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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

    no......its a potassium issue.......and when I get to the Quantum puzzle blog you'll see why........BG is not the major issue. It can be when BG is present in higher temps body temps such as when cytokines are high. Your cytokines are low because you are CT machine. The longer you CT the higher your BG goes but you develop no issues with BG.........because insulin can not hurt you when you control cytokines.

    When energy is used in a quantum cell, it operates coherently and cooperatively as a unit. It becomes destabilizes a bit from its metastable state, and this allows glucose and calcium, to move into the cell in droves. This tells you why I made a big deal about calcium ion frequency resonance in the EMF series. EMF uncouples this normally coupled coherent event.
    Under the control of insulin, glucose adsorption sites on proteins and enzymes become exposed to the environment, and glucose can be burned to replenish the ATP or shunned if the cell is made IR as mentioned above in this thread. When glucose is the fuel, at the same time, carbon dioxide is produced, which functions to stabilize the resting living state. Here is where my cosmology links come back for you to consider........CO2 in cold causes matter in galaxies to condense under the force of the electromagnetic and gravitational forces of physics. In your body the same thing happens in the ABSENCE OF CYTOKINES OR INFLAMMATION. This effect is called the Bohr effect, increases the efficiency with which oxygen is unloaded from the red blood cells, curtailing the production of lactate and protons. Protons are positively charged and consider acids and they do not like Oxygen. In this highly energized coherent state, potassium is preferentially adsorbed to the ionized carboxylate groups on intracellular proteins. This satisfactorily explains why the administration of glucose and insulin can uncomfortably lower blood potassium levels............this is has huge implications for explaining rigor mortis:

    NOW CONSIDER THIS: Carb whores think fructose is the only way to replenish glycogen.......not true. the PPP is the best way because it is the most reducing pathway using electrons to do so.......why does biochemistry miss it? Because modern humans beliefs have kept them from realizing that fructose is how you do it when cytokines are high and saturated fat electrons do it in the cold.........Seasons matter in biochemistry.
    Last edited: Dec 6, 2013
  2. Jack Kruse

    Jack Kruse Administrator

    Cold animals are slow and made quicker with energized photons......we do it by increasing electron energy efficiency because we have better Maxwell demons to catch the free electrons and photons from the environment.
  3. Jack Kruse

    Jack Kruse Administrator

    now to your other excellent point about CT and the surface.......let me ask you to consider the first paragraph of EE 4.......what did I tell you about the thermohaline currents in the ocean? They cycle naturally........just by the nature of the photoelectric effect and water chemistry.........to metabolically couple to move.......to deliver what? Oxygen by using temps...........and nothing else. Your body is made up or 71% water and it collects photons.........you see any homology now?
  4. endless

    endless New Member

    I'm just not getting it....going to need to read this again and again. I've got high FBG....now I'm not sure I should be trying to lower it! How does RS fit into this?
  5. Inger

    Inger Silver

    Christa, I am not getting it theoretically either but intuitively.. and this thread made all my worries about my highish BG disappear. I also researched a bit on ketogenic athlete sites yesterday and there was said BG do not matter when ketogenic.
    From all the research I have done, and my own feeling, I am not one bit worried anymore and I like my blood glucose levels :)
  6. Dali Dula

    Dali Dula Moderator

    There is detailed answer happening over on
    A few questions about the PPP and fat thread.
  7. Jack Kruse

    Jack Kruse Administrator

    Insulin does not work well below 62 F endless.......so this stops glucose from entering the cell and causing problems but leaves your BG high. The second carb to worry about is fructose. It is not affected by insulin......therefore the cold temps have another thermoplastic trick for fructose metabolism. It makes sugar act like a saturated fat using a quantum tunneling shuttle in the PPP. So this brings us to EMF 4, the PPP.
    How the PPP uses cold and fat:The Pentose-phosphate pathway has a wide range of purposes in the cell. It provides a constant supply of NADPH, which is used in biosynthesis. The pathway also produces Ribose-5-phosphate, which is required for nucleic acid synthesis. Also in the Pentose-phosphate pathway two glycolytic intermediates are formed:
    1. Fructose-6-phosphate (the PEAT/Paleo WAY) and
    2.Glyceraldehyde-3-phosphate. (THE KRUSE/Mammal WAY VIA FATS)

    Regulation of the Pentose Phosphate Pathway:

    Due to the first step of this pathway being reversible, it is highly regulated. As a result the enzyme Glucose-6-phosphate dehydrogenase is inhibited by NADPH and also by fatty acid esters of coenzyme A.

