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Thread: Vitamin K2 and Warfarin

  1. #1
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    Default Vitamin K2 and Warfarin

    I know Vit K found in green stuff is something us blood thinner have to keep at a minimum, but does Vit K2 also thicken blood. K2 has many benefits to include preventing hardening of the arteries and slowing cancer developement, thus I would love to take it.

    Anyone know the answer to this?
    Todd Taylor
    Mitral Valve Replacement - Mech St Judes 5/26/2010
    Dr Michael Petracek, Vanderbilt Heart Institue
    "he's more machine than man now" Obiwan Kenobi

  2. #2
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    Sorry Todd I don't have an answer, but I also don't keep my "green stuff" to a minimum.
    Laughter is the Best Medicine

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    There's some evidence that ingesting a reasonable and consistent amount of Vit. K makes it EASIER to maintain a steady INR than avoiding Vit. K. I'm not an expert on K2, and I don't remember which factor of Vit. K does what.
    BAV, extended ARoot, some MV damage.
    68 y.o. (65 @OHS), keen active athlete until shortly pre-op, only symptomatic 1-2 months pre-op.
    AVR (Medtronics Hancock II) Dec. 1 2010 w/ Dr. C.M. Feindel at UHN aka Toronto General. Also a "tuck" on the Aortic root, and a (Dacron) Medtronics Simplici-T ring on my MV. I did ACT for 3 months for the ring, and Metoprolol (BB) for 3 months for A-fib.

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    Quote Originally Posted by hook View Post
    I know Vit K found in green stuff is something us blood thinner have to keep at a minimum, but does Vit K2 also thicken blood. K2 has many benefits to include preventing hardening of the arteries and slowing cancer developement, thus I would love to take it.

    Anyone know the answer to this?
    Keeping Vitamin K intake to a MINIMUM is an OUT OF DATE Philosophy that has been PROVEN to lead to unstable INR.

    Studies have Proven that a "Consistent" level of Vitamin K intake leads to a more stable INR.

    'AL Capshaw'

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    Vitamin K has been shown to be beneficial. Drastically reducing or eliminating it is not good, as others have indicated.

    As Al noted, the important part about Vitamin K (and, really, the rest of your diet) is consistency. If you are consistent in your diet and activities, you will be able to regulate your INR based on your regular dietary intake (and other factors). Just because you take warfarin, this shouldn't mean that you have to change your diet.

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    Quote Originally Posted by hook View Post
    I know Vit K found in green stuff is something us blood thinner have to keep at a minimum, but does Vit K2 also thicken blood. K2 has many benefits to include preventing hardening of the arteries and slowing cancer developement, thus I would love to take it.

    Anyone know the answer to this?
    Just eat your normal diet. If you love green stuff, enjoy those. If you don't, no big deal. I have a friend who pooh-poohs anything green, even iceberg lettuce, which is pretty bland-looking.
    Marsha (7-28-50), MVP 1990/MVR (St. Jude) & ASD repair 6/24/03 Baylor University Medical Center, Dallas Texas. Hometesting since 11/03, first with ProTime 3, now with INRatio.
    John (3-13-46), MV repair 5/10/07, Dallas Presbyterian, port-access incision, Dr. William Ryan. Chordae ruptured 12/05 in car crash.

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    Just one quick point -- warfarin doesn't 'thin' the blood, and Vitamin K doesn't 'thicken' it. What warfarin does is make your blood take longer to clot. Vitamin K works in a different direction, reducing the clotting time. From what I understand, the INR represents a ratio in clotting times compared to a 'normal' 1.0. So, if it takes your blood 10 seconds to clot with a 1.0, an INR of 3.0 should mean that, for the same sized incision, under the same conditions, it'll take your blood 30 seconds to clot. (At least, that's how I've seen INRs explained). The reason we're taking warfarin is to reduce our body's propensity (how's that for a word?) to form a clot (like the clots around your valve, for example).

