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  • Koncentrated K from k-vitamins

    Anybody hear of CAC reversal from using Koncentrated K? High doses of EPA and DHA and D3 too?

  • #2
    Dr. Brewer has a very interesting video on plaque reversal.

    https://youtu.be/ysifMKWKZLY

    And another one on vitamin K:

    https://youtu.be/ulemSPBA3DA


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    • #3
      An interesting podcast on Ivor Cummins where he interviews Patrick Theut who reversed his calcification on main by high dosage of Vitamin K ( K1, MK4, MK7 ) plus among other things like Keto, Mg, B Complex, Vit D etc. Very interesting and hopeful! Planning to buy that K-vitamins. Thoughts?


      Want to Reverse Your Calcification and Heart Disease? Biochemist Patrick Theut put in 16,000 hours of study over many years in order to address and resolve his extensive heart disease issue. And he did it. Fat Emperor Podcast, Episode 21 reveals the solutions which enabled Patrick to reverse his calcification and disease process.
      https://thefatemperor.com/want-to-re...-podcast-ep21/

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      • #4
        In a nutshell I respect Ivor Cummins, and I have been taking a large dose of K vitamins for a while. The problem with the referenced podcast with Patrick Theut is that it ran from the true to conjecture to outright BS at times with Ivor trying to rein in some of the BS along with a heavy dose of conspiracy. Perfect video for the Internet. There was a whole lot of hand waving without any technical notes to back up what the person was saying, and so it becomes difficult to fully understand where the conjecture led on but the outright BS was obvious. Patrick Theut kept throwing in that he is obviously right because he was trained as an engineer and biochemist. It wasn't apparent to me in his explanations that that training helped.

        I am definitely a believer in getting a CAC score done and understanding the risk factors for cardiovascular disease. Unfortunately, often when we try to simplify biology to make it understandable, there are issues (e.g. LDL-C is bad, HDL-C is good; gave rise to the myth that LDL-C doesn't cause heart disease). We don't really understand the context upon which the concept is true and where it enters conjecture (which is so easy to do). In this case the villain is calcium; bad, bad, bad calcium. You would think that calcium kills many people. I will say that in fact, in the right context, calcium has extended the lives of countless millions of people. When we think that calcium is bad, it is sort of the same as saying that a heart is a terrible organ because it gives us heart disease. Ridiculous, right? Context matters a lot, and sadly there is a lack of context when calcium is discussed on these Internet videos.

        When the combination of lifestyle, genetics and age eventually catches up to all of us, we start to develop cardiovascular disease. Dr. Brewer has lots of videos on this, and no point on regurgitating all of that information. Our body tries to lessen the impact of the damage by bringing in calcium to stabilize the soft plaques. As that happens, the soft plaques eventually become more stable calcified plaques with a much lower risk of rupture that would result in a clot causing a heart attack or stroke. How does calcium save so many lives in the right context? Think about people with 90% blockage of one or more arteries in their heart. The blockage(s) are the result of a series of soft plaque deposited which is over time calcified, sort of like tree rings (forensic scientists can count these). What would happen if there were no calcium coming in to stabilize the plaque? Those people would almost surely have died years earlier. I have heard of people living multiple decades with a lot of stents. It rarely is the mostly blocked artery which causes the heart attack contrary to what some people think.

        What do statins do as a beneficial side effect? They typically increase calcification of soft plaque, resulting in a more stable plaque. However, this also causes a CAC score to go up. If a person believes that a CAC score is the end all, be all of cardiovascular disease risk knowledge, then there is an issue. The risk models that were based upon population studies don't include the statin effects. If a person taking a statin has frequent CAC scores done and the score increases, is it because of their lifestyle laying down new soft plaque, older plaque finally being calcified or the statin itself driving the calcification process. I haven't found anybody who knows, and I think that this is an area of interest to many people. I am open to information that is firmly based upon biology and not somebody doing hand waving.

