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Low carb/ insulin resistance

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

  1. Shijin13

    Shijin13 Guest

    SO if I'm physiologically IR, along with CT and Ketosis, as I mitigate non-native EMF - the PPP should be ezpz???
     
  2. Jack Kruse

    Jack Kruse Administrator

    WHY DID I SAY THIS ^^^^^ Re read the fish oil blog.........carefully. I have said time and time again O6's are a PROBLEM WHEN IL 6 and NF KAPPA BETA ARE HIGH. INFLAMMATION IS THE bad O6 trigger mechanism.........to the ugly side of O6's. Get rid of the underlying inflammation, and I dont believe the excess of O6 is still inflammatory and bad. This is why people on paleo fear the o6 monster is fools gold........if they have inflammation under control.......Hey guess what the Epi paleo Rx prescribes? The lowest inflammatory diet ever. Dietary O3's act like NSAIDS..........naturally.
     
    SCRN2007 likes this.
  3. Jack Kruse

    Jack Kruse Administrator

    non native EMF worsens your mitochondria.......and destroys the stem cell supply......this is how you speed up time relative to your biology........quantum time is a function of how good or bad a tunneler you are. It also project how healthy and how long you live.
     
  4. nicld

    nicld Gold

    Very interesting. We will see if there is a difference in mine when I get it tested again next week. I have been doing alot of CT and it is winter here. My last ones were done in July with no CTing and freeking HOT weather.
     
  5. cantweight

    cantweight Gold

    Trying to so hard to make sense of this.

    BG in optimal range
    HbA1c in optimal range

    IR calculated high
    HOMA-IR calculated optimal range

    Suspect poor mitochondria function due to fatigue....so I want my BG to go up in response to CT? But the rest of that stuff is heading where I want it to? Up CT to decrease inflammation, o3/o6 ratio around 1:3 adjust this too....then wait for the magic to happen?
     
  6. Jack Kruse

    Jack Kruse Administrator

    ^^^ WHAT MAIN FACTOR DID YOU LEAVE OUT?


    Non native EMF has the biggest role of electron coupling or decoupling on mitochondria.........BOOM
     
  7. cantweight

    cantweight Gold

    I moved 18 months ago....there is very little left for me to mitigate so i tend to focus and what actions i have still left to take. I just cant tell if all I am doing is working!!!
     
  8. Shijin13

    Shijin13 Guest


    Christi - our problem is where we live - we can only mitigate so much. the DC metro area (and I 95 corridor) are freaking non-native EMF nightmare. it might be more tolerable if we had longer photoelectric season, colder winters, and a geopathic stress zone.... at some point we have to leave the area - the question is how do we do it in a smart way for our health - physically, emotionally - and financially...

    Jack's been beating this one for ever - where we live matters. where we don't live matters too...
     
  9. caroline

    caroline Moderator

    I can't even invite you to OZ ..... we are even worse off here......
     
  10. cantweight

    cantweight Gold

    I get it...theres just little left for me to do there...like you said the physical, emotional, financial trifecta...but I cant accept that I am screwed. People can get healthy...at least healthier in less than optimal places. I am striving for that. I have been fascinated by the lack of thyroid issues where I am now vs a half hour closer to DC. A lot of much older moms out here...with kids that dont have issues...another mind blower.
     
  11. Jack Kruse

    Jack Kruse Administrator

    bingo!!!!!!
     
  12. Shijin13

    Shijin13 Guest


    I've got the message Jack... just trying to understand how everything else fits into the puzzle give my current environment... and planning the escape....
     
