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The metabolic advantage hypothesis

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  • Originally posted by ChocoTaco369 View Post
    Seriously?
    And if what you quoted yourself as saying was the crux of your entire post you could have been correct.... but you kept typing.

    Here is how your rationale usually reads to me:

    Low carb causes physiological insulin resistance that acts in way that is kinda like metabolic syndrome IR. So if you are a low carber and eating carbs makes you more insulin sensitive then people with metabolic syndrome should do the same thing.... eat more carbs to become more insulin sensitive.


    Thats how it comes off anyhow, and there are all sorts of logical problems with that line of reasoning.
    Last edited by Neckhammer; 10-23-2013, 10:47 AM.

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    • Originally posted by ChocoTaco369 View Post
      Who said anything about pathological?
      The statement of yours I quoted came from your reply to Dilberry, who was talking about diabetes. I don't see the purpose of talking about adaptive low carb insulin resistance in the context of diabetes, which involves unrelated pathological insulin resistance. It makes it sound like you think the mechanisms underlying the two are the same. If you do, provide proof. Otherwise, stop confusing people.

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      • Originally posted by Neckhammer View Post
        That however does not equate in any way shape or form to diabetes being "caused" by fat as you stated. You are simply stating the physiological symptoms of the disease once its already in progress. NIDDM is/can be cause by several things either alone or in conjunction.
        That's not what I said at all. I said low carbohydrate dieting increases the rate of FFA's being oxidized for fuel and decreases the rate at which glucose is oxidized for fuel, and insulin resistance is a natural side effect of that process. That is how FFA's are oxidized more rapidly in a glucose-deficient state - by the body becoming less sensitive to insulin (since you can't drop insulin any lower beyond a certain point or you'll die).

        A completely separate point was the cause of diabetes and metabolic syndrome. That is largely caused by polyunsaturated fat intake.

        Why are you trying to turn two completely separate statements into one argument?
        Don't put your trust in anyone on this forum, including me. You are the key to your own success.

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        • Originally posted by ChocoTaco369 View Post
          That's not what I said at all. I said low carbohydrate dieting increases the rate of FFA's being oxidized for fuel and decreases the rate at which glucose is oxidized for fuel, and insulin resistance is a natural side effect of that process. That is how FFA's are oxidized more rapidly in a glucose-deficient state - by the body becoming less sensitive to insulin (since you can't drop insulin any lower beyond a certain point or you'll die).
          So I did misunderstand.

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          • Originally posted by Timthetaco View Post
            So I did misunderstand.
            Yes. But I also think maintaining insulin sensitivity is important, so I am very against low carbohydrate dieting in the overwhelming majority of cases. The effects are physiological rather than pathological, but that doesn't mean they are healthy. Low carbohydrate dieting still creates insulin resistance and high fasting blood glucose, and while that may not be harmful here and there, holding those conditions for years - like so many others - creates a chronic condition. I don't believe that state to be optimal in very many cases.
            Don't put your trust in anyone on this forum, including me. You are the key to your own success.

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            • Where have I seen this style of argument before? Semantics are being argued at this point. Fat molecules are oils so they would be insoluble in the aqueous intestinal environment, so, obviously they have to be broken down and stored and FFAs are the results of the liberation of these fatty acid stores. Insulin resistance is absolutely caused by a fat, polyunsaturated fats, being liberated en masse from these stored fats. FFAs induces a down regulation of insulin signaling pathways.
              Make America Great Again

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              • Thanks SB! Maybe if I ever go hunting I'll catch a moose or elk. Seal is doubtfull!!

                On a semi unrelated note, with no intentions of derailing this amazing debate, Derpamix and Choco, are you guys biologists or to anything to close to that capacity? You guys are fuckin BRAINS. (You better not tell me you guys deliver pizza like Glenn from the walking dead)

                Back to the topic:

                You guys did say it before, but Omega-3 is a Polyunsaturated fat. You guys are saying there is NO benefits from omega-3?