        One final point, as the people who put a lot of emphasis on CAC scores discuss, the ultimate goal would be to try to reduce their CAC score. In theory, a notable goal. Some people have done so, including the video by John Lorscheider on this. What does it mean biologically when a CAC score goes down? We pretty much know what it means when a CAC score goes up, maybe sometimes not why. When a CAC score goes down, obviously calcium is taken out. John mentioned in a video that that result didn't appear to de-stabilize plaque, and John was thorough in his approach to health issues. However, some at least tout that they reduced or even eliminated their heart disease because of reversing their CAC score. Did the calcified plaque which becomes less calcified sort of disappear? I am skeptical of this, but again open to new information that is biology based. If the plaque is still there, then has the risk of heart attack/stroke really been reduced as some people state? I am again skeptical and hoping that some researcher will take a good look at the multiple n=1 self experiments to provide an answer. For those who believe that a CIMT test has validity, it would be interesting to get before and after CIMT tests to assess the plaque burden change. If we think about science and biology of our bodies, be open but skeptical.
        Last edited by Tom; 05-16-2019, 05:57 AM.

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        • #5
          Thanks for your detailed response! I see your larger point! I had similar doubts too! It did sound too good to be true!
          I hope I am proven wrong for rest of the mankind!
          Few of my conjectures based upon what I understood so far....
          Originally posted by Tom View Post
          What do statins do as a beneficial side effect? They typically increase calcification of soft plaque, resulting in a more stable plaque. However, this also causes a CAC score to go up. If a person believes that a CAC score is the end all, be all of cardiovascular disease risk knowledge, then there is an issue. The risk models that were based upon population studies don't include the statin effects. If a person taking a statin has frequent CAC scores done and the score increases, is it because of their lifestyle laying down new soft plaque, older plaque finally being calcified or the statin itself driving the calcification process.
          Assuming a patient after discovering of CAC score with medium risk, corrects his lifestyle with LCHF/IF and lowers TG,A1C < 5.5 and brings TG/HDL ratio < 1.5 , increases Vit D , insulin sensitivity, based upon these markers per Dr Brewers videos and the Ivor's podcast with Theut:
          1. HDL should start reducing this macrophage/plaque ( with help of K2, Mg, CoQ10 )
          2. Vit K, with its extra dosage removes the calcium ( with help of Mg)

          If yes, then statin kinda defeats the purpose by calcifying it and I thought its calcification that hardens the arteries and increases BP. ( coming from biologically challenged guy )

          One final point, as the people who put a lot of emphasis on CAC scores discuss, the ultimate goal would be to try to reduce their CAC score. In theory, a notable goal. Some people have done so, including the video by John Lorscheider on this. What does it mean biologically when a CAC score goes down? We pretty much know what it means when a CAC score goes up, maybe sometimes not why. When a CAC score goes down, obviously calcium is taken out. John mentioned in a video that that result didn't appear to de-stabilize plaque, and John was thorough in his approach to health issues. However, some at least tout that they reduced or even eliminated their heart disease because of reversing their CAC score. Did the calcified plaque which becomes less calcified sort of disappear? I am skeptical of this, but again open to new information that is biology based. If the plaque is still there, then has the risk of heart attack/stroke really been reduced as some people state? I am again skeptical and hoping that some researcher will take a good look at the multiple n=1 self experiments to provide an answer. For those who believe that a CIMT test has validity, it would be interesting to get before and after CIMT tests to assess the plaque burden change. If we think about science and biology of our bodies, be open but skeptical.
          Yup, it may not be CIMT test, but a CT angio is needed to assess the amount of stenosis and plaque built up. So to summarise what I said earlier - Probably the best case scenario is to after altering the lifestyle, take low dosage Crestor for couple of months to stabilise plaque / reduce inflammation and then use K2 to remove the calcium and HDL to remove the plaque?

          I am planning to buy that K2 anyways, do you see any risk with high dosage K?
          Last edited by VenSub; 05-19-2019, 03:44 PM.

