They found no relationship between K1 intake and heart attack incidence. K1 is the form found in leafy greens and other plant foods. They found that each 10 microgram increase in daily vitamin K2 consumption was associated with a 9% lower incidence of heart attack. Participants consumed an average of 29 micrograms K2 per day, with a range of 0.9 to 128 micrograms. That means that participants with the highest intake had a very much reduced incidence of heart attack on average. Vitamin K2 comes from animal foods (especially organs and pastured dairy)and fermented foods such as cheese, sauerkraut, miso and natto. Vitamin K is fat-soluble, so low-fat animal foods contain less of it. Animal foods contain the MK-4 subtype while fermentation produces longer menaquinones, MK-5 through MK-14.
There's quite a bit of evidence to support the idea that vitamin K2 inhibits and possibly reverses arterial calcification, which is possibly the best overall measure of heart attack risk. It began with the observations of Dr. Weston Price, who noticed an inverse relationship between the K2 MK-4 content of butter and deaths from coronary heart disease and pneumonia in several regions of the U.S. You can find those graphs in Nutrition and Physical Degeneration.
The 25% of participants eating the most vitamin K2 (and with the lowest heart attack risk) also had the highest saturated fat, cholesterol, protein and calcium intake. They were much less likely to have elevated cholesterol, but were more likely to be diabetic.
Here's where the paper gets strange. They analyzed the different K2 subtypes individually (MK-4 through MK-9). MK-7 and MK-6 had the strongest association with reduced heart attack risk per microgram consumed, while MK-4 had no significant relationship. MK-8 and MK-9 had a weak but significant protective relationship.
There are a few things that make me skeptical about this result. First of all, the studies showing prevention/reversal of arterial calcification in rats were done with MK-4. MK-4 inhibits vascular calcification in rats whereas I don't believe the longer menaquinones have been tested. Furthermore, they attribute a protective effect to MK-7 in this study, but the average daily intake was only 0.4 micrograms! You could get that amount of K2 if a Japanese person who had eaten natto last week sneezed on your food. I can't imagine that amount of MK-7 is biologically significant. That, among other things, makes me skeptical of what they're really observing.
I'm not convinced of their ability to parse the effect into the different K2 subtypes. They mentioned in the methods section that their diet survey wasn't very accurate at estimating the individual K2 subtypes. Combine that with the fact that the K2 content of foods varies quite a bit by animal husbandry practice and type of cheese, and you have a lot of variability in your data. Add to that the well-recognized variability inherent in these food questionnaires, and you have even more variabiltiy.
I'm open to the idea that longer menaquinones (K2 MK-5 and longer, including MK-7) play a role in preventing cardiovascular disease, but I don't find the evidence sufficient yet. MK-4 is the form of K2 that's made by animals, for animals. Mammals produce it in their breast milk and other animals produce it in eggs all the way down to invertebrates. I think we can assume they make MK-4, and not the longer menaquinones, for a reason.
MK-4 is able to play all the roles of vitamin K in the body, including activating blood clotting factors, a role traditionally assigned to vitamin K1. This is obvious because K2 MK-4 is the only significant source of vitamin K in the diet of infants before weaning. No one knows whether the longer menaquinones are able to perform all the functions of MK-4; it hasn't been tested and I don't know how you could ever be sure. MK-7 is capable of performing at least some of these functions, such as activating osteocalcin and clotting factors.
I do think it's worth noting that the livers of certain animals contain longer menaquinones, including MK-7. So it is possible that we're adapted to eating some of the longer menaquinones. Many cultures also have a tradition of fermented food (probably a relatively recent addition to the human diet), which could further increase the intake of longer menaquinones. The true "optimum", if there is one, may be to eat a combination of forms of K2, including MK-4 and the longer forms. But babies and healthy traditional cultures such as the Masai seem to do quite well on a diet heavily weighted toward MK-4, so the longer forms probably aren't strictly necessary.