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                • The most comprehensive model to date for pathological IR and subsequent NIDDM is the oxidative stress model IMO. I'm not sure what/how you guys are trying to push all the blame on PUFA only. Seems like your missing all kinds of things there.
                  Last edited by Neckhammer; 10-23-2013, 04:35 PM.

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                  • Originally posted by Neckhammer View Post
                    The most comprehensive model to date for pathological IR and subsequent NIDDM is the oxidative stress model IMO. I'm not sure what/how you guys are trying to push all the blame on PUFA only. Seems like your missing all kinds of things there.
                    It was my understanding that type 2 diabetes was a result from chronically elevated insulin levels, desensitizing the insulin receptors to not allow glucose from entering most cells (since they're topped off) and instead go to fat cells to be stored.

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                    • Originally posted by Neckhammer View Post
                      The most comprehensive model to date for pathological IR and subsequent NIDDM is the oxidative stress model IMO. I'm not sure what/how you guys are trying to push all the blame on PUFA only. Seems like your missing all kinds of things there.
                      I am personally alluding to hepatic insulin resistance, which is induced by the excess accumulation of FFAs. Within the hepatocyte, metabolites of the FFA re-esterification accumulate. These excess FFAs cause relocation of several protein kinase isoforms, from the cytosol to the membrane compartment. The membrane isoforms phosphorylate the intracellular portion of the insulin receptor which results in impairment of insulin receptor interaction with downstream insulin signaling proteins. These are all cut of the same thing, usually anyway. Obesity is just hypoxia of the cell leading to the activation of cellular stress response pathways causing autonomous inflammation and the release of pro-inflammatory cytokines, much the same as the interference from FFAs.

                      On a semi unrelated note, with no intentions of derailing this amazing debate, Derpamix and Choco, are you guys biologists or to anything to close to that capacity? You guys are fuckin BRAINS. (You better not tell me you guys deliver pizza like Glenn from the walking dead)
                      Thanks man, but I don't think much of myself personally. I am basically a higher paid pizza delivery guy. I'm currently saving money to move off the grid and start a farm.
                      Last edited by Derpamix; 10-23-2013, 05:57 PM.
                      Make America Great Again

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                      • Originally posted by Prime-Animal View Post
                        It was my understanding that type 2 diabetes was a result from chronically elevated insulin levels, desensitizing the insulin receptors to not allow glucose from entering most cells (since they're topped off) and instead go to fat cells to be stored.
                        Yes hyperinsulinemia tends to lead to insulin resistance or perhaps more vice versa. That is the physiological route. In a biochemical sense oxidative stress is the "why" of how the cells become insulin resistant. This is a good one by Chris Masterjohn. BTW he gets into the oxidative stress stuff around minute 20:00



                        If you take this view then you don't have to agree with everything he says, but you can recognize that IR is the result of nutrient deplete and toxic energy sources that creates a high oxidative load in the cell. This could be due to either carbs or fats, but usually both.... and that is what the evidence supports IMO.
                        Last edited by Neckhammer; 10-23-2013, 06:08 PM.

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                        • Hyperinsulinemia is hexosamine biosynthesis insulin resistance.
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                          • Now put it in your own words.

                            Showing results for hyperinsulinemia is hexosamine biosynthesis insulin resistance.
                            Search instead for perinsulinemia is hexosamine biosynthesis insulin resistance.
                            Scholarly articles for hyperinsulinemia is hexosamine biosynthesis insulin resistance.
                            … in transgenic mice leads to insulin resistance. - ‎Hebert Jr - Cited by 273
                            Hexosamines and insulin resistance - ‎McClain - Cited by 302
                            … hyperinsulinemia and peripheral insulin resistance. - ‎Tang - Cited by 63
                            Search Results