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          • #6
            I agree that getting the right micro nutrients (vitamins, minerals, etc.) and macro nutrients (carbs, protein and fats) along with a healthy lifestyle (sleep, exercise, stress reduction, etc.) will make a huge difference in managing any chronic disease including cardiovascular disease. I will have to do some searching as I don't recall seeing studies that indicated that vitamin K2 will pull macrophages out of plaques. I have been taking vitamin K1/K2 under the assumption that the vitamin K2 will direct more calcium to my bones rather than have calcium coming out of the bones and into the blood stream. The macrophage/plaque response is an inflammatory response, and there is a generic resolution of inflammation using resolvins (associated with fish oils). If a person in particular lowers their cardiovascular inflammation, then along with a healthy lifestyle they can see a reduction in their plaque burden over time. Two drugs are known to reduce cardiovascular inflammation, statins and ACE inhibitors. Our arteries getting stiffer with age, probably due to a lot of reasons. If calcified plaque is stable and doesn't impair blood flow too much, then I see no reason to try to mess with it because it is the soft plaque that will cause a heart attack or stroke. Preventing additional soft plaque from being laid down should be the real health goal.

            After thinking about this for a while, it seems to me that the MESA risk model is based on people not changing their lifestyle. So if you have a CAC score of x and you don't change your lifestyle, then your risk of getting a heart attack in the next ten years is some amount for your age cohort (since age is one of the most determinant factor for heart attacks). The risk associated with that CAC score is not really based upon your calcified plaque as that likely won't hurt you, it is based on an expectation that you will continue to lay down new soft plaque. If you change your lifestyle and significantly lower cardiovascular inflammation, you might well have a much lower real risk than the MESA risk model would suggest. That is a big IF though for most people.

            Since vitamin K1 is associated with blood clotting, which is why the body prioritizes the use of vitamin K1 over K2, there is obviously going to be a health impact at high doses of vitamin K1. There are probably toxic doses of vitamin K2, but a standard supplement will usually be ok. I take the Life Extension Super K version, and one of those daily is as much as I think necessary and healthy for that matter.
            Last edited by Tom; 05-17-2019, 02:33 AM.

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            • #7
              One other thing to watch is the balance between vitamin k, vitamin d, and magnesium (and probably others). The way I understand it, in my simplistic way, is that magnesium optimizes vitamin d, vitamin d frees up calcium, and vitamin k directs it to the right place.

              I have to take 15000 iu of vitamin d in the winter and 10000 iu in summer to maintain vitamin d at optimal level. Another one of those darn snps! I wonder if taking such a high dose of vitamin d for several years without vitamin k might have added to my arterial and valve calcification.

              Comment


              • sthubbar
                sthubbar commented
                Editing a comment
                rich, this amount of Vitamin D is shocking since ConsumerLab. com says 25ng/ml is an ideal level and taking 100 IU/day should increase Vitamin D by 1ng/ml. This would mean if you started with 0 ng/ml and took 15,000 IU per day you should have a level of 150 ng/ml, or 6x their recommended level. What is your target level?

            • #8
              Dr. Brewer covered vitamin D in a video, and I personally think that 25 ng/ml is low (low side of the "normal" level). I personally want 40-60 ng/ml, and some people go a little higher. There are a relatively few people to my understanding who have SNPs for which they have very low conversion efficiency for vitamin D. Those few people do need to take more vitamin D, and I have heard of the above quoted daily amount for a very few people. I can only say go slow on increasing and get your vitamin D level checked often if you think that you need more than the standard recommended amount of vitamin D supplements. I personally take 3000/4000 IU daily, many others take 5000 IU daily.

              Comment


              • rich
                rich commented
                Editing a comment
                This gene encodes for the vitamin D binding protein which affects the delivery of 25-hydroxyvitamin D (precursor to vitamin D hormone) and activated vitamin D (1,25-dihydroxyvitamin D) to target organs, as well as clearance of vitamin D metabolites from the circulation.
                This*genotype, rs2282679(A;C), is associated with an*increased risk of vitamin D deficiency.
                It is known that supplementing with 1,000 IU of vitamin D3 per day generally raises serum 25-hydroxy vitamin D levels by around 5 ng/ml.*This may not be the case for people with the affected genotypes, rs2282679(A;C) and rs2282679(C;C), which may require higher vitamin D supplementation doses to achieve the same serum levels as individuals without these polymorphisms. The best way to assess vitamin D status is to get a blood test.
                Blood levels of 25-hyroxyvitamin D below 20 ng/ml are considered deficient, less than 30 ng/ml is inadequate. Individuals with levels between 30-60 ng/ml are considered adequate. Meta-analyses have shown that people with serum levels between 40-60 ng/ml have the lowest all-cause

              • sthubbar
                sthubbar commented
                Editing a comment
                rich, where is this quote from?

