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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

    Working on an Infographic for this one as well....

    Dali- I'm wondering if my issues - are directly related to the flares I've been having - I seriously wonder if I don't actually have hashis? I also have the high FBG - even though I'm on both Met and Cycloset.... my PCP is actually testing me on the 16th to look at my beta cells - she wants to rule out any potential problems w/ expensive labs before the year ends..
     
    Josh (Paleo Osteo) likes this.
  2. Jack Kruse

    Jack Kruse Administrator

    There is a big step to make......It is the redox potential of the inner mitochondrial membrane. I have not given you enough yet to go further.......but that post is coming and it is a doozy. But I will wet your appetite with this: The drop in inner mitochondrial membrane voltage is very protective against reverse electron transport through cytochrome one. This is why T2D need lots of ketones. It limits superoxide generation from reversal of flow. The transitional metals in Cytochrome are all targets for non native EMF and the the flow of electrons is controlled by the electromagnetic force. The direction of the current is controlled by the redox potential or voltage across this membrane. I've been talking redox here for a while.......now you know why.
     
  3. Jack Kruse

    Jack Kruse Administrator

    This last step in mitochondria confuses the obesity researchers all the time because they do not understand the key is the electromagnetic force. They look for a biologic switch that does it....This ketone effect is an enigma to them because as MCTs spike insulin levels in this case at a period of time where glucose can be high or low. It actually does not matter. The effect is a QED quantum tunneling effect.......they do not understand one iota of this. This is why.
     
  4. Shijin13

    Shijin13 Guest

    SO WAIT? Are you saying the Superoxide generation from Cytochrome 2 as part of the voltage drop at the inner mitochondrial membrane, and increasing electron transport through quantum tunneling a la transition metals is a redox pathway?????

    ETA assuming you've mitigated the effects of non-native emf????
     
  5. Jack Kruse

    Jack Kruse Administrator

    Its been well known from the 1990's that high insulin levels for any reason at all cause phosphorylation of the cytochromes.........and guess what? This is what is a problem. What did I tell you about CT and insulin? below 62 degree insulin can not work.......therefore insulin can not phosphorylate the cytochromes regardless........this is the magic of CT. It has a direct effect on quantum tunneling to increase the flow of electrons using the Hall current found by Becker.
     
  6. Jack Kruse

    Jack Kruse Administrator

    To gain control Gretch of BG you need to induce physiologic insulin resistance to have a normal blood sugar. An altered ASI and melatonin screw that up and so will even a small amount of the wrong seasonal carbs with your ketotic diet........The end result will still be the failure to develop the essential physiological insulin resistance which is needed to keep blood glucose normal as we see in fasting animals and humans.
     
  7. Shijin13

    Shijin13 Guest

    so CT is the key, along with diet and a perfect ASI and Melatonin panel - to achive physologic insulin resistance. should be doing my Salivary ASI/Melatonin tomorrow or Thrusday....
     
  8. cantweight

    cantweight Gold

    Feeling the universe juice today, just walked in from the docs with labs in hand. Gretch...I am an AI mess in the last month out of left freaking field. Swollen hands, painful knees and knuckles, the most crazy cystic acne, my skin burns, lupus eyelids (dont know what it actually called)...etc. I am a mess.

    PCP had labs galore (I am also PCOS)
    hsCRP high at 2.8, Lp-PLA high , lipid profile optimal, metabolic and renal optimal
    Glycemic control labs all optimal, beta cell function all optimal.

    free fatty acid moderately high
    a-hydroxybutyrate high
    oleic acid moderately high
    linoleoyl-gpc high
    IR score calculated high
    HOMA-IR score calculated optimal

    Everything else shows me as the healthiest fat person I could hope to be.

    Also MTHFR C677T and MTHFR A1298C

    So completely IR also adipose IR and low risk of T2D...I am both happy and confused. Going to re-read this thread and some blogs. It is always going to come back to Ct and mitochondria for me....accepting this :)
     
  9. Jude

    Jude Gold

    It's hard to believe that you actually found an Aussie GP to order all those tests for you....just amazing......haven't even heard of some of those tests you've had! Do those results..... high fats ........mean yr o6/o3 ratio is out?
    free fatty acid moderately high
    a-hydroxybutyrate high
    oleic acid moderately high
    linoleoyl-gpc high
    IR score calculated high
    HOMA-IR score calculated optim
     
  10. cantweight

    cantweight Gold

    Im in the states Jude. Yeah my o6/o3 is off. All within ranges but doc said EPA and DHA need to come up and o6 could go down. Total omega-3 9% total omega 6 33%
     
  11. JanSz

    JanSz Gold

    I have found this on 23andme.
    How serious is having TT genotype?
    Is it still worth to eat Metformin?



    Contrary Studies None
    Applicable Ethnicities European
    Marker rs4585


    In this study, researchers examined metformin response in 3,920 individuals of European ancestry with type 2 diabetes. A positive response was defined as achieving an HbA1c level below 7%. The researchers found that individuals with the
    GG genotype at rs4585 (which is equivalent to the SNP reported by the researchers) in the ATM gene had 1.35 times higher odds of having a positive response to metformin treatment
    compared to individuals with the GT genotype,
    and individuals with the TT genotype had about 0.75 times the odds of having a positive response.


    ....
     