Well if you've made it this far, you're a hero (or a nerd)! Now for some humor. From the paper:
The concept of proposing beneficial effects to vitamin K2 seems to have different basis as for vitamin K1. Vitamin K1 has been associated with a heart-healthy dietary pattern in the earlier work in the USA and this attenuated their associations with CHD. Vitamin K2 has different sources and relate to different dietary patterns than vitamin K1. This suggests that the risk reduction with vitamin K2 is not driven by dietary patterns, but through biological effects.They seem confused by the fact that people who ate foods high in saturated fat and cholesterol had less CHD, yet people consuming green vegetables didn't. Here's more:
Thus, although our findings may have important practical implications on CVD prevention, it is important to mention that in order to increase the intake of vitamin K2, increasing the portion vitamin K2 rich foods in daily life might not be a good idea. Vitamin K2 might be, for instance more relevant in the form of a supplement or in low-fat dairy. More research into this is necessary.Translation: "People who ate the most cheese, milk and meat had the lowest heart attack rate, but be careful not to eat those things because they might give you a heart attack. Get your K2 from low-fat dairy (barely contains any) and supplements."
I've got to link this instanter!
Sounds like "special K" to me - ;-)
Another bulls eye Stephan! An interesting study. I wonder how much a mother's diet influences the amount of K2 in her milk? With the emphasis on low-fat diet these days, that might be a problem.
Alright, I guess I'm a nerd. That was great.
Man it seems like anything coming from an animal is bad when people write about diet for the mainstream public lately (unless it's modified to be considered good in some way - like skim milk).
Are there any other vitamins similar to K which have more then one form? Like, are all vitamins different in plants versus animals and are they at all as complex as K seems to be? Just wondering, if you knew.
And Bryan, I was reading in this gigantimous book about Dietary Fats - and it was mentioning breast feeding in one of the documented presentations, and it did say that low-fat, high-carbohydrate diets effected breastmilk and was not as calorie dense as it needed to be (probably less rich in nutrients as well - being that if fat makes up a bulk of the milk and calories, and K2 is fat-soluble, then it's probably less existent). Then again it didn't get into much detail about what high-carbohydrate diet it was - so I'm sure that must be important (like refined versus not) since there are indigenous people who do get a lot of carbs as energy.
Nice post. I too am skeptical that there should be a big difference between MK 4 and MK 5-14. As I understand it the napthoquinone ring structure is the active part of the molecule and the 4-14 is simply the number of side chair repeats. The number of side chair repeats influences the soluability characteristics of the molecule and its half life but not its basic mechanism of action. They all carboxylate gla proteins. So ANY methaquinone will inhibit calcification of endothelial cells and facilitate calcification of bone matrix.
Also, our own intestines work to further metabolize our methaquinones. Anerobic fermentation by our gut friendly bacteria may well change MK 4 into 5,6,or 7. Exactly how I am not sure. So the methaquinone you eat may well not be the methaquinone your arteries see.
Regardless of whether the K2 was M-4 or 7-9, most of it came from cheese right?
Any idea if -8 and -9 are found in the same places (i.e. cheese) as -7? In other words, if you're eating cheese that has been fermented with a bacterial culture, is it going to contain all three?
One of the things that puzzled me in the study is that they seemed to get quite a bit of -8 and -9, but almost no -7. Any guesses to how that could be?
Just some more info on K2. Most of the studies on K2 are either Dutch (Dr Vermeer's Group) ( Look up the Rotterdam Heart Study) or Japanese. The Dutch, of course study intake of fermented cheese, the Japanese study intake of Natto. Fermented cheeses include almost all imported cheese with holes in them. Hard cheese has more K2 that soft cheese. Processed cheese has none.
Examples of fermented cheese include Aged Goat cheese, Camembert,Blue Cheese, Stilton,Port du Salut, Feta, Aged Cheddar,Parmesian, Romano. Surprisingly Provolone, Ricotta, and Mozorella have no K2.
Hard fermented cheese has about 5mcg of MK4 and 40-75mcg of MK 8/9. Only fermented soy beans contain MK 7. To be more specific, only natto contains MK 7. The more palatable fermented soy products don't have any. (Miso, tempeh)
So rnikoley, the reason a dutch study shows no MK7 is because only the japanese can eat natto.
Stephan, infants can survive on pure MK 4 because of the bacteria in their in their intestines which can ferment MK 4 into its longer sidechain relatives.
Unfortunately we cannot directly measure K2 in the blood. The closest we can get is to measure undercarboxylated osteocalcin. How does K2 work? It carboxylates a substrate in tissue which is involved in whether or not calcium will be laid down at that specific site in the body. So in the heart, K2 STOPS calcium from being laid down. In the bone it FACILITATES its deposition. So, as I understand it, vitamin D lets the calcium in from the intestine, vitamin K2 tells it where to go.
For all you people who are wondering how such a crucial compound as K2 could be important in paleolithic evolution. After all primitive man did not ferment cheese or soybeans. The answer to this question lies within you. Anerobic fermentation in our intestines. We are host to more cells than we have stamped with our own DNA.
