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New Research Agreeing Paleo is the way to reduce instances of T2 Diabetes

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  • New Research Agreeing Paleo is the way to reduce instances of T2 Diabetes

    Added fructose is 'a principal driver of type 2 diabetes'

    In Mayo Clinic Proceedings, experts urge drastic reductions in the consumption of added sugars

    See the article here: Added fructose is 'a principal driver of type 2 diabetes' | Elsevier Connect

    If you read into the recommendations at the end of the article, it says: reduce sugar intake, no processed foods, whole foods, fruit and veg... Sound vaguely familiar?
    Fortune Favours the Brave
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    I can only talk from my acquired knowledge and experiences. You may have a different view or experience and I will respect that. Please respect mine.

  • #2
    Good post. Thank you. I saw that, too, and it's caused some questions in my head.

    Emphasis needs to be placed on a key word, "added". Fructose, as a component of fruit, isn't the problem, as they identify it. Rather, it is fructose as a huge component of table sugar and HFCS, added to so many processed foods.

    But, fructose bypasses the usual insulin spike that glucose causes so I'm a little fuzzy how it fits in with the Diabetes or insulin resistance issue. Since fructose is paired with glucose in both sugar and HFCS, I still wonder which is the greater culprit. One, or both?

    I understand that excess fructose can cause liver issues, but how does that relate to diabetes?
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    • #3
      Originally posted by John Caton View Post
      But, fructose bypasses the usual insulin spike that glucose causes so I'm a little fuzzy how it fits in with the Diabetes or insulin resistance issue.
      Insulin does not cause insulin resistance. That's an old model that was speculative but never validated. Free fatty acids cause insulin resistance. It's called the Randle Cycle.
      Originally posted by John Caton
      I understand that excess fructose can cause liver issues, but how does that relate to diabetes?
      Fatty liver causes insulin resistance in the liver. Insulin resistance itself is type 2 diabetes.

      It should be noted that increased intake of magnesium and other nutrients can alleviate these problems.
      My opinions and some justification

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      • #4
        Originally posted by John Caton View Post
        I understand that excess fructose can cause liver issues, but how does that relate to diabetes?
        Are you thinking of non-alcoholic fatty liver disease? I had read quite a bit a couple of years ago about an association between excess dietary fructose intake and NAFLD, but I've since read studies to the contrary.

        Of course, "dietary fructose" can mean many different things, as you said.
        Life is not a matter of having good cards, but of playing a poor hand well.

        - Robert Louis Stevenson

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        • #5
          It should be noted that increased intake of magnesium and other nutrients can alleviate these problems.

          Comment


          • #6
            Is this true? I thought that fat in the liver and pancreas made insulin production problematic but that insulin resistance could happen in different parts of the body.

            Human muscle can become insulin resistant and require more and more insulin to function. Additional fat makes you more insulin resistant.

            Beta cells might not respond well to insulin, so more and more is produced.

            I've seen this debate play out and no one can confirm that insulin resistance is definitely not due or exacerbated in some part due to excess insulin.

            It stands to reason that too much of any one hormone flooding the system over time could be problematic.


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            • #7
              Originally posted by SanjayK View Post
              Is this true? I thought that fat in the liver and pancreas made insulin production problematic but that insulin resistance could happen in different parts of the body.

              Human muscle can become insulin resistant and require more and more insulin to function. Additional fat makes you more insulin resistant.

              Beta cells might not respond well to insulin, so more and more is produced.

              I've seen this debate play out and no one can confirm that insulin resistance is definitely not due or exacerbated in some part due to excess insulin.

              It stands to reason that too much of any one hormone flooding the system over time could be problematic.


              Sent from my iPad using Marks Daily Apple Forum
              This experiment directly demonstrates that insulin does not cause insulin resistance, but rather, the opposite:
              Increased insulin responsiveness in vivo and in vitro consequent to induced hyperinsulinemia in the rat.
              On the eighth day an in vivo insulin tolerance test (0.5 U/kg) was performed. Insulin-infused rats responded with a hypoglycemia that was both more pronounced and longer sustained than in saline-infused controls...Glucose uptake by adipocytes from insulin-infused rats was similar to that of controls under basal (zero insulin) conditions, but showed an increase in the maximum response to insulin. Glucose incorporation into total lipid and fatty acid was greater in adipocytes from insulin-infused rats than in controls under both basal (zero insulin) and insulin-stimulated conditions.
              My opinions and some justification

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              • #8
                Originally posted by Elliot View Post
                This experiment directly demonstrates that insulin does not cause insulin resistance, but rather, the opposite:
                Increased insulin responsiveness in vivo and in vitro consequent to induced hyperinsulinemia in the rat.
                That is not what I get from this experiment.