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    That's a great article. I've been struggling with maintaining a stable INR since surgery. I have not been taking a multivitamin since surgery. I was doing well maintaining if I ate 1 salad a day. Then when I was in the hospital for a-fib for 10 days, they would not let me eat my salads and my INR shot up to 4.5. I will look into taking a vitamin with a small amount of K to see if it helps.
    1997: At 33 yo, diagnosed Bicuspid Aortic Valve w/ Severe Aortic Stenosis (1.0cm2)
    2010: BAV w/ SAS (.7 cm2), mean Pressure gradiant: 42mm HG.
    2011: Mechnical valve, On-X, AVR Scheduled Jan 13, w/ Dr. J Alan Wolfe at NorthEast Georgia Medical Center
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  10. #10
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    drivetopless........

    Hope each day you are doing better.
    If you enjoy your salads and had one a day when you had stabalized your INR, why not go back to enjoying your salads rather than taking a supplement? Too bad they were so 'out of date' with INR stabalization in the hospital and denied you salads. Must have been very frustrating for you.

    Sending you best wishes for no more bumps.......

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    Quote Originally Posted by Greg a View Post
    Great article Greg. From what I have learned thus far, it seems taking the K2 will help in many ways. thanks
    Todd Taylor
    Mitral Valve Replacement - Mech St Judes 5/26/2010
    Dr Michael Petracek, Vanderbilt Heart Institue
    "he's more machine than man now" Obiwan Kenobi

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    This is one of my favorite subjects. I take a multivitamin with 25 mcg Vit K (1-not 2) AND a supplement of 100 mcg Vitamin K. I take them every day, without fail. This has helped me maintain a steady amount of Vit K and my warfarin dosage is adjusted to take this into account. The recommended minimum daily amount of Vit K is 80-90 mcg. My INR is much more stable doing this. I don't consume a consistent amount of Vit K through food so this helps me level off. When I do take in a 'more than normal' amount of dietary Vit K the shock to my system is much less. The light bulb analogy helps to explain it. If you're in a room with a 75 watt bulb and then increase it to 100 watts, you've only made a 33% increase. If you're in a room with a 50 watt bulb and then increase it to 100 - you now have a 100% increase. AND if you're in a room with a 25 watt bulb and then increase it to 100 it it a whopping 400% increase. Works pretty much the same with Vit K - so don't limit your veggies...or supplements - give your body the benefits of Vit K as well. Just maintain some sort of consistency.

    BTW most Vit K1 is from vegetable sources and most Vit K2 is from meat, dairy, & eggs.
    Cris

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    St. Jude Mitral Valve 5/16/05

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    Ok, this was the kind of research I was looking for. I know this is a rat study, but it is getting closer to the answer I seek. K1 into the liver creates a protien that aids in clotting, and coumadin blocks/slows that protien conversion. K2 in the liver creates a protien that conveys calcium in the blood and arteries into bone where it belongs. I would like to know if coumadin blocks the protien conversion in the liver for K2 as it does K1.

    here is the rat story

    In the new study, the researchers induced arterial hardening in rats by interfering with vitamin K-metabolism, by adding the vitamin K-antagonist warfarin to the diets. Vitamin K is reported to act on a protein called matrix Gla-Protein (MGP), said to be the strongest inhibitor of arterial calcification.

    Initially, the rats were divided into two groups, a control group with vitamin K added to the diet, and a warfarin treated group to induce calcification. After six weeks of treatment with warfarin, the researchers report that the rats showed signs of significant arterial hardening.

    The warfarin treated rats were then further divided into four groups and assigned to one of four intervention groups for a further six weeks: a standard diet plus warfarin, a standard diet plus vitamin K1 at normal dose (5 micrograms per gram of food, purchased from Sigma), a standard diet plus high-dose vitamin K1 (100 micrograms per gram of food), or the standard diet plus high-dose vitamin K2 (MK-4, 100 micrograms per gram of food, gifted from Eisai, Japan).

    Schurgers and his co-workers report that during the second six week period, the calcifications in the warfarin-treated control group continued linearly, as did the calcification in the normal dose vitamin K1 group, indicating that dietary vitamin K1 intake had no effect.

