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Low carb/ insulin resistance

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

  1. As long as it is working for you, all the more power to you! I'm all for n=1's as they offer the most thorough information available... for the individual (although extrapolations can be made; I enjoy reading case studies in the literature as there is more 1 on 1 analysis and less room for error than a couple researchers surveying a few thousand people).

    I suppose my comments were made for those who are experiencing these symptoms; though I'm sure the amount of grounding you do, your Magnetico, and they type of exercise you do (MoveNat), are largely benefiting you.

    There are a lot of things that don't add up for me, though. For instance, I posted studies on the FaceBook group about Cold Thermogenesis actually enhancing carbohydrate metabolism as opposed to fat metabolism. It increases the uptake of glucose to muscle and BAT cells. This coincides with the Sherpa's true, not-so-fictional largely vegetarian, carb based diet, along with Wim Hoff's vegan diet. I agree with Jack's points in the early CT blogs about extremophiles and viewing extremes, or 'outliers', with an objective eye and applying that knowledge to us. The thing is, there is extremely strong evidence of life evolving near and at volcanic bases, as opposed to the oceans, and thus it renders a lot of things we are learning not so useful (though I still believe in CT, oxytocin, hebbian learning, etc.).

    For instance, in 1965 and 1973, Sidney Fox showed that polymerization of amino acids into protein is energetically costly in water, but it creates structures, with bilayer 'membranes' and catalytic action, in dry environments. Earlier, in 1904, Nathansohn made an observation that water-soaked lecithin lost it's oily properties and became rather hydrophilic; the membrane should exclude water-soluble molecule while 'allowing' oil-soluble molecules.

    I just don't see why one would want to invoke insulin resistance to somehow control blood glucose levels... especially when seasonal eating is advocated. You won't spontaneously be insulin sensitive when spring/summer roles around just because the light cycle says so - the longer the duration of, and the more extreme the severity of IR, the worse of your pancreatic beta-cells will be, and that is mostly irreversible. It just seems as though living a life of cold, darkness, and extreme nutrient restriction (carbs) is just a life of stressors that are only useful if buying into the "Rate of Living Hypothesis" and expending energy leads to a shorter life.
     
  2. Danco3636

    Danco3636 Silver

    I know Ray Cronise talks about non shivering CT burning primary fat and once shivering starts glucose is burned form the blood and muscles. Now this may be different for someone already depleted of glucose through a keto diet and PPP adapted. Perhaps a different pathway or the PPP works different in the mitocondria and ATP production.

    But I am glad to see your questions as I am
    curious as well.
     
  3. I have not read this in its entirety as I have to finish some exams and get to bed, so don't quote me, but this seems to indicate that glucose metabolism is associated with the PPP, which coincides with the Wikipedia page stating that the PPP is an anabolic alternative to glucose metabolism, creating pentoses and reducing equivalents:

    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC290807/pdf/jcinvest00305-0030.pdf

    Very first portion of the study: "Mature human erythrocytes possess the enzymes necessary to catabolize glucose to CO2 via pentose phosphate pathway (...)It has been demonstrated that human erythrocytes deficient in glucose-6- phosphate dehydrogenase (G6PD) are unable to maintain their level of reduced glutathione upon incubation with a variety of agents."

    You can see glucose metabolism's role in the PPP here: http://en.wikipedia.org/wiki/File:Pentose_Phosphate_Pathway.png (in fact, you can see fructose's role, as well)
     
  4. yewwei.tan

    yewwei.tan Gold

    This makes me think of an old comment from Lyle McDonald regarding dieting to achieve a contest bodybuilder's level of leanness (5% bodyfat). He often talked about how it was better to be systemically insulin resistant, because it essentially reduced the ability for the muscle to uptake glucose, and thereby allow for greater burning of body fat. I could possibly see how the same mechanism is playing a role in someone who has too much fat.

    I also remember John Keifer talking about you can get the best of both worlds, by eating a generally ketotic diet, and only consuming carbs after up-regulating GLUT-4 translocation in skeletal muscle (through weights training) as a non-insulin mediated way to shuttle any carbs that are consumed into muscle cells (the keywords here being "non-insulin mediated").