K2 probablly has more mysteries to reveal since it is also important in cell signaling involving growth or apoptosis. We just don't understand yet. Also it may be a partial answer to the french paradox.
Hope this helps. Bye now
Looks like those guys are suffering from the same debilitating brain condition as poor Dr. Cordain.
I'm also glad that Stephan came to the same conclusion I did when reading the paper; gives me confidence. :-)
I'm not surprised ricotta and mozzarella cheese have no K2. They're fresh cheeses, not aged; I've made them many times. Ricotta in particular is super easy - no cheese cultures even needed, just an acid medium. I use vinegar to "crack" the milk.
Interesting about infants surviving on pure MK-4 synthesizes from gut bacteria. Wonder about the difference in gut bacteria in vaginally-born infants (GI tract innoculated right away with mother's vaginal flora) compared to c-sectioned infants, or breastfed vs. formula fed (I seem to remember reading that it used to be a practice in Japan that mothers didn't wash their breasts for a month after birth, which would greatly facilitate bacterial GI innoculation in a nursing infant - don't remember the source, though, maybe Ron Schmid's Untold Story of Milk?). Birth method and early infant feeding variables are associated with a huge difference in infant gut bacteria population number and species balance.
Interesting about infants surviving on pure MK-4 synthesizes from gut bacteria.
I think you read that wrong. MK-4 is synthesized by the mother, not the child. It's in the milk.
Infants originally colonize their intestinal tracts primarily during the birth process through exposure to maternal vaginal flora. The pregnant uterus and fetal GI tract do not contain bacteria. The maternal vagina like it or not is colonized by the maternal GI tract. So if mom has a healthy gut, so does the infant. There are very few anerobic (fermenting) bacteria floating around on our skins. It is mostly staph and strep. It's the anerobic e coli, possibly the bifidobacter, and probably a whole host of other bacterial "denisons of the deep" which enter through the infant's mouth and nose to colonize the gut to help ferment a small amount of K1 into K2 and produce whatever form of K2 is ultimately used in the body. But you are right, breast feeding certainly does help. Very interesting point about not washing the breast!
Now here comes the modern labor and delivery deck. Mom has a low grade fever?, Mom needs a C/Section? You guessed it. Here comes the antibiotics. OOPs.
I don't know, but that's a good question. It's probably influenced by the amount of K1 and K2 in the diet. The human mammary gland is one of the more efficient tissues at making K2 from K1.
There are number of vitamins that have several forms. Vitamin E for example has 8 forms. Most of the research has focused on alpha-tocopherol, one of the eight. There are different forms of vitamin A as well. Plant precursors of vitamin A, the carotenoids, are commonly referred to as vitamin A but the human body converts them inefficiently to true vitamin A. Then true vitamin A can be in the form of retinyl ester, retinal, retinol, or retinoic acid. I think you can see why it's difficult to be too reductionistic about nutrition, it's extraordinarily complex.
The length of the side chain affects how the menaquinones are transported and metabolized. The longer ones (longer than 7) tend to get stuck in the liver, while 4 through 7 hang out in the circulation and are absorbed by tissues (although no one knows to what extent MK-7 is absorbed by various tissues). If you feed vitamin K-deficient rats MK-7, you find MK-4 in their bone, suggesting they convert MK-7 to MK-4.
Do you have evidence to support your statement that intestinal bacteria convert MK-4 to longer menaquinones? The most current data indicate that bacterial menaquinones from the intestine make a negligible contribution to vitamin K status in humans and rats. Researchers once thought rats absorbed K2 through the intestine but it turns out they get it by eating their own poop-- if you prevent coprophagy and don't feed them K1, they rapidly become K deficient (even though their colon is full of bacterial K2). The same seems to be true for humans, although we have a rather large store so it takes longer to deplete.
So I'm skeptical about what you said about babies converting MK-4 to longer menaquinones. Do you have evidence to support that? Rats seem to do just fine without any longer-chain menaquinones. When you feed them warfarin and MK-4, they only have MK-4 in their blood and tissues, no longer-chain menaquinones.
MK-4 came mostly from dairy and meat, the longer menaquinones came mostly from cheese.
My guess is the cheese microbes just preferred making MK-8 and MK-9 to MK-7. The menaquinones produced depend on the bacterium that's doing the fermenting.
Thank you for this wonderful blog. I'm finding answers to many of my questions, but they are being replaced with more questions.
