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  1. #31
    Registered User FemmeFatale's Avatar
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    Originally Posted by DannySampsonite View Post
    If metformin is helping you, then you may not have insulin resistance: you may have type II diabetes. If a ketogenic diet is helping you lose weight so easily, then it is even more likely that you are diabetic or pre-diabetic. You should probably get a glucose tolerance test done. Type II diabetes at age 24 isn't unheard of, but it's incredibly rare.
    From what I remember from my "biology of eating disorders and obesity" neuroscience class, insulin (and even the other neuropeptide you mentioned) is NOT the only hormone at work when it comes to fat storage and satiety. If it was, nobody would be able to get fat beyond a certain point. There are at least 40 neurotransmitters/neuropeptides at work, if I remember, though we only talked in depth about insulin, leptin, serotonin, NPY, PPY, and CCK in that class. So elevated insulin levels do not *always* and *exclusively* lead to more satiety/less fat storage. It's a lot more complicated than that. Additionally, it was explained to me by both my general doctor and my endocrinologist that elevated insulin levels can stimulate hunger for a number of reasons, including (but not limited to) because they can cause your blood sugar to drop a LOT and can make you lethargic (less activity).

    As for diabetes/pre-diabetes: I am NOT diabetic; I have been tested. And massive insulin-resistance _is_ 'pre-diabetic' (see also PCOS, metabolic syndrome, syndrome-x) as this is what happens on the way to type-II diabetes.

    The metformin is both a quality of life enhancer (I can eat about twice as many carbs as before without adverse effect - though that's still ridiculously low), and a preventative measure to keep me from crossing the line into diabetes.

    Oh, and I never meant to imply that insulin resistance is the ONLY thing that causes or facilitates obesity, I just mean I think it is a LOT more prevalent than society at large may realize. And for sure, once I was fat and couldn't lose any weight following conventional nutritional wisdom, there were some seriously bad decisions made that didn't help. ("I'm a fatass anyway, and nothing I do works...So if I'm gonna be fat forever, sure I'll have another slice.")
    Last edited by FemmeFatale; 02-09-2013 at 11:09 PM. Reason: edited to add details and correct a typo.
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  2. #32
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    I'd love to know how people know exactly what they are,insulin resistant, insulin sensitive etc.
    I wouldn't be able to hang me hat on any statement like that.
    Obviously they're more knowledgable than me on this subject.
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  3. #33
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    Originally Posted by DannySampsonite View Post
    Well, in the case of ketosis, it actually has nothing to do with the glycerol either, which is gluconeogenic at the level of triose phosphates.

    Ketosis is an overflow pathway whereby so much lipolysis and b-oxidation has occurred that acetyl-CoA levels are too high in the liver. The liver does not use the acetyl-CoA for energy because it doesn't need it, and the presence of acetyl-CoA blunts other pathways (e.g. pyruvate decarboxylase). So, in an effort to get rid of the excess acetyl-CoA, the liver converts them to ketone bodies and exports them to tissues with high metabolic demand.
    Yes, you're right. That dawned on me about ten minutes after I made that post, and had gone out the door to go out of town. Glycerol is one of the substrates used for hepatic gluconeogenesis, which is one of the four major energy pathways present during lipolysis...
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  4. #34
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    Originally Posted by DannySampsonite View Post
    God shut up retard. The number one cause of insulin resistance is obesity. Who here is obese?

    The number one booster of insulin sensitivity is exercise. Who here exercises?

