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Low carb/ insulin resistance

Discussion in 'The New Monster Thread' started by Dali Dula, Dec 1, 2013.

  1. Jack Kruse

    Jack Kruse Administrator

    I would think the whole apple is fine......as long as you dont alter the apple to make it something it is not.
  2. Hemming

    Hemming New Member

    Does boiling them to make 'mashed apples' count as altering it into something it is not?
  3. SeaHorse

    SeaHorse Gold

    I would think yes....cooking concentrates sugars...think of a quince: sour and inedible raw...cooked it becomes sweet without any additional sugar. Meat too...onions...carrots...
  4. Hemming

    Hemming New Member

    That was also what I was thinking.
  5. Jack Kruse

    Jack Kruse Administrator

    ..............So let us talk about what Dali Dula really wants to talk about.......T2D. How does superoxide work in a screwed mitochondria Remember in T2D the transition metals in the cytochromes do not work well to tunnel electrons. This means that electron flow is slow. IT means it actually can reverse at times. This cause cytochrome one to leak more. cytochrome 1 is right next to mitochondrial DNA. When a lot of leak occurs it cause generation of positively charged molecule called oxidants of free radicals. This destroys mitochondrial epigenetic expression of its DNA. MtDNA has only 13 genes. Guess what those genes code for? Cytochrome parts. If the expression is altered you become unable to make properly functioning cytochromes to tunnel electrons. Remember QED requires precision to tunnel electrons. So what happens? Cytochrome 1 becomes quickly demolished and non functional in a T2D.

    So what does a doc do to help a T2D? METFORMIN

    Metformin is an inhibitor of cytochrome I of the ECT. It aborts glycolysis to lactate because pyruvate is not much use to mitochondria with blocked first cytochrome. Acute exposure to metformin in tissue culture happens to also generates a ton of superoxide. And superoxide production is what benefits a T2D who has a blown up cytochrome 1
  6. Jack Kruse

    Jack Kruse Administrator

    Metformin does not stop fatty acid oxidation as guys like Morley the magnesium man tells folks. You do need some minimal cytochrome I activity to provide the NAD+ for beta oxidation to function and it does do this. There is no evidence for a complete block of cytochrome I by metformin.
  7. Jack Kruse

    Jack Kruse Administrator

    When a diabetic keeps eating carbs.....it drives the TCA cycle intermediates and this makes positively charge ions that are free radicals and this still generates NADH which causes the reversal of flow of electrons in cytochrome 1.
  8. Jack Kruse

    Jack Kruse Administrator

    So if you are following along......metformin acts like a high fat diet for a T2D even when the person is non compliant and eating carbs they should not eat. This is the reason I have told many of you metformin is a godsend for T2D and those with PCOS. Metformin makes levels of superoxide that are comparable to fat metabolism.

    Now you may begin to see why I said earlier superoxide is the cause of IR. IR protects a T2D from a broken first cytochrome in this particular context..........it can act like the devil in other cases.
  9. Jack Kruse

    Jack Kruse Administrator

    Fat cells become IR under metformin direction. This means they act just like cold does. It causes fat cells to empty its fat content so the free fatty acids feed electrons to cytochrome 2 to keep the ECT humming making ATP.
  10. Jack Kruse

    Jack Kruse Administrator

    So what does all this fancy QED directing biology mean? It means metformin directs function and not insulin.......and this is why treating diabetics with insulin is an epic mistake in my opinion. We want a diabetic to be in a constant state of IR to empty fat cells of free fatty acids. It also shows you why the Epi paleo Rx protects them when they eat within cycles.
  11. Jack Kruse

    Jack Kruse Administrator

    The brain is an organ that I told you is an electromagnetic computer. Therefore it really does not like a lot of positively charged superoxide around. For the same reasons it does not really like glucose, contrary to paleo biochemistry dogma, nor does it like free fatty acids. What does she like? My members know......KETONES. Think Energy and Epigenetics 1. How do ketones work in the brain? simple.....they come in cross the BBB easy and hit the brick wall called the neural glial cells which turn all ketones to lactate. Glial cells in your brain are like mini livers. They make ketones for the brain like the liver does for the body.
  12. Jack Kruse

    Jack Kruse Administrator

    The reason the brain does this is because beta oxidation of free fats turns on apoptosis and this is not good for the brain that needs to keep long term neurons from being eaten alive. Now this is precisely what happens when the brain has a neurodegenerative disorder from glucose.
    Danco3636 likes this.
  13. Jack Kruse

    Jack Kruse Administrator

    High BG drives superoxide production.
  14. Jack Kruse

    Jack Kruse Administrator

    When glucose is the main Ferrari fuel to the brain it drives huge amounts of NADH production. This amount of NADH can't be utilized once Cytochrome 2 (FADH2 from succinate dehydrogenase) reaches some critical level in neuronal mitochondria. This gets back to the Oprah blog. The mitochondria say no to glucose calories to limit brain mitochondria to superoxide and becomes they become insulin resistant as a protectant.
  15. Jack Kruse

    Jack Kruse Administrator

    Ketones turn into lactate which in turn gets metabolized to supply acetyl-CoA along with production of a couple of extra NADH molecules in the glial cells. Turns out lactate metabolism does not need glucose metabolism. So this is good news for the brain hence why lactate pathway is big and no one seems to know it. This action means it shuts down FFA flow into cytochrome 2 via FADH2. Lactate is the purest form of metabolic fuel for a sick cytochrome 1. This is why ketosis helps the human brain. EE 1 alert.
  16. Jack Kruse

    Jack Kruse Administrator

    Superoxide generation is the primary marker of energy excess at the cellular level from any cause. It also turns out superoxide generation is directly proportional to the ratio of FADH2 generated to the amount of NADH generated for a given substrate put in to mitochondria. This is the key metabolic pathway for electron tunneling......when this goes awry......shit hits the fan
  17. Shijin13

    Shijin13 Guest

    OMG - THIS IS EPIC. I'm gonna have to re-read this.

    but If I understand what your saying - Metformin - produces superoxide - thus increasing the potential for NADPH+ and access to the PPP - for those who are T2D or PCOS.

    does dosage - time duration change the benefit? is night dosing of Metformin more beneficial or would it be more beneficial to take Metformin through out the day????
    SCRN2007 likes this.
  18. nicld

    nicld Gold

    Head is hurting a little bit. I see a flow map coming to straighten it all our for me.

    What would be going on if while someone was on Metformin blood sugars were still high while eating low carb? Does it all have to do with seasonality of the carbs?

    How is the mechanism for physiological IR and pathological IR differ?
  19. Dali Dula

    Dali Dula Moderator

    Thank you, Jack. Will need another read.

    Nicid great questions. If you do the flow chart please post.

    I doubt what I am experiencing has to do with carbs. I am on a real clean 80%+ fat diet. I could have failing beta cells and T2D is a progressive disease. So many variables.Hashi's too. Keep paying attention, keep hacking. Heading for my outdoor tub @ 34f for a soak.
  20. How does cannabidiol effect this process?

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