    However, in both high-dose groups (K1 and K2) no continued calcification occurred, but the existing hardening was found to be reversed by about 40 per cent after six weeks of supplementation.

    Interestingly, vitamin K2 concentration in the tissues of both groups were similar, which showed the vitamin K1 was converted into vitamin K2.

    “The effect of K1 and the conversion rate of K1 to K2 was due to the extremely high dose of K vitamins used in this model,” said Schurgers. “This would be probably less in a normal diet, even with supplemental K1. In contrast, the Rotterdam study showed a significant protective benefit with Natural Vitamin K2 at just 45mcg per day, whereas K1 had no correlation at all.”
    Todd Taylor
    Mitral Valve Replacement - Mech St Judes 5/26/2010
    Dr Michael Petracek, Vanderbilt Heart Institue
    "he's more machine than man now" Obiwan Kenobi

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    This study seemed to show that high dose Vit. K2 overcame the Coumadin to protect the arteries, and "the Rotterdam study showed a significant protective benefit with Natural Vitamin K2 at just 45mcg per day". I don't know if the 45mcg per day was a human dose or a rat dose, but isn't that your answer?
    Last edited by normofthenorth; February 9th, 2011 at 06:58 PM.
    BAV, extended ARoot, some MV damage.
    68 y.o. (65 @OHS), keen active athlete until shortly pre-op, only symptomatic 1-2 months pre-op.
    AVR (Medtronics Hancock II) Dec. 1 2010 w/ Dr. C.M. Feindel at UHN aka Toronto General. Also a "tuck" on the Aortic root, and a (Dacron) Medtronics Simplici-T ring on my MV. I did ACT for 3 months for the ring, and Metoprolol (BB) for 3 months for A-fib.

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    here is another article

    Part II: The Vitamin K Connection to Cardiovascular Health
    Introduction
    First recognized by German researchers as a nutrient required for normal blood “koagulation,” vitamin K is actually a family of structurally similar, fat-soluble compounds, some of which (the K2 forms) play essential roles in cardiovascular health, primarily through regulating the body’s use of calcium – both promoting its integration into bone and preventing of its deposition within blood vessels -- and also by exerting anti-inflammatory and insulin-sensitizing actions.1

    In nature, vitamin K appears primarily in two forms: K1 (phylloquinone [phyllo – relating to a leaf] and K2 (the menaquinones [mena – in reference to their methylated napthoquinone ring structure]). While all forms of vitamin K share 2-methyl-1,4-naphthoqinone as their common ring structure, individual forms differ in the length and degree of saturation of a variable aliphatic side chain attached to the 3-position.

    K1, a single compound that contains a monounsaturated side chain of four isoprenoid residues, is found primarily in plants and algae in association with chlorophyll. Dietary sources of K1 include green leafy vegetables, such as broccoli, kale and Swiss chard, and unhydrogenated plant oils, including canola and soybean oil.

    K2, the menaquinones (MKs) are classified based on the length of their unsaturated side chains into 15 different types denominated as MK-n, with “n” denoting the number of isoprenyl residues in the side chain. The most common MKs in humans are the short-chain menaquinone, MK-4, which is now thought to be primarily produced via the systemic conversion of K1 to K2 in the body} 2 3 4 and the long-chain menaquinones, MK-7 through MK-10, which are exclusively synthesized by bacteria and gut microflora in all mammals, including humans. K2 (primarily its long-chain forms, MK-7, MK-8 and MK-9) is found in fermented foods, notably cheese and natto (fermented soybean); the latter is the richest dietary source of vitamin K presently known, almost all of which occurs in the form of MK-7.45