  13. Jack Kruse

    Jack Kruse Administrator

    I want you to go back and re read the Oprah blog.......what was it teaching you? How you went abby normal from normal. What is normal? In healthy cells (FOR JAKE: Tunneling is working well) the signal to reject excess calories picks specifically on glucose metabolism, in the form of the "physiologic development" of insulin resistance. Why did Lady evolution chose glucose? Well cytochrome one, the first one is where glucose and its Krebs cycle intermediates all fill in to the mitochondria. So putting the switch signal there makes the most sense. How does the switch work? Excess energy of electrons from glucose increase superoxide generation at cytochrome complex I of the mitochondria. What is so damn unique about cytochrome 1? Meet our first transition metal complex made of iron and sulphur: It's called iron sulphur cluster N-1a. Not a catchy phrase but tells you what is in it. What is the target of this complex? You guessed it.......the transition metal and sulphur. When the iron sulphur group is functioning well, it creates a small amount of leak to generate ROS to signal mitochondrial biogenesis. This is orderly. What happens when the transition metal does not work, or say sulphur is off because of a lowered redox potential in the inner mitchondrial membrane which slows electron flow for any reason at all? The mitochondria play to avoid a breakdown is to use cytochrome number two. This is where FADH2 lives and where electrons from fats enter the Electron chain transporters for tunneling. So how do you best avoid a broken complex one? You go to two. One big problem......electrons from carbs can not go thru a broken one.......if they do you can expect lots of ROS. This makes more signal that cause more mitochondrial inflammation which stimulate permanent destruction of cytochrome 1. If and when this happens you need to eat like a great white shark and live like a polar bear to take advantage of the HALL EFFECT. This is how you increase electron current on the ETC when your redox potential sucks and/or your cytochrome 1 is broken for any reason. The simple fix is to feed your mitochondria a lot of saturated fat to generate a lot of FADH2. Why? Because FADH2 is the substrate that Lady evolution used to build complex two. When you feed electrons in cytochrome two guess what happens? electrons flow toward cytochrome one backwards and toward cytochrome 3 forward. This means that flow is bidirectional. It also means when flow is bidirectional it can not be as fast as if it were unidirectional. So what increases flow when it is slow? The HAll effect or the cold effect of semiconduction. When electrons flow reverse thru cytochrome 1 guess what happens? We shut down glucose electron acceptance from foods to the cell. Now you might see why insulin does not work below 62 F either......why? COLD is designed to do this NATURALLY!!!! It is built by design not hormetic as the "paleo leaders" tell you.
     
  14. Jack Kruse

    Jack Kruse Administrator

    See why this question was not ask Jack worthy?
     
  15. Jack Kruse

    Jack Kruse Administrator

    FOR JAKE THE PEATATARIAN: WHY IS FRUCTOSE A KILLER? Fructose is the number one insulin resistance generators in biology. Fructose free falls through glycolytic pathway to levels that the cells really cannot expect to use immediately. Most of it gets off loaded as lactate but because of how it is handled there is still way more pyruvate present than a cell can oxidize readily. Fructose effect on mitochondrial are dose related. Eating the occasional autumn fruit will not kill you, but the orange juice PEAT told you is fine. will set you up for the path of destruction.

    Lady evolution to fructose comes from the action of the molecular demons. It limits fructose damage by shutting down glucose electrons by compensating for the amount of fructose supplied to the cell. This is done the same way mentioned earlier. We use FADH2 to shut down complex one. This massively reduces complex 2. Simultaneoulsy Glucose 3 Phosphate dehydrogenase does this directly from the cytoplasm. This shuttle acts just like electron transferring flavoprotein dehydrogenase, (cytochrome 2 like) to shut down complex one both ways.
     
  16. SeaHorse

    SeaHorse Gold

    For me you have reached a critical mass of writing on the blog....I'm following what you are saying and I'm understanding so much more of the contextual physiologic and pathologic information with IR, BG etc....Some of these recent threads have been super useful and important.

    It's not like everything is optimal with me yet, but I'm not frustrated by the time it's taking to turn things around. I feel like I know what it is I need to do, where i've fallen off the path and what I've done so far that's made me feel so much better. Even with things crashing and burning every now and then, I know I'm moving forward....How can we expect all these systems to operate well after decades of messed up signalling. Even though I'm at a fairly low energy charge these days....my sleep is fantastic and that gives me great hope despite cytochrome 1 being a disaster zone.
     
  17. nonchalant

    nonchalant Silver

    Lucky for us sunlight completely bypasses cytochrome 1...

    No, wait... Photons do power mitochondria....
    Must read more...
     
  18. nicld

    nicld Gold

    Yep but thank you for explaining all of it to us even if it takes a bit to sink in.
     
    SCRN2007 likes this.
  19. Dali Dula

    Dali Dula Moderator

    My life for the past 2 1/2 years has been guided by what I can do or not do to lower my BG. For most of that time I have kept an a1c of 5.6 avg. 6 months ago this started rising. My last two labs in June and September a1c rose to 6.0 and 6.1.
    waking FBG is now typically 140 to 170. I haven't seen a BG reading at anytime below 100 in many months. This does not seem correlated with seasonality or light cycles. Non glycemic meals will produce post prandial spikes of 30-50 points.
    I work all the protocols. I eat a kerogenic diet. I have always believed the lower the BG the better as long as we don't go hypo. Is neuropathy and organ damage not a risk at a1c of 6 +? Is there a protective mechanism I have missed?
     
  20. Amy

    Amy Silver

    Trying to connect some threads here and have some questions. Any thoughts appreciated.
    1. Hall effect predicts improved electron flow with cold. Insulin not functional below 62 degrees. If CT only cools skin and Core temperature actually rises during CT, how does CT improve electron flow (anywhere other than skin) and how would it affect insulin action in entire body?
    does loading the skin semi conductors give rise to increased charge internally? In regards to insulin is this some sort of spooky quantum at-a-distance action? All I can come up with...
    2. Cold blooded animals are slow and lethargic at low temps. Is this consistent?
     

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