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A fairly simple explanation of methylation?

Discussion in 'Beginners Area' started by sooperb, Mar 15, 2014.

  1. sooperb

    sooperb New Member

  2. Shijin13

    Shijin13 Guest

    Nice.... but they do miss the context of how methlyation turns on or turns off dna and rna... as Jack discussed in the Sept 2013 Webinar....
    seanb4 and Danny like this.
  3. cantweight

    cantweight Gold

    That's great Sue...I like a concise breakdown...too much info sends my ADD brain off in too many directions and I sometimes miss the point!
    I like to call it the MoTHerF****R gene.
    A whole house full of us. Some hetero, some homo, and some compound....fun. Finding N=1 x 5 is a math a equation I have not yet mastered. I hate math.

    Dr K has said Sam-e forever and I have yet to add that one...as well as molyb....think I'm gonna have to give them a go.

    Just got labs back on my youngest this week and his B12 was high, mag and D low, and t3 low. Thinking the t3 may be a result of biotoxin and not a thyroid issue. Holding off on dosing the cytomel until we get the C4a and Alcat mold panel back.

    Oh the joy of figuring all of this crap out! Sometimes I wish I was one of those people that didnt have to think so damn much about everything. It can be exhausting!
    Angie Medler, Cpt.Tired and Danny like this.
  4. Lahelada

    Lahelada New Member

    I like the simple explanations too. Reading Jack after that I can fill in the missing blanks or see what the error /omission was of whatever I read somewhere else.
    Mike David and seanb4 like this.
  5. Josh

    Josh New Member

    This podcast is Dr. Kruse's "simple" version:


    Tim Jackson's:


    Nancy Mullan's:


    Amy Yasko's


    Kendall Stewart:


    As blind people, putting our hand on the different parts of the elephant gives us a fuller idea of what we are touching and feeling.....
    Last edited: Mar 15, 2014
    Amber Ament, seanb4, Danny and 3 others like this.
  6. Shijin13

    Shijin13 Guest

    These are great resources!!!!
  7. Melanie Procter

    Melanie Procter New Member

    OMG. This thread is the real 101 to this topic. Thanks for everyone who has compiled these links into this thread. I will use this as a resource. I like the way Jack described the biochemistry approach to this health challenge. He stated we are looking at a 30 foot view. I am compiling all three of these interviews to put together a protocol for myself. I have started with Jack's approach as it something I can do with diet. Thanks again everyone for this compilation. We are a lucky group of people to have each other, Jack, Misty and all the experts they are bringing to us.
  8. Jack Kruse

    Jack Kruse Administrator

    Well I am going to warn you now.......Prior to the May 2014 webinar it will be required you re-listen to what I said to Tim in that blog talk radio podcast......because if you listen closely.......i was just swimming on the surface. In the May 2014 webinar we are at the ocean floor drilling into the mantle. It will be probably the best webinar I have done. It was that good. March thru April are all linked conceptually.
    Danny likes this.
  9. Melanie Procter

    Melanie Procter New Member

    I have already listened to it twice. I will definitely listen again as it really is a good one. Actually, your approach is much easier than the biochemistry approach. Although, I wonder if you feel we need to combine the two if we have the defect. If we get on the diet you suggest in the blogtalk podcast, would we most likely still need all the transdermal supplements? Will taking on a 90 percent water based ketogenic diet bring about a solution to the MTHFR defect? Or will supplementation still be required in most cases? I am guessing that such a large percentage of caucasians have this defect as our ancestors lived off carbohydrates just 2-3 months of the year so we were fat burners. Perhaps this enzyme wasn't necessary for our "fat burning ancestors". If the story is really that simple, then becoming a a fat burner could potentially solve the problem. I hate to be too simplistic. I am just thinking that the protocols suggested in this blog do allow the solutions to be a bit simpler.
  10. Sujoe123

    Sujoe123 New Member

  11. Sujoe123

    Sujoe123 New Member

    Do some reading on methlymalonic acid....there is a difference between absolute and functional deficits. MTHFR is not the only methylation SNIP that can affect B12 status.....just the most famous one.
    Last edited: Nov 20, 2016
  12. Jack Kruse