    Vitamin K1, MK-4 and MK-7 are available as supplements: MK-4 as a synthetic version called menatetrenone, and MK-7, as the natural compound extracted from natto. MK-7 has a much longer half-life than either K1 or MK-4, which share similar molecular structures (both contain 4 isoprenoid residues, 3 of which are saturated in K1 but contain a double bond in MK-4) and therefore similar physiokinetics. In contrast, the longer-chain menaquinones, including MK-7, are much more hydrophobic and are handled differently by the body. In vivo, they have longer half-lives and are incorporated into low-density lipoproteins in the circulation, resulting in much more stable serum levels and accumulation to 7- to 8-fold higher levels during prolonged intake.5

    K3 (menadione), a third, much simpler form of the vitamin, is considered a synthetic analogue, although intestinal bacteria can produce minute amounts from K1.6 K3 has been utilized in research on vitamin K's anti-cancer effects because it potentiates the cytotoxic activity of chemotherapeutic agents and vitamin C (when acting as an antioxidant, vitamin C is oxidized to dehydroascorbate, a potent free radical that is spontaneously reduced by glutathione as well as in reactions using glutathione or NADPH7; however, because of its toxicity, the FDA has banned its use in nutritional supplements.8

    Although, following intestinal absorption, both K1 and K2 are taken up in the triglyceride fraction from which they are rapidly cleared by the liver, only the K2 forms are also taken up and systemically redistributed by low-density lipoproteins.910 Compared to K1, whose primary activity is the carboxylation of blood coagulation factors (II [prothrombin], VII, IX, and X, the anticoagulant proteins C, S and Z), which are synthesized in the liver, K2 has a much wider range of action, playing a significant role in bone formation and protection against bone loss, arterial calcification, and oxidation of LDL cholesterol.11 12 In addition, K2 is a 15-fold more powerful antioxidant than K1 and is the predominant form of vitamin K in all tissues, except the liver.13 Finally, K2 is better absorbed than K1 and remains biologically active far longer; K1 is cleared by the liver within 8 hours, while measurable levels of the MK-7 form of K2 have been detected up to 72 hours after ingestion.
    14
    Todd Taylor
    Mitral Valve Replacement - Mech St Judes 5/26/2010
    Dr Michael Petracek, Vanderbilt Heart Institue
    "he's more machine than man now" Obiwan Kenobi

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    So - after all this (and it was certainly interesting material) - we should NOT avoid sources of K1 or K2 - and perhaps should even take supplements because the K provides benefits that are probably not available without it. It goes back to the issue of consistency -- if you take a regular source of K (as it appears we all should) - then you should adjust your warfarin dose to compensate for the effects on the INR.

    (Now -- what about Vitamin E?)

  17. #17

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    I'm not exactly sure what you are trying to figure out. Are you asking since you are on Coumadin would it be a good idea to take Vit K2? Or asking if K2 has an effect on coagulation and does Coumadin block it (or any of the other benefits) like it does K1?

    Do you have a link to the rat study, or the article you quoted in your last post (#13) If I'm reading it correctly, it seems for the 2nd 6 weeks, when they broke into the 4 groups, only the first group still took Coumadin and the other 3 didn't, they just took different levels of vit K 1 or a high dose of K2?

    "The warfarin treated rats were then further divided into four groups and assigned to one of four intervention groups for a further six weeks: a standard diet plus warfarin, a standard diet plus vitamin K1 at normal dose (5 micrograms per gram of food, purchased from Sigma), a standard diet plus high-dose vitamin K1 (100 micrograms per gram of food), or the standard diet plus high-dose vitamin K2 (MK-4, 100 micrograms per gram of food, gifted from Eisai, Japan)."

    Schurgers and his co-workers report that during the second six week period, the calcifications in the warfarin-treated control group continued linearly, as did the calcification in the normal dose vitamin K1 group, indicating that dietary vitamin K1 intake had no effect.
    Lyn
    Mom to Justin 25 TGA,VSDs, pulmonary atresia/stenosis ect, post/Rastelli, 5 OHS, pacer in and out ... and surgery w/muscle flap for post op infection (sternal osteomyelitis with mediastinitis) www.caringbridge.org/nj/justinw

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    Here is the link

    http://www.lmreview.com/articles/vie...-risk-part-II/

    Putting all the techno mumbo jumbo aside, my root question is simple; foe a person taking coumadin, would taking 45mcg of K2 help prevent calcium build-up in arteries and valves.