                And as to the randal cycle, I believe you may be confounding a biochemical pathway with clinical lifestyle risk factors that leads to those biochemical changes. For example....your rational is the same as "fat makes you fat", or better yet you would expect eating more fat to aid in producing higher triglyceride blood count, but it is carbohydrate that drives such as we all have seen. Or, and this is to molify the carb group, AGEs where once implicated as being a product of primarily carbohydrate, but we now know that protein can be a large contributor.
                Last edited by Neckhammer; 02-26-2015, 07:58 AM.

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                • #9
                  Originally posted by Neckhammer View Post
                  That is not what I get from this experiment.

                  And as to the randal cycle, I believe you may be confounding a biochemical pathway with clinical lifestyle risk factors that leads to those biochemical changes. For example....your rational is the same as "fat makes you fat", or better yet you would expect eating more fat to aid in producing higher triglyceride blood count, but it is carbohydrate that drives such as we all have seen. Or, and this is to molify the carb group, AGEs where once implicated as being a product of primarily carbohydrate, but we now know that protein can be a large contributor.
                  Then what do you get from this experiment? The rodents which were previously exposed to extra insulin showed greater insulin sensitivity. I don't see another way to interpret it. Can you explain your reasoning?

                  You also claim that carbohydrates cause insulin resistance. If free fatty acids cause insulin resistance, and insulin causes free fatty acids to remain hidden in fat cells, then insulin should prevent free-fatty-acid-induced insulin resistance. Carbohydrates promote insulin, so carbohydrates should then prevent free-fatty-acid-induced insulin resistance.

                  I agree that people eating certain diets often develop insulin resistance, and these diets are often high-carb, but that is not enough to conclude the carbohydrates are at fault. What people say usually sounds like "These foods are bad and these foods have carbohydrates. Therefore all carbohydrates are bad." That's invalid reasoning. Meanwhile, magnesium promotes insulin sensitivity. How do you know the carbohydrates are responsible and not the change in magnesium intake, or any other variable?

                  People here also talk about "physiological" insulin resistance on a ketogenic diet. You can call it "physiological" if you want, but it's still insulin resistance. If carbohydrates cause insulin resistance, then a zero-carb diet should promote maximum insulin sensitivity. But that's not what we see.
                  Last edited by Elliot; 02-26-2015, 11:06 AM.
                  My opinions and some justification

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                  • #10
                    No, I never said it was just carbohydrates. Insulin resistance is desirable because it beats the alternative. In the case of pathological insulin resistance the alternative is cell death. In this case insulin resistance is brought about by cell messengers associated with this level of oxidative stress happening in the cell. This stress is produced by too much enegy and not enough cofactors to process that energy efficiently. Refined carbohydrate simply blows through these cofactors at a much greater rate than any other energy source. That's why refined carbs and sugar hold such a high correlation with insulin resistance. It's also why starchy vegetables and fruit which come with prepackaged cofactors and fiber to slow the bollus of absorption for processing to ATP are not as highly correlated. For physiological insulin resistance i.e. Muscular insulin resistance only....this is brought about simply to preserve glucose for other body parts, not because it's uptake would cause cellular death....that's a pretty big difference.
                    Last edited by Neckhammer; 02-26-2015, 11:30 AM.

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                    • #11
                      Originally posted by Neckhammer View Post
                      No, I never said it was just carbohydrates. Insulin resistance is desirable because it beats the alternative. In the case of pathological insulin resistance the alternative is cell death. In this case insulin resistance is brought about by cell messengers associated with this level of oxidative stress happening in the cell. This stress is produced by too much enegy and not enough cofactors to process that energy efficiently. Refined carbohydrate simply blows through these cofactors at a much greater rate than any other energy source. That's why refined carbs and sugar hold such a high correlation with insulin resistance. It's also why starchy vegetables and fruit which come with prepackaged cofactors and fiber to slow the bollus of absorption for processing to ATP are not as highly correlated. For physiological insulin resistance i.e. Muscular insulin resistance only....this is brought about simply to preserve glucose for other body parts, not because it's uptake would cause cellular death....that's a pretty big difference.
                      I'm still curious as to how you interpret the experiment I posted. Very frequently, I hear people say that insulin causes insulin resistance, and by that mechanism, all carbohydrates promote insulin resistance. The experiment I posted seems to directly contradict that. You've said you disagree with this interpretation, but you haven't specified how.