    As Jack said, the key is to get the fat cell to become insulin resistant. It's all about getting rid of old fat cells and their cellular signalling mechanisms.

    I need to take a look at some of Peter Attia's writing. If I recall correctly his experiments showed insulin sensitivity improving during his 2-year ketogenic protocol.
     
    SCRN2007 likes this.
  5. Hemming

    Hemming New Member

    Yes, Peter's markers improved a lot. From having metabloic syndrome (more or less) he reversed it so to having pretty good markers on everything.
     
  6. Jack Kruse

    Jack Kruse Administrator

    Gretchen I think you're missing another key point.......you want your BG high if you have T2D and PCOS. The whole point of a ketogenic diet in these particular cases is to induce starvation-appropriate physiological insulin resistance to protect your mitochondria from the bad side of superoxide due to poor quantum tunneling. If the BG stays up despite your actions it means you might have ruined your mitochondrial DNA genes for transcription of the Cytochrome proteins.
     
  7. Jack Kruse

    Jack Kruse Administrator

    dude you continually mix data of those with proper quantum tunneling and those who dont...........STOP. Realize there is a difference.
     
  8. Jack Kruse

    Jack Kruse Administrator

    And then Ray tell you to eat a diet that screws the good cold advice up..........BAD.
     
  9. Jack Kruse

    Jack Kruse Administrator

    Gretch: Failure to develop physiological insulin resistance during starvation is instructive to those with bad mitochondria because both clinical cases results in hypo-glycemia and cravings/hunger. So the raised BG in you helps you reverse these things because your mitochondria not so good.....This is a basic reason the Leptin Rx and CT work in unison.
     
    SCRN2007 likes this.
  10. Jack Kruse

    Jack Kruse Administrator

    Hypoglycemia is a signal of impending doom for the brain.......never forget it. That is why when someone has to eat 6 times a day......youre in deep shit.
     
    SCRN2007 likes this.
  11. Shijin13

    Shijin13 Guest


    Ok. I think I understand Jack but want to verify. that a High FBG with T2D/PCOS while eating Keto is a good thing. however, if I'm eating this way, and taking Met/Cycloset - and the FBG doesn't come down - its a bad thing b/c it means I can't by pass the leakiness at Cytochrome 1 using Met/cycloset? which means any superoxide I make - from met highlights my dehydration, and poor quantum tunneling. I understand how the high FBG in T2D/PCOS is beneficial when Cold Adapted - I get that. but what's confusing me is I think you're saying that If while on the Met/Cycloset - if my FBG doesn't come down in the cold its a bad thing? This year we've noticed on my labs - that as we've moved into winter my FBG is Higher than summer. If I'm ketotic - wouldn't that be expected. We've seen small changes in my HbA1C since starting on cycloset. Prior to the cycloset it was 5.6 for the past year the spring/summer HbA1C drops to 5.2 and rises to 5.4 in the fall, and drops to 5.3 in the winter.

    I'm just trying to figure my body's responses over time/seasons. I know from testing at home my FBG always runs higher (consistently over 95) toward the end of my cycle (After cd 21 -which is when we run these labs.) maybe I should be running fBG/HbA1c at different points in my cycle to see if the FBG is constantly high - or only high after CD21?

    I also know from my lab work prior to going high fat low carb moderate protein - my FBG ranged btwn 85-89. but as I went below 25g of carbs the FBG increased....
     
  12. Shijin13

    Shijin13 Guest

    so If my cravings are entirely fat/seafood related what does that mean? You know that I used to crave dark chocolate like it was going out of style - there are days 90% - on up to raw cacao nibs are gross - the thought of eating them is un appealing. but 2-3lbs of sahsimi -game on!; seaweed its on. butter, ghee, coconut oil, bacon fat, duck fat - check. I'm now eating 2-4TBS of pure fat w/every meal b/c its what my body wants - and nothing else. my next question is how do carbs that turn SCFA, such acetic, propionic and butyric acid play into this???? you've mentioned before that carbs that convert to butyric acid can be a good thing - when in season. Going back to how Glucose is use to protect when Cold adapted and in Ketosi and fructose can buy pass the protective mechanisms of COLD and KETOSIS.....
     