    Even with open heart surgery and all the meds that come with it, I feel strongly a patient can reach a relatively high level of health with the right lifestyle. If coumadin does indeed contribute to calcium deposits in the wrong places, and contributes to weak bones, then I want to do what I can to stop it. All I am suggesting is a collective input to help one another.
    Last edited by hook; February 10th, 2011 at 02:03 PM.
    Todd Taylor
    Mitral Valve Replacement - Mech St Judes 5/26/2010
    Dr Michael Petracek, Vanderbilt Heart Institue
    "he's more machine than man now" Obiwan Kenobi

  19. #19

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    Quote Originally Posted by hook View Post
    Here is the link

    http://www.lmreview.com/articles/vie...-risk-part-II/

    Putting all the techno mumbo jumbo aside, my root question is simple; if a person taking coumadin, can K2 help prevent calcium build-up in arteries and valves, and it be effective.

    Even with this surgery and all the meds that come with it, I feel strongly a patient can reach a relatively high level of health. If coumadin does indeed contribute to calcium deposits in the wrong places, and contributes to weak bones, then I want to do what I can to stop it.
    Thanks, do you have the link to this article or study? I would like to read it.
    "here is the rat story

    In the new study, the researchers induced arterial hardening in rats by interfering with vitamin K-metabolism, by adding the vitamin K-antagonist warfarin to the diets. Vitamin K is reported to act on a protein called matrix Gla-Protein (MGP), said to be the strongest inhibitor of arterial calcification...."

    The short answer is Coumadin does inhibit Vit k2 from doing its jobs, like it does K1 and the role it plays in coagulation.
    Also IF you increase your Vit K2 I believe, most likely you will also have to increase the amount of Coumadin you need to stay in range.
    Last edited by Lynlw; February 10th, 2011 at 02:45 PM.
    Lyn
    Mom to Justin 25 TGA,VSDs, pulmonary atresia/stenosis ect, post/Rastelli, 5 OHS, pacer in and out ... and surgery w/muscle flap for post op infection (sternal osteomyelitis with mediastinitis) www.caringbridge.org/nj/justinw

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    That was also my short answer, Lyn. But I think I assumed they continued the Coumadin dosing of the non-control rates (even groups 2, 3, & 4). Your contrary reading may be right. I'm not sure it affects the "bottom line", except that (I think) my way it's about overcoming the ingoing effects of Coumadin, and your way it's about reversing the past effects.
    BAV, extended ARoot, some MV damage.
    68 y.o. (65 @OHS), keen active athlete until shortly pre-op, only symptomatic 1-2 months pre-op.
    AVR (Medtronics Hancock II) Dec. 1 2010 w/ Dr. C.M. Feindel at UHN aka Toronto General. Also a "tuck" on the Aortic root, and a (Dacron) Medtronics Simplici-T ring on my MV. I did ACT for 3 months for the ring, and Metoprolol (BB) for 3 months for A-fib.

  21. #21

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    Quote Originally Posted by normofthenorth View Post
    That was also my short answer, Lyn. But I think I assumed they continued the Coumadin dosing of the non-control rates (even groups 2, 3, & 4). Your contrary reading may be right. I'm not sure it affects the "bottom line", except that (I think) my way it's about overcoming the ingoing effects of Coumadin, and your way it's about reversing the past effects.
    That's why I was asking for a link to the study.
    I "think" they would have mentioned "+ coumadin" for groups 2, 3, 4, since they mentioned "standard diet" each time. IF they were able to not only prevent more calcification but also able to reverse the past effects while the rat was still taking same amount of coumadin, I would think that would make a big difference compared to adding high dose Vit K but not having to overcome also taking Coumadin.
    Lyn
    Mom to Justin 25 TGA,VSDs, pulmonary atresia/stenosis ect, post/Rastelli, 5 OHS, pacer in and out ... and surgery w/muscle flap for post op infection (sternal osteomyelitis with mediastinitis) www.caringbridge.org/nj/justinw

  22. #22

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    Quote Originally Posted by hook View Post
    Here is the link

    http://www.lmreview.com/articles/vie...-risk-part-II/

    Putting all the techno mumbo jumbo aside, my root question is simple; foe a person taking coumadin, would taking 45mcg of K2 help prevent calcium build-up in arteries and valves.