    Yeah, you do the math you parroting ketard
    Oversimplification. Obesity correlates with insulin resistance, it doesn't cause it. That's WHY type II diabetes also occurs in the non-obese/overweight. Obesity is caused by a rise in leptin resistance, which, like insulin, is an anorexigenic hormone. So, it becomes a matter of understanding the nutritional patterns that cause the rises in anorexigenic hormonal resistance. Not understanding this makes people thermo-tards, (oversimplified thermodynamics) if you simply believe its an issue of thermodynamics. This is not meant to be an insult, merely using the same subjective standard you've used as a sociopathic opportunity to insult people.
    Last edited by KLMARB; 02-11-2013 at 05:02 AM.
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  5. #35
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    Originally Posted by Mickqc1 View Post
    I'd love to know how people know exactly what they are,insulin resistant, insulin sensitive etc.
    I wouldn't be able to hang me hat on any statement like that.
    Obviously they're more knowledgable than me on this subject.
    It's called a "Glucose Tolerance Test" if your doctor performs it. There's a method you can use youself, in order to get a general idea if you have anorexigenic hormonal resistance, including insulin. You simply restrict/eliminate carbs (calories replaced with fat) and see what happens when you become hypoglycemic.

    When you deplete dietary glucose and become hypoglycemic, you switch over to glucagon secretion. This enables glycogenolysis, which is glycogen depletion. When that is finished, you become lipolytic, and start burning fat (either dietary or stored, NOW thermodynamics comes into play) and consequentially begin the process of reduction of anorexigenic hormonal resistance, (which was due to chronic, insulin-based lipogenesis) which caused the overweight, diabetic states in the first place.

    It's the degree of reaction you experience upon becoming hypoglycemic that is the indicator. Since the body, in a balanced state, should be able to be lipogenic and lipolytic (either burning carbs or fat) with equal efficiency, it's the degree of the withdrawal reaction that is the guide. The more energy issues/the worse you feel, the higher degrees of anorexigenic hormonal resistance issues..If you've got it, then the answer is a sustained lipolytic nutritional pattern, in order to get to the point that there is little difference to your body, as to burning either fats or carbs.
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  6. #36
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    Originally Posted by KLMARB View Post
    It's called a "Glucose Tolerance Test" if your doctor performs it. There's a method you can use youself, in order to get a general idea if you have anorexigenic hormonal resistance, including insulin. You simply restrict/eliminate carbs (calories replaced with fat) and see what happens when you become hypoglycemic.

    When you deplete dietary glucose and become hypoglycemic, you switch over to glucagon secretion. This enables glycogenolysis, which is glycogen depletion. When that is finished, you become lipolytic, and start burning fat (either dietary or stored, NOW thermodynamics comes into play) and consequentially begin the process of reduction of anorexigenic hormonal resistance, (which was due to chronic, insulin-based lipogenesis) which caused the overweight, diabetic states in the first place.

    It's the degree of reaction you experience upon becoming hypoglycemic that is the indicator. Since the body, in a balanced state, should be able to be lipogenic and lipolytic (either burning carbs or fat) with equal efficiency, it's the degree of the withdrawal reaction that is the guide. The more energy issues/the worse you feel, the higher degrees of anorexigenic hormonal resistance issues..If you've got it, then the answer is a sustained lipolytic nutritional pattern, in order to get to the point that there is little difference to your body, as to burning either fats or carbs.


    Thanks for the response.
    I don't seem to have any issues when reducing my carbs to sub 20g and going hypoglycemic.
    I feel a bit foggy in the head for a few hours and headaches.
    I will know better again when i do a carb up on wed after 3 weeks of keto.
    I have read that if you have no issues moving in and out of keto then a standard low carb (100g carbs) would work equally as good as keto.
    I understand that keto is meant to be more muscle sparring and fat burning than low carb diets or any other below maintenance diet.
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  7. #37
    Registered User FemmeFatale's Avatar
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    In addition to a glucose tolerance test, another test I had was simply fasting insulin levels. Generally, a nondiabetic with hyperinsulinemia while fasting can be presumed insulin resistant. And yes, a lot of the diagnostic criteria is subjective too - for instance, my having done a ton of N=1 experiments on myself with my carbohydrate tolerance.

    I wasn't just calling myself insulin resistant out of nowhere. Anyone who suspects that they are should have these tests done for sure.
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  8. #38
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    I've got a question for the group. When my friend says she has a "fast metabolism" doesnt this really mean that she has excellent insulin sensitivity and nutrient partitioning.