Here's one-from reading this and doing some quick searches it seems that the standard practice of injecting babies with K1 at birth is just about worthless, right? If K2 is what is needed for clotting, then we need to be addressing the lack of K2 in the mothers diet. After my son became dangerously jaundice after his vit K shot, I rejected it for my 2 daughters. I just can't believe that babies are born so faulty that they need immediate "fixing".
Should the Korean soybean product "chunkukjung" contain K2 as well? There is also a Chinese fermented soybean food. All are prepared slightly differently. The Korean version is often ground into a powder after fermentation and then salted.
Vitamin K1 is effective for activating liver clotting factors, it's the rest of the K-dependent proteins that can't use it effectively. I can't say for sure why babies are born clotting deficient, maybe it's because mothers tend to be K2 deficient and K2 would be a significant contributor to clotting factor activation in infants?
K1 crosses the placental barrier in rats but there has to be a lot of it in circulation for that to happen significantly. Humans don't absorb much K1 from food so it's possible K1 wouldn't contribute much to infant clotting status. Just speculating.
I don't know. It would depend on the organism it's cultured with. Natto is made with Bacillus subtilis. If those are made with B. subtilis then they would probably contain lots of MK-7 like natto. Otherwise, it would depend on how much and what type of menaquinone the specific microorganism in those foods produces.
I'm new at blogging and can only get the google blogger to work on my home computer. Alot of my reference material is at work so if you ask me a question for a reference there may be a delay.
"MK 7-10 are synthesized by bacteria in the colon." Schurgers LJ, Z Kardiol 2001,90,suppl 3,57-63. This is the same Dutch group whose latest study prompted this post. Another tidbit from the same article: Pancreas, testes, and arterial vessel walls convert Vitamin K1 to MK4. But once you are out of the intestines and into the body you can't get MK4 to convert into the longer methaquinones.
Natto interests me for reasons other than MK7. My reading is that it is fermented by bacillus natto whereas other fermented soy products do not use b natto. (I don't know if b. subtilis is just another name for b. natto or if they are just close cousins. Probably doesn't matter.) I'd like to know more about nattokinase. Nattokinase is a PAI1 inactivator. PAI1 is prothrombotic but acts at a different point in the clotting cascade.
The take home message for me is this. I'll eat more fermented cheeses. Natto is interesting but I just can't bring myself to eat it. I'm leary of supplementing with a gelcap because we don't know yet what form is best and what dose is optimal.
"I'm leary of supplementing with a gelcap because we don't know yet what form is best and what dose is optimal." - homertobias
If you believe the data in The Rotterdam Heart Study, then a threshold of 32.7 micrograms of K2 from fermented hard cheese (MK-7) is associated with a 52 percent lower risk of severe aortic calcification, a 41 percent lower risk of CHD, and a 51 percent lower risk of CHD mortality.
Dr. Leon Schurgers (www.menaq7.com) seems to favor MK-7 at a daily dose of 45-90 mcg. http://www.google.com/products?hl=en&q=menaq7&scoring=p
Weston Price used animal fat (concentrated butterfat (MK-4) from ruminants grazing on fast growing pasture) in his "Activator X" calcium metabolism studies. David Wetzel of Green Pasture Products seems to be a good source of natural MK-4 at a controlled dose that Price may have used in his experiments. No need for "supplementing with a gelcap" if you get an 8oz. bottle. I consider this butter oil more as a food source than a supplement anyway:
David Wetzel is not a doctor, but has an interesting theory. That, the benefits from Price's Activator X is actually from a group of fat soluble nutrients (found in vitamin A, E, K and COQ) that have yet to receive much attention called quinones:
Gut bacteria synthesize longer menaquinones, but are you sure they make it from MK-4? Bacteria can make menaquinones from scratch. Besides, by the time bacteria are making menaquinones, they're too far down the gut for us to absorb them.
B. natto is the older name for B. subtilis. The thing I don't understand about nattokinase is how can an ingested enzyme do anything other than act in the gut? Enzymes don't cross into circulation, so how could it have the effects that are ascribed to it? I don't know anything about it, just curious.
Thanks for the links. I am enjoying poking around in them. The Rotterdam study used cheese not supplements and the dutch certainly make delicious cheese.
I buy raw butter (Pasture fed) at either Sprouts or Whole Foods markets. Wonderful stuff.
For me the jury is still out on injesting Vitamin A. Of course that could be a post in itself.