                            Hexosamine biosynthesis pathway flux contributes to insulin ...
                            www.ncbi.nlm.nih.gov/pubmed/19036880‎
                            by P Bhonagiri - ‎2009 - ‎Cited by 8 - ‎Related articles
                            Nov 26, 2008 - Hexosamine biosynthesis pathway flux contributes to insulin resistance via ... in hyperinsulinemic cell culture models of insulin resistance.
                            Transgenic mice with increased hexosamine flux specifically ...
                            www.ncbi.nlm.nih.gov/pubmed/10969833‎
                            by J Tang - ‎2000 - ‎Cited by 63 - ‎Related articles
                            To determine the effects of hexosamines on insulin synthesis and secretion, ... in hyperinsulinemia, insulin resistance, and (in males) mild type 2 diabetes.
                            Hyperinsulinemia Diminishes Phosphoinositide-Regulated Actin ...
                            professional.diabetes.org/Abstracts_Display.aspx?TYP=1&CID=51010‎
                            Hyperinsulinemia Diminishes Phosphoinositide-Regulated Actin Structure and Insulin Sensitivity Via Increased Hexosamine Biosynthesis. Year: 2005. Abstract ...
                            Trivalent Chromium Modulates Hexosamine Biosynthesis Pathway ...
                            http://www.scirp.org/journal/PaperIn...D=35078‎
                            by BA Penque
                            Trivalent Chromium Modulates Hexosamine Biosynthesis Pathway Transcriptional ... hyperinsulinemia-induced cholesterol biosynthesis and insulin resistance.
                            Hexosamine biosynthesis pathway flux contributes to insulin ...
                            https://www.docphin.com/.../Hexosami...-con...‎
                            Hexosamine biosynthesis pathway flux contributes to insulin resistance via altering ... dysregulation and insulin resistance induced by hyperinsulinemia.
                            Insulin Resistance and Hyperinsulinemia - Diabetes Care
                            care.diabetesjournals.org/content/31/7/1433.abstract‎
                            by SH Kim - ‎2008 - ‎Cited by 36 - ‎Related articles
                            We analyzed the correlation between insulin resistance and insulin response in ... Hexosamine Biosynthesis Impairs Insulin Action via a Cholesterolgenic ...
                            Evidence coupling increased hexosamine biosynthesis pathway ...
                            www.sigmaaldrich.com/catalog/papers/21712361‎
                            Hyperinsulinemia is known to promote the progression/worsening of insulin resistance. ... increased glucose flux through the hexosamine biosynthesis pathway (HBP) causes PIP(2)/F-actin dysregulation and subsequent insulin resistance.
                            Download - Journal of Clinical Investigation
                            www.jci.org/articles/view/118876/pdf/render‎
                            by LF Hebert Jr - ‎1996 - ‎Cited by 273 - ‎Related articles
                            to weight-dependent hyperinsulinemia in random-fed mice. .... Increased Hexosamine Synthesis Results in Insulin Resistance. 931. DNA and RNA analysis.
                            Advances in Hyperinsulinism Research and Treatment: 2013 Edition: ...
                            books.google.com/books?isbn=1481670727
                            2013 - ‎Medical
                            Evidence reveals a hidden cost of hyperinsulinemia on plasma membrane (PM) ... whether increased glucose flux through the hexosamine biosynthesis pathway (HBP) causes PIP(2)/F-actin dysregulation and subsequent insulin resistance.
                            Hexosamine Biosynthesis Pathway Flux Contributes to Insulin ...
                            europepmc.org/articles/PMC2659275/
                            Nov 26, 2008 - Hexosamine biosynthesis pathway flux contributes to insulin resistance via altering membrane phosphatidylinositol 4,5-bisphosphate and ...

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                            Last edited by Terry H; 10-23-2013, 07:12 PM.

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                            • Originally posted by Terry H View Post
                              Now put it in your own words.
                              Those are his own words. Your problem if you cannot comprehend.


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                              • Originally posted by turquoisepassion View Post
                                Those are his own words. Your problem if you cannot comprehend.


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