another. So for example, if you’re really, really full and you just had really big meals over the last three days, you’re not going to be very interested in eating more food. Whereas if you hadn’t done that―or let’s say, you didn’t eat anything for three days, you’re going to be very, very interested in eating more food.
    IMO this is not quite right, as obese people can pretty much eat again even after having a really big meal. So even though they are full, they are still wanting to snack/graze more foods soon after.

    Dr.Eades explains why:

    Let’s look back at the non-obese person to explain. A non-obese person eats, uses the energy from the food and stores the rest. During the time between meals and during sleep, the non-obese person draws on the stored fat to provide energy. When the fat cell mass decreases to a certain critical point, the body signals the brain that the fat cells need a refill, so the brain initiates the hunger response. The non-obese person eats, uses some energy for immediate needs, fills the fat cells with the rest, uses the stored energy as needed, and then the cycle repeats.

    It doesn’t work that way in the obese. Obese people eat, use the energy required for immediate needs and store the rest. But–and this is the extremely important ‘but’– during the time between meals and during sleep, obese people can’t access their fat stores because their baseline insulin is too high. When they can’t get to their stored fat, the lack of access to energy sets in motion all the same biochemical signals in the obese person that get sent in the non-obese, who have depleted the energy storage in their fat cells. And these signals are converted by their brains into the drive to feed, i.e., intense hunger. They have to eat to provide for their immediate energy needs because, thanks to chronically elevated insulin levels, they can’t get into to their own stored fat, even though it’s there waiting in massive quantities.

    To use an analogy, it would be like being out of cash when you desperately needed it yet having a huge amount of money in the bank. You hustle to an ATM machine and find your card won’t work. It’s the same with the obese – they have plenty of energy to go without eating for months, but their fat ATM cards don’t work. And since their fat ATM cards don’t work, the only option they have for immediate energy is to eat.

    So fat people are fat not because they overeat – they overeat because they’re fat.

  7. #17
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    Ignore them both.

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