  12. Danco3636

    Danco3636 Silver

    I just get confused. I seem to have so much to learn or so much to question on my own knowledge. But one thing I am good at is applying.
    So in the mean time it is 100% ketosis epi-Paleo diet with no carb refeeds. CT as much and often as I can. Minimize EMF as best as I can. Ground - connect to nature and the outdoors daily. That and have a good attitude and rock this life. My quest to optimize the PPP for health and performance.
    Thanks Jack for dropping these "bombs". Though I may not complety understand it doesn't stop me from applying and seeing the effect. My n=1
     
  13. caroline

    caroline Moderator

    This is what JK said in the Q&A.......we don't have to understand it all - but we do have to learn how to apply it to ourself for the best outcome...
     
  14. This is confusing me entirely. I don't mean this offensively, so please no one take it that way. I feel as though I'll get banned after this, but, so this is the logic:

    To reduce blood glucose and insulin levels, prevent diabesity and metabolic syndrome, we must go low or very low carb and enter ketosis. According to recent posts in this thread, ketones will and should create lactate for use; we do this even though ketosis replicates the metabolism of diabetics, and diabetes produces lactic acidosis (Scale T, Harvey JN. Diabetes, metformin and lactic acidosis. Clin Endocrinol (Oxf). 2011 Feb;74(2):191-6 & rawford SO, Hoogeveen RC, Brancati FL, Astor BC, Ballantyne CM, Schmidt MI, Young JH. Association of blood lactate with type 2 diabetes: the Atherosclerosis Risk in Communities Carotid MRI Study. Int J Epidemiol. 2010 Dec;39(6):1647-55. Epub 2010 Aug 25). So, we are to replicate the metabolism of diabetics through dietary choices, and then are left in the blue as to why we develop diabetic-like symptoms...?

    There are, of course, different forms of insulin resistance; Lucas Tafur has very thorough blogs on this, so one eating a high-fat diet must be wary of this simple (yet complex) facet of metabolism. Regardless, I see no reason why one would want to induce insulin resistance as a therapeutic modality. Frayn KN, Williams CM, Arner P. Are increased plasma non-esterified fatty acid concentrations a risk marker for coronary heart disease and other chronic diseases? Clin Sci (Lond). 1996 Apr;90(4):243-53. Plasma FFA are typically elevated in obesity, diabetes, and old age. I think Chris Masterjohn and Paul Jaminet's perspectives serve as an interesting read on this topic (I'll leave Dr. Peat out of it for now:))

    Have any of you checked your thyroid thoroughly? TSH is a very poor and inaccurate marker for thyroid health, as are most (if not all) blood tests, as they don't establish tissue levels which can be far off. Body Temp, pulse, the Achilles reflex test, T wave on an electrocardiogram, are all good. Blood tests for total thyroxine and T3 are okay, too. I suggest reading McGavack's The Thyroid is a good read, I'm about to go through it. Dr. Broda Barnes books are definitely worthy as well.
     
  15. Danco3636

    Danco3636 Silver

    Interesting BigPapaChakra777 I am a bit confused on it too.
     
  16. The most logical thing to glean from the literature in addition to peoples experiences are: ketosis = a short term super-fuel, and a long-term degenerative fuel. I think ketones are great, but there are ways to achieve that without carb restriction (BHB-salts, ketone esters, MCT Oil, coconut products, exercise, etc.). Or, perhaps the long-term negative effects of ketogenic diets are from non-esterified PUFAs which are damaging to the body:

    Hong-Mei Zhang1, Howard Dang2, Chih-Ko Yeh3,4, Bin-Xian Zhang1,4. Linoleic Acid-Induced Mitochondrial Ca2+ Efflux Causes Peroxynitrite Generation and Protein Nitrotyrosylation. PLoS ONE 4(6): e6048. doi:10.1371/journal.pone.0006048.
     
  17. caroline

    caroline Moderator

    Dr. Jackson has told us a couple of times now that a TSH is useless ...it only confirms that the brain and thyroid are talking - nothing else.
     
  18. Danco3636

    Danco3636 Silver

    Seems Jack in the past has advocated full time epoi paleo ketosis when in an altered field. Which is really for most all of us in these times. But to really express the benifits and make it work we need CT..... That is my understanding they need to work together to make the dance and to really express the benifits and unfold the potential of the PPP. So hopefully I don't have it wrong because thatnisnwhatbinhave been doing for a while now and feel pretty dang good!
    Again I am just learning and trying to get my head around it.
     
  19. Danco3636

    Danco3636 Silver

    Some Notes:

    Cold makes proteins and enzymes bend in different ways than occurs in warm states.

    Enzymes adapt at extremes to allow for ideal function and ideal signaling to improve metabolic efficiency.

    The best food source then for a cold adapted mammals biochemistry would be a ketogenic paleolithic diet that has a high omega 3 content.

    Ketosis is most efficient mammalian fuel in the cold not carb loading.

    Many think this is reversed because all the research is done on warm adapted humans eating the wrong diet.

    Burning fat actually increases our VO2max when the cold adaption is induced. Being adapted to fat is better for performance too. It increases strength and power because the cold increases the steroid receptor for steroid binding. This means your Growth Hormone and testosterone levels surge as you cold adapt over 2-3 years. No one studies it that long.

    This is my experience so far - "My experiment of one".

    It's not for everyone but we will see where it goes.
     
  20. Danco3636

    Danco3636 Silver

    One more of my notes:

    You must become a fat burner using the PPP because this will limit excessive ROS mitochondrial leak when you environment is littered with man made EMF waves.

    This means that a high fat diet is the preferred diet to mitigate an excessive man made EMF risk to biology. This means that what we have believed to constitute a healthy diet can no longer be true in an altered field.
     

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