    Glycerol is a precursor for synthesis of triacylglycerols and of phospholipids in the liver and adipose tissue. When the body uses stored fat as a source of energy, glycerol and fatty acids are released into the bloodstream. In some organisms, the glycerol component can be converted into glucose by the liver and, thus, provide energy for cellular metabolism.
    Before glycerol can enter the pathway of glycolysis or gluconeogenesis (depending on physiological and environmental conditions), it must be converted to their intermediate glyceraldehyde 3-phosphate in the following steps:
    Glycerol To Glycerol kinase To Glycerol-3-phosphate To Glycerol-3-phosphate dehydrogenase To Dihydroxyacetone phosphate To Triosephosphate isomerase To Glyceraldehyde 3-phosphate

    Now the next step.......in understanding:

    FATS STOP THE NEED FOR THE physiologic FRUCTOSE PATH...................What is this tied to? COLD WEATHER CHANGES!!!!!! but it COLD and the activation of Brown fat that liberates fats!!!! Cold empties adipocytes to make the reducing elements........need for maintanence of the redox potential. COLD increases blood flow to BAT to released nitric oxide synthetase and we empty fat by burning it at BAT sites. Insulin is not the main actor here.......nitric oxide, blood flow and the sympathetic nervous system are in COLD. HERE you see CT at work. This is tied to sympathetic nervous system response to cold. I spoke about this in CT 6. Any biochem book has it, but it is not SPELLED out. You have to read between the lines and see that electrons are handled in this metabolic trap door differently than in the first fructose PPP path.

    This glycerol 3 phosphate molecule has a special shuttle that PeataTarians forget. Paleo too. This is a metabolic pathway controlled by transition metal maxwell demons. It allows electrons to skip cytochrome 1. Using it allows cytoplasmic NADH to enter the electron transport chain. Little known area of the PPP is in play here folks...........

    They happen to have two special glycerol 3 phosphate dehydrogenases which make up the shuttle. Free in the cytosol there is cytosolic G3P dehydrogenase, which actually uses NADH to add a pair of hydrogens to a glycolysis intermediate (dihydroxyacetone phosphate) to form G3P directly.

    The other G3P dehydrogenase really does dehydrogenate G3P, back to dihydroxyacetone phosphate. But this second G3P dehydrogenase is embedded in the outer surface of the inner mitochondrial membrane. KEY POINT!!! Anyone guess why? Think what I told you special in the quantum electron blog 2 years ago about FADH2? And it contains an FAD/FADH2 moiety which takes these two hydrogens and uses them to reduce the CoQ couple, feeding electrons in to the electron transport chain. FADH2 is our special fat pathway quantum tunneler......it allows glucose to act like saturated fat when the shuttle is active in cold environments or during starvation.

    When the shuttle is working we pump electrons from cytosolic NADH directly in to the mitochondrial respiratory chain through the FADH2 tunneler. When you do this............it is electron only required and no pumping of protons. Anybody see WHY yet?

    The G3P shuttle is the key to understanding the QED mystery of the PPP.

    In leptin sensitive cells with low cytokines the signal to reject excess energy from food picks on glucose at cytochrome one because it is first in the chain. When it happens we get the development of insulin resistance from superoxide production of cytochrome 1, specifically at the iron sulphur cluster N-1a (Transition metal alert) . Lady evolution used Occams razor and made it simple for those who were willing to dig for this pathway............. to access this maxwell demon by burning saturated fats (NOT PUFA's) to generate a lot of FADH2. When you do this little molecular demon trick it cause backward bidirectional flow of a few electrons through complex I and it completely shuts down the fructose carbohydrate pathway unknown to most physical culture people, paleo, and the fruitatarians.

    You can make glucose act as if it were bacon lard or butter through the G3P shuttle. This is why cold is not hormetic.....it is primordial for all eutherian mammals. I think you have heard this statement made many times beginning in CT 4........The holy Trinity.