    Even with open heart surgery and all the meds that come with it, I feel strongly a patient can reach a relatively high level of health with the right lifestyle. If coumadin does indeed contribute to calcium deposits in the wrong places, and contributes to weak bones, then I want to do what I can to stop it. All I am suggesting is a collective input to help one another.
    Todd, i don't know if this helps answer your basic question

    here is the 'rat" study

    http://bloodjournal.hematologylibrar...ull/109/7/2823
    Regression of warfarin-induced medial elastocalcinosis by high intake of vitamin K in rats

    "To induce vascular calcification, rats (n = 30) received a diet containing warfarin (3 mg/g food) and vitamin K1 (1.5 mg/g food; the minimal dose required for rats is 0.5 g/g food), according to the method described earlier by our group.25 These animals are designated as the W&K group. Control rats (n = 18) received no warfarin and a normal dose of vitamin K1 (5 g/g food; this is equivalent to the vitamin K amount in normal standard rat food). From the control group, 6 rats where killed at the start of the experiment to measure the baseline calcium content of the abdominal aorta and left carotid artery. After 6 weeks of treatment, 6 control rats and 6 W&K rats were killed to monitor the effect of treatment. The remaining rats in the W&K group (n = 24) were subdivided into 4 groups of 6 rats for another 6-week treatment. One group continued the W&K diet, whereas warfarin was discontinued in the remaining 3 groups: one group received normal vitamin K1 (5 g/g food), one group received high vitamin K1 (100 g/g food; the dietary vitamin K requirements for rats are 0.5 g/g food to maintain normal blood clotting), and the last group received high vitamin K2 (menaquinone-4, 100 g/g food). In addition, the remaining 6 control rats continued their diet for another 6 weeks "

    I "believe" the reason they stopped the Coumadin for the 3 groups, was they weren't really interested in Coumadin and Vit K, they just used the Coumadin to cause the vascular calcification, so they could see what effect the different levels of Vit k1 and high dose K2 would have on the calcification.

    From the intro

    "The rat arterial calcification model, as developed by Price et al20 and used by others,21,25,29 has thus far only looked at the development of arterial calcification. The aim of the present study was to use the rat arterial calcification model to investigate whether maximal MGP activity, ascertained by high–vitamin K intake, may stop the progression or even induce a reversal of warfarin-induced arterial calcification and the associated decrease in arterial distensibility"

    Also for the Rotterdam study mentioned above (hooks post #13) that showed the benefit with just 45mcg of K2 a day

    “The effect of K1 and the conversion rate of K1 to K2 was due to the extremely high dose of K vitamins used in this model,” said Schurgers. “This would be probably less in a normal diet, even with supplemental K1. In contrast, the Rotterdam study showed a significant protective benefit with Natural Vitamin K2 at just 45mcg per day, whereas K1 had no correlation at all"