    Jack Kruse Administrator

    This will be no surprise to my members but it may be new to you. Vitamin B12 and Vitamin D 3 are linked to solar exposure. If you lack sunlight, leptin resistance develops and diseases that ruin the NAD+/NADH redox couple at cytochrome 1 becomes ruined. Obesity and T2D are diseases of darkness due to a lack of sunlight. Obesity and T2D are effectively spectral solar deficiency diseases. A lack of solar light during the day is one side of T2D and obesity, but the presence of blue light at night effects another pathway that the human eye uses at night to optimize the mitochondrial in melanopsin, RPE, and the central retinal pathways that control the eye clock mechanism that controls circadian cycles. The absence of blue light at night is critical light effect needed to catalyze the solid state conversion of serotonin by using the process of methylation. Methylation during darkness mediates circadian clock plasticity both in the SCN and in the peripheral clocks. This solid state biochemical process requires a large exclusion zone (EZ) and the presence of vitamin B12 and folate. B12 is made in the liver under the presence of SOLAR daylight. Folate, on the other hand, is destroyed by full spectrum sunlight and it is produced under darkness when blue light is ABSENT. These are the two chemical arms that tell the quantum clinician if a patient is solar deficient and/or blue light toxic. Obesity and T2D are two such quantum diseases that manifest when this situation occurs in humans. B12 and Vitamin D3 are linked to specific sunlight frequencies and this is why pernicious anemia is associated with a lack of sun. In fact, most anemias are related to a lack of proper solar exposure. This link to anemia and B12 was found by Fritz Hollowich in the 1940's. In fact, I have found a link to low solar exposure and low B12 that dates back to 1927. It seems these links are well published on a long time ago but seem to be unknown by modern humans. It is nice to see medscape making the connections. T2D and obesity are epigenetic diseases of light that ruin cytochrome 1 and the Q-cycle. http://www.medscape.com/viewarticle/872008
  13. Sujoe123

    Sujoe123 New Member

  14. Sujoe123

    Sujoe123 New Member

    A methylmalonic acid test ( serum) is a functional marker for B12 deficiency. The type of B 12 in most vitamins is not methylated. (cyanocobalamin) and can still show high serum levels of B12 but it is not usable....There is a difference in an absolute deficiency and a functional deficiency. There are many SNP's that can effect this....upstream, downstream, point of conversion.....The SNP(s) can be too fast or too slow in their enzymatic efficiency.
  15. Jack Kruse

    Jack Kruse Administrator

    simple version is in reality series.......who saw it?
  16. Sujoe123

    Sujoe123 New Member

    The one with Tim Jackson??? yes listened today!
  17. Chase Gozon

    Chase Gozon New Member

    good read, thanks!
  18. Jack Kruse

    Jack Kruse Administrator

    The Patreon explanations are foundational for MTHFR and so where the member conversations on the beach in Jan 2018
  19. BrunoB

    BrunoB New Member

  20. Lois Hollan

    Lois Hollan New Member

    One has to be very careful in understanding forms of "folate" here. The synthetic folic acid that we eat like candy--and put in lots of our foods--is fine for some people, but deadly for those with the MTHFR polymorphism. That's because--with the polymorphism--we cannot break down the synthetic form of folate (folic acid) and it builds up in our systems, thus becoming a carcinogen. (Recall the scare years ago--that was the discovery that prompted the scare.) So it works for those with the normal C677T genes, but not for those with the mutation. If one has one or both mutations, avoidance of folic acid in synthetic form is necessary. It can be taken--and the person will feel great for a short time--then begin to feel absolutely terrible and wonder why. With the MTHFR mutation, one must take the natural form of folate--methylfolate. It is available. And many good researchers suggest methlyflolate and folinic acid. But there's one critical thing: Do not take a lot! Take very, very little every day. It will help. So, the warning is that this inability to synthesize folate is fixed only by supplementation of the natural form and is hurt by supplementation of the readily-available, drugstore form of folic acid. I can go on about this, but this is enough for now! Happy to answer any questions to the best of my ability.

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