    CITES: 1.Journal of Applied Physiology (1984) vol. 56 (1) pp. 78-83 (shows fats do not need glycogen hammering a paleo and exerciser belief)
    2.http://www.physiologicalchemistryandphysics.com/pdf/PCP8-115_ling_will.pdf (LING's PAPER SHOWING INSULIN ACTS AT HIGHER TEMPS AND ONLY WHEN IT IS PRIMED BY 7 PRIMERS WITH A SPECIFIC -OH chemistry at carbon 3......Should make BOB feel a lot better link!!)
    3.http://www.cell.com/cell-metabolism/abstract/S1550-4131(11)00261-0 (PET SCAN SHOWING BAT BURNS SUGAR IN COLD)
    4.http://ajpendo.physiology.org/content/285/1/E216 (COLD lowers insulin and stimulates feeding which is reduced when you EAT FAT AND PROTEIN!)
  8. Jack Kruse

    Jack Kruse Administrator

    I personally think physics explains this easier than biochemistry above ^^^^^ but both arguments lead to the same conclusion........COLD BURNS FATS INDEPENDENT FROM INSULIN..........because insulin does not work well in cold by evolutionary design. Ling was the first cat who showed it needed higher temps and cytokine activation to work as biochemistry says it does in a book 100% of the time............well that is their belief.........and here is a new reality. It does not. “If you thought that science was certain - well, that is just an error on your part.”
    ― Richard P. Feynman
  9. HoneyChild

    HoneyChild Gold

  10. Danco3636

    Danco3636 Silver

    Copy, paste, print, study time.
  11. yewwei.tan

    yewwei.tan Gold

    So essentially, the surface of our body cools during CT, which cools and "stabilizes" the tissue and blood in that region, and then this more coherent blood circulates and brings energy to the rest of the body?
  12. nonchalant

    nonchalant Silver

    Nice, yewwei. Sounds like we get an oxygen and energy infusion while we CT. Sounds a bit like HBOT.
  13. Inger

    Inger Silver

    That it how it feels, indeed :)
    super energizing
  14. Jack Kruse

    Jack Kruse Administrator

  15. freesia

    freesia Old Member

    My experience of CT has felt similar to HBOT in lots of ways. :)
  16. endless

    endless New Member

    Yes, I think that is my next course of action :)
  17. yewwei.tan

    yewwei.tan Gold

    This is the first time I can honestly say that I'm not looking forward to summer as much as winter. :)

    WRT to ketosis and insulin resistance, I've been measuring blood ketone and glucose levels for more than a month now, and personally seem to get pretty much above 2.0mM every day on the blood ketone measurements, with blood glucose in the 90-100mg/dL range all the time (fasting, post-prandial, etc ...) Before going keto, I would get fasting blood glucose readings of 80-90mg/dL, so there's a slight increase there, possibly an artefact of the insulin resistance mechanisms that Peter and Dr Kruse talk about. I'm personally not too worried about it so long as ketones stay elevated.

    Another sidenote would be that I've been putting the "protein knocks you out of ketosis" theory to a test. Breakfasts these last 2 days have been literally 500g of fish (weighed raw), with very minimal carbs through the day. BHB ketone readings 2 hours after were still just below 2.0, and by the afternoon, they were back to the 2+ range.

    Contrast that to one of my prior experiments, whereby I tested for a BHB of 2.1mM before eating some beef liver and onions for dinner, and then tested at 0.6mM two hours after the meal. So 2 small onions, or around 50g of easily assimilated carbs pretty much took me out of ketosis, despite both protein and energy load being quite low for that meal (I'd say 30g protein, and maybe 600kcal for the meal). I was back into full ketosis by the next day though.

    Finally, I had a bout of protein-only overfeeding a week ago, whereby I probably consumed 1.5kg of fish and meat for dinner. Carbs were kept minimal. Ketones went down to 0.2mM the next morning, but re-bounded pretty quickly to the 2+mM range by that same afternoon. Obviously my body was able to "clear out" the protein and jump straight back to burning fat. That said, I'm still a young guy (22) sitting at 85kg and 13-15% body fat, which could possibly allow me to get away with higher protein loads.
    Last edited: Dec 9, 2013
  18. Hemming

    Hemming New Member

    Thanks a lot for sharing your measurings. Its really interesting to read other people's biohacking!
  19. yewwei.tan

    yewwei.tan Gold

    No problem. Today was pushing the limit again, with 150g protein at breakfast (2 lamb chops, almost a pound of salmon). This was at 7am.

    Right after breakfast, BHB was 0.9mM
    At 10:30am (3.5 hour post), BHB was 1.1mM, which is basically back in ketosis by most definitions
    At 3pm (8pm), BHB was 2.7mM, which is back to pretty therapeutic levels of ketosis

    Hunger is obviously nonexistent with that level of protein. Still not hungry now at 5:30pm. Now that I know my protein limits, it's time to back down the protein level until I actually get hungry by dinnertime.
  20. Jude

    Jude Gold

    2 lamb chops...and a pound of salmon as well.!.....wow ..great white shark eating there.

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