    Here is a link to the Abstract http://www.ncbi.nlm.nih.gov/pubmed/15514282

    Vitamin K-dependent proteins, including matrix Gla-protein, have been shown to inhibit vascular calcification. Activation of these proteins via carboxylation depends on the availability of vitamin K. We examined whether dietary intake of phylloquinone (vitamin K-1) and menaquinone (vitamin K-2) were related to aortic calcification and coronary heart disease (CHD) in the population-based Rotterdam Study. The analysis included 4807 subjects with dietary data and no history of myocardial infarction at baseline (1990-1993) who were followed until January 1, 2000. The risk of incident CHD, all-cause mortality, and aortic atherosclerosis was studied in tertiles of energy-adjusted vitamin K intake after adjustment for age, gender, BMI, smoking, diabetes, education, and dietary factors. The relative risk (RR) of CHD mortality was reduced in the mid and upper tertiles of dietary menaquinone compared to the lower tertile [RR = 0.73 (95% CI: 0.45, 1.17) and 0.43 (0.24, 0.77), respectively]. Intake of menaquinone was also inversely related to all-cause mortality [RR = 0.91 (0.75, 1.09) and 0.74 (0.59, 0.92), respectively] and severe aortic calcification [odds ratio of 0.71 (0.50, 1.00) and 0.48 (0.32, 0.71), respectively]. Phylloquinone intake was not related to any of the outcomes. These findings suggest that an adequate intake of menaquinone could be important for CHD prevention.

    heres the fulltext http://jn.nutrition.org/content/134/11/3100.long

    I'm not sure if it helps with your question tho, since they studied the general population and their diets and not people on Coumadin, for their study. So if their study showed 45 mcg a day lowerred their risks, I don't know what effect Coumadin would have on it, since it blocks the Vit K from doing its job. Most likely someone on Coumadin would need more than the 45 a day.
    Also IF you increased your levels of Vit K2, most likely you would have to increase your Coumadin to keep your INR in range so it MIGHT be a catch 22 type of thing.
    Lyn
    Mom to Justin 25 TGA,VSDs, pulmonary atresia/stenosis ect, post/Rastelli, 5 OHS, pacer in and out ... and surgery w/muscle flap for post op infection (sternal osteomyelitis with mediastinitis) www.caringbridge.org/nj/justinw

  23. #23
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    You bring up the million dollar question. Will increased K2 require increased Coumadin, and will that increase in Coumadin cancel out all actions of the K2. The catch 22 if you will

    From what I can simplify, the Coumadin does its work in the liver where Vit K1 activates the proteins that work on blood coagulation. I have read in a couple other articles that the K2s structure has a much longer half life, and is metabolized into the body in other places other than the liver. With that said, it may be possible an added dose of K2 may be able to do its job for the body, even if a little extra Coumadin is required.

    I have a home INR tester, and have a small surplus of strips. I am going to start 45mcg of K2 and test every other day for two weeks to gather results. If this causes only minor changes in INR I will try the 90mcg. If I am able tolerate this with only minor increases in Coumadin, I will make this part of my regiment just to play it safe. I don't eat many greens, so this could be my primary source of K that we have all learned we need to maintain our levels. In a few years they will determine I was either wasting my money, or that I may have helped stop a deadly progression of calcification. We will see
    Todd Taylor
    Mitral Valve Replacement - Mech St Judes 5/26/2010
    Dr Michael Petracek, Vanderbilt Heart Institue
    "he's more machine than man now" Obiwan Kenobi

  24. #24

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    Quote Originally Posted by hook View Post
    You bring up the million dollar question. Will increased K2 require increased Coumadin, and will that increase in Coumadin cancel out all actions of the K2. The catch 22 if you will

    From what I can simplify, the Coumadin does its work in the liver where Vit K1 activates the proteins that work on blood coagulation. I have read in a couple other articles that the K2s structure has a much longer half life, and is metabolized into the body in other places other than the liver. With that said, it may be possible an added dose of K2 may be able to do its job for the body, even if a little extra Coumadin is required.

    I have a home INR tester, and have a small surplus of strips. I am going to start 45mcg of K2 and test every other day for two weeks to gather results. If this causes only minor changes in INR I will try the 90mcg. If I am able tolerate this with only minor increases in Coumadin, I will make this part of my regiment just to play it safe. I don't eat many greens, so this could be my primary source of K that we have all learned we need to maintain our levels. In a few years they will determine I was either wasting my money, or that I may have helped stop a deadly progression of calcification. We will see
    But Coumadin Blocks/ inhibits vit K (1- K2) from doing its job anywhere NOT just the liver. Coumadin inhibits vitamin K(1 and 2) from activating the Vit K dependent proteins (like Matrix Gla Protein) to do their jobs (coagulation, protect from calcification etc)