  13. Jack Kruse

    Jack Kruse Administrator

    Pkarlson asked about the cabinnoids earlier in the thread........so here ya go: The hypoglycemia biologic message has to be converted to the chemical neurotransmitter in the brain and SC to alter firing and affect behavior in the frontal lobe. Remember neurons that fire together wire together. Oddly enough, a derivative of linoleic acid is a neurotransmitter. Linoleic acid is the parent molecule of the endocannabinoids. Linoleic acid (LA) is an unsaturated omega-6 fatty acid. So a diet in excessive O6's is an issue.......Most people have heard of the munchies, well this is where it comes from. In my opinion biology will find out shortly that eating linoleic acid will often lower your blood glucose level. This low GB is what stimulates the munchies due to endocabinnoids from the action of linoleic acid in the brain.

    In my opinion this is the number one way T2D get made in the USA.......PUFA to excess.......and by PUFA I am not speaking of omega 3 PUFA which I told you in BG 5 is not USED FOR METABOLIC FUEL.........IT IS RESERVED FOR THE BRAIN!!!!! In humans.
     
    Last edited: Dec 4, 2013
  14. Jack Kruse

    Jack Kruse Administrator

    Going real low carb made your BG spike because your body is telling you your mitochondria are TOAST. So you need physiologic IR to stay well.
     
  15. Jack Kruse

    Jack Kruse Administrator

    COLD AND KETOSIS IS FOR THOSE WITH BAD QUANTUM TUNNELING
    ...........how many ways do I have to say it?
     
    Danco3636 likes this.
  16. Shijin13

    Shijin13 Guest

    OBviously this today - my brain isn't firing on all cylinders....
    Ok so I need Cold and Ketosis (I've got that and you know I get into the cold tank & eat my fat/seafood) to get into a physiological Insulin Resistance. How do I test to verify that I've moved from pathological IR to Physiological IR???? What Am I looking for diagnostically?
     
  17. Jack Kruse

    Jack Kruse Administrator

    You already did it..........!!!! your BG is high! it means your peripheral cells are IR..........already!!!
     
  18. Jack Kruse

    Jack Kruse Administrator

    Key point for O6's: This is where JanSz needs to pay attn......and where Patricia Kane is on thin ice. The balance of O6's to O3's is critical. They advocate higher levels of O6's than I am comfortable with in those with bad mitochondria......now I dont think Jansz has bad mitochondria......so that is why he touts Kane's work..........but People who cant tunnel well on their inner mitochondrial membrane need to BEWARE of the this. DALI DULA alert. THis is where we get a lot of T2D. EXcessive or unbalanced Omega 6 fats appear to be great for putting fat in to adipocytes. Adipose hyperplasia appears to be the key to maintaining insulin sensitivity during weight gain. Omega 6 fats are great for generating adipose hyperplasia. What do O3 from seafood prevent? They alter M1 and M2 macrophages so they help maintain IR peripherally.......and they make you insensitive to insulin while the O6's diets allow you to become very very insulin sensitive and you get fatter and sicker.........The people with a better O3/O6 ration get fatter but they don't develop metabolic syndrome because of the macrophage change.......if you got an AI on top of all this it is another layer of complexity.
     
  19. Jack Kruse

    Jack Kruse Administrator

    BG being high is good for those with bad mitochondria.......because it is a signpost that your cells are IR protecting your mitochondria......modern medicine and obsesity researcher have the world thinking high BG is bad........It is not......It will be higher in colder climates or in those who CT like MAD.
     
  20. Jack Kruse

    Jack Kruse Administrator

    I told you long ago in the mitochondrial series that aspirin is an uncoupler of ETC.........go look.......why is that a big deal to those who cant tunnel if you're following me? The obesogenic effect of omega 6s can be blocked by drugs like NSAID's, a cyclo oxygenase inhibitor. This is why if your mitochondria are bad you need to have a doc to understand this nuance.......NSAID's are also two edged swords for humans.......they can help or they can kill you based upon your context.
     

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