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

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

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    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?
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    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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    Quote 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.
    Quote 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.

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

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    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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    Quote 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.


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    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.

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    Quote 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 at 06:58 AM.

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    Quote 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 at 10:06 AM.

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    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 at 10:30 AM.

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