    There are tons of articles about coumadin + Vit K but this is easy http://cjasn.asnjournals.org/content/3/5/1504.full
    Vitamin K-dependent proteins (VKDPs) require carboxylation to become biologically active. Although the coagulant factors are the most well-known VKDPs, there are many others with important physiologic roles. Matrix Gla Protein (MGP) and Growth Arrest Specific Gene 6 (Gas-6) are two particularly important VKDPs, and their roles in vascular biology are just beginning to be understood. Both function to protect the vasculature; MGP prevents vascular calcification and Gas-6 affects vascular smooth muscle cell apoptosis and movement. Unlike the coagulant factors, which undergo hepatic carboxylation, MGP and Gas-6 are carboxylated within the vasculature. This peripheral carboxylation process is distinct from hepatic carboxylation, yet both are inhibited by warfarin administration. Warfarin prevents the activation of MGP and Gas-6, and in animals, induces vascular calcification. The relationship of warfarin to vascular calcification in humans is not fully known, yet observational data suggest an association...
    The most well-known vitamin K-dependent proteins (VKDPs) are the coagulant factors II,VII, IX, and X. Produced by the liver, they are converted into their biologically active forms by the carboxylation of glutamic acid residues, a process requiring vitamin K as a cofactor. By interfering with this carboxylation process, warfarin has become the mainstay of anticoagulant therapy. However, beyond these coagulant factors, there are other VKDPs with widespread physiologic activities. Recent studies have focused on two particularly important VKDPs, Matrix Gla protein (MGP) and Growth Arrest Specific gene 6 (Gas-6) protein. These proteins have many diverse biologic functions, yet with the recognition that they are produced by vascular smooth muscle cells, their roles in vascular biology are being increasingly explored. MGP functions primarily as a vascular calcification inhibitor. Gas-6 affects vascular smooth muscle cell movement and apoptosis. Together, these proteins constitute a new mechanism of local vascular regulation, where the blood vessel defends itself against injury and participates in self-repair. A failure of these local mechanisms might be an important first step in a cascade of events culminating in vascular calcification, and supports the notion that vascular calcification is an active, regulated process.

    To become biologically active, both MGP and Gas-6 undergo carboxylation, a process that occurs at the blood vessel level. Like hepatic carboxylation, this peripheral carboxylation is inhibited by the administration of warfarin, yet whereas warfarin's anticoagulant effect is well known, its effect on the vasculature is less certain.
    Last edited by Lynlw; February 12th, 2011 at 11:03 AM.
    Lyn
    Mom to Justin 25 TGA,VSDs, pulmonary atresia/stenosis ect, post/Rastelli, 5 OHS, pacer in and out ... and surgery w/muscle flap for post op infection (sternal osteomyelitis with mediastinitis) www.caringbridge.org/nj/justinw

  25. #25
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    Todd, I think that's a great plan, given what I've gleaned from those studies. I think K1 is more involved in INR, and Warfarin interferes with both "even-handedly", so you should end up with more K2 (and its metabolites) in your blood, the same INR, and a slightly increased ACT dose.

    Those of us who have been trying to quantify and clarify the risks of ACT here haven't even mentioned this one, though it's important to the choices people make. (If you choose a mech. valve because you never, ever want another OHS, but the ACT means that you need a multiple bypass 10 years later, then you blew it!) ... But your approach may well reduce that risk to normal levels -- or even lower, if you end up with better K2 levels than the population as a whole. (Now I wonder why nobody's thought of this and acted on it before!)
    BAV, extended ARoot, some MV damage.
    68 y.o. (65 @OHS), keen active athlete until shortly pre-op, only symptomatic 1-2 months pre-op.
    AVR (Medtronics Hancock II) Dec. 1 2010 w/ Dr. C.M. Feindel at UHN aka Toronto General. Also a "tuck" on the Aortic root, and a (Dacron) Medtronics Simplici-T ring on my MV. I did ACT for 3 months for the ring, and Metoprolol (BB) for 3 months for A-fib.

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