                      Do you believe insulin causes insulin resistance?
                      My opinions and some justification

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                      • #12
                        Originally posted by Elliot View Post
                        Do you believe insulin causes insulin resistance?
                        My response covers this. Short answer is no.

                        Originally posted by Elliot View Post
                        I'm still curious as to how you interpret the experiment I posted. Very frequently, I hear people say that insulin causes insulin resistance, and by that mechanism, all carbohydrates promote insulin resistance. The experiment I posted seems to directly contradict that. You've said you disagree with this interpretation, but you haven't specified how.
                        What I think people frequently say is that hyperinsulinemia indicates you already have insulin resistance, and that hyperinsulinemia itself is detrimental to health as well. What I've also seen stated is that this prolonged hyperinsulinemia may promote beta cell burnout in the pancreas. I think this experiment shows some indication that prolonged hyperinsulinemia is in fact detrimental to health. But I don't pretend to like mouse experiments....what does an 8 day experiment translate to in human years? Does it really tell us much of anything? I'm afraid that with just this rat study, and an abstract only at that, I cant reach any solid conclusion.
                        Last edited by Neckhammer; 02-26-2015, 12:39 PM.

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                        • #13
                          Originally posted by Neckhammer View Post
                          My response covers this. Short answer is no.



                          What I think people frequently say is that hyperinsulinemia indicates you already have insulin resistance, and that hyperinsulinemia itself is detrimental to health as well. What I've also seen stated is that this prolonged hyperinsulinemia may promote beta cell burnout in the pancreas. I think this experiment shows some indication that prolonged hyperinsulinemia is in fact detrimental to health. But I don't pretend to like mouse experiments....what does an 8 day experiment translate to in human years? Does it really tell us much of anything? I'm afraid that with just this rat study, and an abstract only at that, I cant reach any solid conclusion.
                          Then we can agree to some extent. I agree that hyperinsulinemia indicates insulin resistance. Regarding beta cells, I don't know if hyperinsulinemia causes beta cell death. But free fatty acids do, in a process called lipotoxicity. Free fatty acids also cause insulin resistance, which would cause the hyperinsulinemia, so this seems to come back to free fatty acids as a more fundamental cause.

                          Your earlier post seems to say that carbohydrates are only problematic if obtained in isolation, i.e. without the other essential nutrients. If this is what you meant, then I agree. Flour and refined sugar are bad.
                          My opinions and some justification

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                          • #14
                            @Elliot or Neckhammer

                            I've been following your exchange. I generally understand there being a link between FFAs and insulin resistance. Aren't FFAs practically non-existent. Fatty acids are either bound to glycerol or to a protein. When are they free to cause insulin resistance? Or, is it possible that insulin resistance just increases FFAs?
                            Stop by to visit at http://primalways.net
                            Old Paths ... New Journeys

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                            • #15
                              Originally posted by John Caton View Post
                              @Elliot or Neckhammer

                              I've been following your exchange. I generally understand there being a link between FFAs and insulin resistance. Aren't FFAs practically non-existent. Fatty acids are either bound to glycerol or to a protein. When are they free to cause insulin resistance? Or, is it possible that insulin resistance just increases FFAs?
                              Instead of "free," think "non-esterified."

                              In vitro, a cell's response to insulin diminishes as the amount of non-esterified fatty acids in the medium increases.
                              In vivo, a body's overall response to insulin diminishes as the amount of non-esterified fatty acids in the serum increases.
                              In rodents which have been genetically modified to have extra lipoprotein lipase in specific tissues, those tissues have increased insulin resistance.

                              Mechanism of free fatty acid-induced insulin resistance in humans. - PubMed - NCBI
                              Therefore in contrast to the originally postulated mechanism in which free fatty acids were thought to inhibit insulin-stimulated glucose uptake in muscle through initial inhibition of pyruvate dehydrogenase these results demonstrate that free fatty acids induce insulin resistance in humans by initial inhibition of glucose transport/phosphorylation which is then followed by an approximately 50% reduction in both the rate of muscle glycogen synthesis and glucose oxidation.
                              My opinions and some justification

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