Vitamin K2 and Warfarin

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hook

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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?:confused2:
 
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.
 
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?:confused2:

Keeping Vitamin K intake to a MINIMUM is an OUT OF DATE Philosophy that has been PROVEN to lead to unstable INR.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'
 
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.
 
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?:confused2:

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.
 
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).
 
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.
 
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....... :)
 
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.
 
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.”
 
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?
 
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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
 
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?)
 
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.
 
Here is the link

http://www.lmreview.com/articles/view/vitamin-d-and-vitamin-k-team-up-to-lower-cvd-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.
 
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Here is the link

http://www.lmreview.com/articles/view/vitamin-d-and-vitamin-k-team-up-to-lower-cvd-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.
 
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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.
 

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