    Said friend is also a fantastic athlete, but also is a wimp when it comes to not eating for a little bit (aka feels nauseous if she doesnt eat within 3hrs of wake._
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  9. #39
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    Originally Posted by DustyChicago View Post
    I've got a question for the group. When my friend says she has a "fast metabolism" doesnt this really mean that she has excellent insulin sensitivity and nutrient partitioning.

    Said friend is also a fantastic athlete, but also is a wimp when it comes to not eating for a little bit (aka feels nauseous if she doesnt eat within 3hrs of wake._
    Too many possibilities, too little information. At the risk of generalization, "fast metabolism" often equates to being genetically fortunate, as not to have the trait of rapidly rising leptin resistance when following a carb-based nutritional pattern...
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  10. #40
    IFBB Amateur, M. Physique ArchangelEST's Avatar
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    Originally Posted by KLMARB View Post
    Oversimplification. Obesity correlates with insulin resistance, it doesn't cause it. That's WHY type II diabetes also occurs in the non-obese/overweight. Obesity is caused by a rise in leptin resistance, which, like insulin, is an anorexigenic hormone. So, it becomes a matter of understanding the nutritional patterns that cause the rises in anorexigenic hormonal resistance. Not understanding this makes people thermo-tards, (oversimplified thermodynamics) if you simply believe its an issue of thermodynamics. This is not meant to be an insult, merely using the same subjective standard you've used as a sociopathic opportunity to insult people.
    Obesity isn't usually caused by leptin resistance. Leptin resistance usually follows the onset of obesity and helps to drive it forward. It's an evolutionary mechanism as the accumulation of fat stores resulted in greater survivability.

    In order to become Obese, an individual first has to repeatedly consume energy above his daily requirements. Leptin levels help manage a healthy appetite, but it's effect in blunting excess appetite is limited. An individual with sufficient psychological stimulus - as in desire for good tasting foods, emotional problems, boredom, etc - can easily consume excess energy, even if circulating leptin levels discourage it. After a while the body becomes less sensitive to leptin even though there is more of it now. Basically Leptin is a weak set of breaks for the overconsumer - enough to stop the average individual from consuming too much calories - but hardly enough to stop someone with enough stimulus from other factors.
    For the dieter the Leptin is a much more effective as a Gas pedal. As body-fat drops it drives hunger forward much more strongly than it could ever halt it in the over-consumer.

    If the body has become leptin resistance through other medical ailments it can contribute to obesity, but only in people with a low level of self control and no knowledge of proper nutrition/training. After all, feeling hungry all the time doesn't mean you are destined to become fat. It certainly makes the average person more likely to consume more calories, but many people do have plenty of self control to just say no to the extra cookie.

    While many things can contribute to obesity - the basics are simple. People just eat way too much for their activity level. Whether they eat too much because they have emotional issues, or because they simply do not comprehend the basics of nutritional value of foods or their activity level or whatever - it's still the matter of simply eating too much.
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  11. #41
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    Actually keto diets cause temporary Insulin Resistance when carbs are reintroduced.
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  12. #42
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    Originally Posted by ArchangelEST View Post
    Obesity isn't usually caused by leptin resistance. Leptin resistance usually follows the onset of obesity and helps to drive it forward. It's an evolutionary mechanism as the accumulation of fat stores resulted in greater survivability.

    In order to become Obese, an individual first has to repeatedly consume energy above his daily requirements. Leptin levels help manage a healthy appetite, but it's effect in blunting excess appetite is limited. An individual with sufficient psychological stimulus - as in desire for good tasting foods, emotional problems, boredom, etc - can easily consume excess energy, even if circulating leptin levels discourage it. After a while the body becomes less sensitive to leptin even though there is more of it now. Basically Leptin is a weak set of breaks for the overconsumer - enough to stop the average individual from consuming too much calories - but hardly enough to stop someone with enough stimulus from other factors.
    For the dieter the Leptin is a much more effective as a Gas pedal. As body-fat drops it drives hunger forward much more strongly than it could ever halt it in the over-consumer.