Stephan. Interesting about nattokinase.
I find it curious that the Japanese seem to be promoting MK4 and the Dutch MK7.
What do you guys think of liverwurst? I found a source for grass-fed organic liverwurst, here's the ingredients:
grass-fed beef trim (30%),liver (30%), heart (20%) and kidney (20%), water, sea salt, onion powder, honey, white pepper, coriander, marjoram, allspice
I bought some and I'm trying to figure out how to eat it. It is inoffensively bland with a slightly weird distinctive smell, but the texture is pretty soft.
I love liverwurst, especially with brown seed mustard! I even loved it as a kid, but didn't like liver.
I think liverwurst is a good way to eat liver, esp if regular liver is too strong. My SIL in Norway and a German-raised friend here feed liverwurst spread on bread (of course) to their kids for breakfast and snacks. Then again they also eat fish ( pickled herring, etc.). Wish I could get my kid to go for that sort of thing, but at least we're backed away from the cold cereals...some things take time. But I think savory breakfasts (like fish and liver) are important to start very young, or else taste for it is hard to develop later.
The best grocery store liverwurst I can find is Boar's Head brand (only marginally better than the Farmer John's and Oscar Mayer, with preservatives, sugars, and additives I wouldn't want). I'd eat those options once in a while, but it isn't what I'd want for regular consumption.
The liverwurst you mention and US Wellness Meats look like good options, though I haven't tried them yet. Need to do so, or learn to make it myself (I have a good sized meat grinder). I think it probably freezes well, and would likely slice into 3-day sized portions with just a bit of thawing, so a bulk purchase is a reasonable option. I know US Wellness Meats often has coupons for regular customers and many like their products and ordering system.
"I buy raw butter (Pasture fed) at either Sprouts or Whole Foods markets. Wonderful stuff." -homertobias
I'm sure raw pastured butter is wonderful.
But a lot of people can't get raw dairy. I.e., My home state of Maine, due to maximizing their covert efforts to discourage local dairy farmers from selling raw products, has made it very difficult for someone like myself. And, it's against US federal law to ship/transport raw dairy across state lines.
But, I believe those who can't find local raw pasture should NOT be discouraged because, AFAIK, Vitamin K2 is heat stable.
Organic Valley widely distributes a limited edition pasture butter (May-September cream) that has been minimally pasteurized:
We can also order summer/pasture butter online from Pastureland:
If you like ghee (and can afford it) this looks like a good place to order pasture ghee online (I've never personally ordered from them... yet):
I just bought Carlson K2 - MK-4 in the 5mg dose. 5mg is 5 milligrams, right? If so, 5mg = 5,000 micrograms, right? But if every daily 10 micrograms dose lowers my risk of heart attack 9%, I should have virtually no chance of having a heart attack, right?
I have a feeling that I'm misunderstanding something here. Can anyone shed some light on this?
Your risk of heart attack will be in the negatives, haha! The study was observational so I can't say for sure that taking K2 will reduce your risk. I think there's good reason to believe that K2 is a factor. But remember, these people were getting K2 from diet, which comes in conjunction with a number of other nutrients that act together with K2 (A, D, minerals). Who knows what taking 5 mg of isolated K2 will do; that's an unnatural dose. The Japanese trials showed that 45 mg per day is well tolerated over a period of a couple of years (i.e. no detectable negative side effects on average). But again, 5 mg of straight K2 is outside your body's normal operating parameters.
Stephan, the "natural dose" of K2 something I've actually been wondering about. Have you seen any estimates on what the "natural" intake of K2 is in H/G diets?
I'm not sure, because K2 hasn't been measured in many foods. I give a rough estimate of 500 micrograms per day as the reasonable upper limit from food, but that requires neolithic foods like foie gras and pastured butter.
Certain organs contain a high concentration of K2 but to my knowledge it hasn't been measured in wild animals that would have been prey to HGs. I'd be surprised if HGs consistently got more than 100 micrograms per day. I also suspect that there may be something in wheat, sugar or both that increases the need for K2.
Thanks for posting this! Maybe I am forgetting/misunderstanding statistics, but isn't it the case that when this is present: "Hazard Ratio (HR) of 0.91 [95% CI 0.85-1.00]" then this study is largely, well, useless? Am I correct in understanding that because of that 1.00 there, this study has absolutely no statistically significant implications?