            • #9
              Originally posted by Tom View Post
              I will have to do some searching as I don't recall seeing studies that indicated that vitamin K2 will pull macrophages out of plaques.
              You are correct, I mistyped and now corrected. I meant to say -
              1. HDL should start reducing this macrophage/plaque ( with help of K2, Mg, CoQ10 )
              2. Vit K, with its extra dosage removes the calcium ( with help of Mg)

              If you find time, hear that podcast or better watch it in YT. He explains the logic: https://youtu.be/X4RipKub_Y8
              Last edited by VenSub; 05-19-2019, 03:43 PM.

              Comment


              • Tom
                Tom commented
                Editing a comment
                I did watch the podcast, and I commented on it at length on my May 16 post at 4:31 AM. I agree that HDL particles over time with a very healthy lifestyle and likely some drugs (statins and perhaps ACE inhibitors for hypertension) will reduce the problem. I think that the immune system is really what quietens down the macrophage activity, not HDL particles per se which sort of help clean up the cholesterol (really cholesteryl ester) that is causing/driving the inflammatory response. I am not a big fan of trying to purposely removing calcium from plaques as I haven't seen anything that shows that reduces cardiovascular disease. The calcium is a marker, helpful in stabilizing plaques, and removing the marker at best doesn't resolve the disease from what I can tell. Hopefully more hard biology-based information on this will come out over time and we will know for sure.

            • #10
              originally posted by sthubbar
              rich, where is this quote from?
              It's from my report using Dr Rhonda Patrick's app. I'm not sure what source she used. I thought it was SNPedia, but don't find that specific wording there.

              Comment


              • sthubbar
                sthubbar commented
                Editing a comment
                rich, Ok. Google to the rescue found this:

                https://www.apoe4.info/forums/viewto...=2341&start=10

                Hi Circ,
                I'm not sure. I ran "Rhonda's Genetic Report" using my 23&me results. I'll include the more detailed information she provided below.
                Chris

                This gene encodes for the vitamin D binding protein which affects the delivery of 25- hydroxyvitamin D (precursor to vitamin D hormone) and activated vitamin D (1,25- dihydroxyvitamin D) to target organs, as well as clearance of vitamin D metabolites from the circulation.
                This genotype, rs2282679(A;C), is associated with an increased risk of vitamin D deciency.
                It is known that supplementing with 1,000 IU of vitamin D3 per day generally raises serum 25-hydroxy vitamin D levels by around 5 ng/ml. This may not be the case for people with the aected genotypes, rs2282679(A;C) and rs2282679(C;C), which may require higher vitamin D supplementation doses to achieve the same serum levels as individuals without these polymorphisms.

                Blood levels of 25-hyroxyvitamin D below 20 ng/ml are considered deficient, less than 30 ng/ml is inadequate. Individuals with levels between 30-60 ng/ml are considered adequate. Meta-analyses have shown that people with serum levels between 40-60 ng/ml have the lowest all-cause mortality. Regardless of an individuals genotype for this particular SNP, a 25-hydroxy vitamin D blood test available from most health care providers can be useful for providing insight in how to optimize overall vitamin D levels.
                Read more on SNPedia (http://www.snpedia.com/index.php/Rs2282679).

            • #11
              Yup, Calcium is better than soft plaque. I see your point! Wonder why Ivor did not press him on that!
              However once its calcified doesn't it harden the arteries and the stenosis/blocakge is there.
              Wouldn't removing Ca help softening the arteries and possibly reduce B.P?

              Comment


              • #12
                The calcium may well have both good and bad effects like a lot of metabolic issues we deal with for our health. In theory it sounds good to reduce calcium to make the arteries more flexible, but I haven't seen anything to indicate that removing calcium results in a positive outcome. The presence of calcium in plaques and in the arteries in general may well be dynamic over a long period of time vs. static, and with a healthy lifestyle/low cardiovascular inflammation slowly decrease on its own. Perhaps this aspect will get studied a bit, but I suppose the cardiovascular disease problem, as huge as it is, will dominate the discussion and funding.

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