    If the body has become leptin resistance through other medical ailments it can contribute to obesity, but only in people with a low level of self control and no knowledge of proper nutrition/training. After all, feeling hungry all the time doesn't mean you are destined to become fat. It certainly makes the average person more likely to consume more calories, but many people do have plenty of self control to just say no to the extra cookie.

    While many things can contribute to obesity - the basics are simple. People just eat way too much for their activity level. Whether they eat too much because they have emotional issues, or because they simply do not comprehend the basics of nutritional value of foods or their activity level or whatever - it's still the matter of simply eating too much.
    It's more complex than that. True, overeating causes weight gain. The point is, for those with the genetic trait of rapidly rising leptin resistance, once a degree of that is established, energy issues/withdrawal reactions come into play. These are often misinterpreted as orexigenic (starved state) secretions, rather than the anorexigenic resistance withdrawal reactions that they really are. The practical effect is prevention of lipolysis, if the individual's response is to eat more carbohydrates. That is the real issue, understanding that these resistance states exist, and to understand how to reduce them. The point is to keep the orexigenic/anorexigenic hormones in balance, so you experience a normal leptin response when you eat carbohydrates as well. That's a response essentially disabled in the obese, due to their high degree of leptin resistance.
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  13. #43
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    Originally Posted by IgboMeso View Post
    Actually keto diets cause temporary Insulin Resistance when carbs are reintroduced.
    Yes, and that response, over literally millions of years of human evolution, has been an evolutionary positve, up until modern times. It enables humans to take advantage of temporary carb sources and efficiently store them as body fat.
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  14. #44
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    Now im totaly confused. What i know about IS/IR:
    - more carbs you consume, less sensitive insulines receptors become and otherwise
    - more often you eat carbs, less sensitive insulines receptors become and otherwise
    - more exersice of muscle, more sensitive insulines receptors in that muscle

    So, as i understand, the short way to restore sensitive of insuline receptors is Keto-diet and Intermittent fasting.
    Im like a dog, easy to understand english language, but hard to say )

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  15. #45
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    Originally Posted by Kostya1981 View Post
    Now im totaly confused. What i know about IS/IR:
    - more carbs you consume, less sensitive insulines receptors become and otherwise
    - more often you eat carbs, less sensitive insulines receptors become and otherwise
    - more exersice of muscle, more sensitive insulines receptors in that muscle

    So, as i understand, the short way to restore sensitive of insuline receptors is Keto-diet and Intermittent fasting.
    as usual, keto + IF for the win =D
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  16. #46
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    Originally Posted by Kostya1981 View Post
    Now im totaly confused. What i know about IS/IR:
    - more carbs you consume, less sensitive insulines receptors become and otherwise
    - more often you eat carbs, less sensitive insulines receptors become and otherwise
    - more exersice of muscle, more sensitive insulines receptors in that muscle

    So, as i understand, the short way to restore sensitive of insuline receptors is Keto-diet and Intermittent fasting.
    Yes, determining the degree of resistance can easily be done by following the method I outlined in post #35...
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    Here's a study I dug out of my files that goes into the leptin-insulin resistance-obesity issue in more detail...http://www.pnas.org/content/94/9/4637.full.pdf
    I'll take arrogance and the inevitable hubris over self-doubt and lack of confidence, anyday.......
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    Brain keto expert Shenpen's Avatar
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    Originally Posted by KLMARB View Post
    Here's a study I dug out of my files that goes into the leptin-insulin resistance-obesity issue in more detail...http://www.pnas.org/content/94/9/4637.full.pdf
    From the abstract it looks very interesting! Thanks!
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    Registered User EVlL's Avatar
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    Hi guys l am a type 2 diabetic currently taking metformin is there any way l build muscle? I have been suffering from this desease for years and I'm to the point where l feel like giving up! Just let this be!
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