Aha, a skeptical reader, I like it! That hazard ratio is per 10 micrograms of K2. I believe what they did was first establish that K2 is significantly inversely associated with CHD risk in general. The mean intake was 29 micrograms, with quite a bit of variability, so people with the highest intake had a better HR than 0.91 with a more solid 95% CI.
Then they went back and tried to quantify the risk reduction per unit K2, which yielded the 0.91 HR. I agree this kind of analysis is a bit shaky, but it doesn't detract from the inverse association between K2 and CHD.
Stephan: How would one measure Vitamin K2-MK7 cardiac protective effect unless you established a baseline with a cardiac catherization and found disease, then took Vitamin K2-MK 7 supplements for a period of time, then redid the cardiac catherization. No insurance would pay for research catherizations. What other objective measureable test would you suggest in place of that?
You could do a controlled clinical trial with MK-7 vs placebo where they look at cardiac outcomes like mortality. It's been done with a number of other isolated nutrients.
Greetings Dr. Stephen,
I come to you by way of Richard Nikoley's blog. I was reading one of his pieces on vitamin supplements, and got interested in the K1 vs. K2 since the vitamins my family has been taking all have K1.
My question is, might the benefits of dietary K2 intake relative to dietary K1 be coincidental? It seems bacteria in the gut process K1 into K2 for absorption? If that is the case, maybe the better health from those that "eat" K2 is not from the K2, but from other things (lipids) that come along with the food they eat?
Has a study been done to this effect? Can K2 levels be measured in the blood? Has anyone measured the K2 levels of people that ingest K1 vs. those that ingest K2?
Um, sorry never mind that last post. I see it was covered in other's comments. Feel free to delete.
In a word, no. K1 to K2 conversion tops out at 100 mcg/day or so. That keeps your bones from dissolving, but it's not the optimal dose. We don't know for sure what the optimal dose is, but Weston Price's studies suggested that the 'cultural wisdom' of native peoples pegged it between 500 and 1000 mcg/day.
Independent studies in Japan and the Netherlands confirm the benefits of high-dose K2 supplementation. Way higher than the body can convert on its own.
It seems you don't know Mr. expert but vitamin K is found in lettuce, parsley..
Leafy green vegetables (kale, collards, spinach, turnip greens, beet greens, mustard greens, dandelion greens green leaf lettuce), Brussels sprouts, broccoli, green onions, parsley, asparagus and sauerkraut contain more than the RDA of vitamin K for men or women.
The post is about vitamin K2 MK-4, which is only found in animal foods. The plant foods you mentioned contain none.
I am curious to know if K-2 in
menatetrenone (fermented brown rice) form has the same effect as K-7. Is it true that vitamin K plays a role in gamma-carboxylating all of the amino acids?
Thanks for this amazing blog, my interest is the nutrient content of wild foods and therefore how traditional cultures prepared wild foods, also being a vegan (of over 10 years) i am always looking for plant derivatives of all nutrients and how to access them and since finding your blog i have not been able to ‘ put it down’ the articles and dialogues that follow are possibly the most interesting stuff i have read on the subject ever. that this site was so Paleo didn’t occur to me straight away(i hadn’t even heard of the term before visiting here)but i am also concerned with meat and dairy too, because my family are all meat and dairy eaters . Anyway putting the two quotes of some of your words (Stephan) together,
“If you feed vitamin K-deficient rats MK-7, you find MK-4 in their bone, suggesting they convert MK-7 to MK-4.”
“Natto is made with Bacillus subtilis.If those are made with B. subtilis then they would probably contain lots of MK-7 like natto”
Do you think we can convert MK-7 natto to M-4? Because if i have this correct that would mean that we can indirectly get MK 4 from a plant resource and not have to eat meat for it? it would also mean that i have to start eating natto...yesterday!
I'm seeing a lot of people post about K2 being produced in the gut but bacteria. Problem is, the vast majority of people have taken anti biotics at some point in their lifetime, and unfortunately the volume of bacterial colonies destroyed probably kill any chance of you manufacturing it in the gut.
I know we have pre and probiotics but the few they sell on the shelves are nothing compared to the thousands upon thousands of species lost following anti biotic use.
Sadly unless you can get a hold of live breast milk or colostrum you're probably not going to be able to manufacture K2 in the gut and that's possibly why heart disease is at an all time high besides the volume of junk they sell on shelves these days.
Which leaves us with supplementation where K2 is concerned if you're needing to keep your arteries clean. The other point is it is the methionine in red meat that causes inflammation in the arteries and omega 6 fats (which have been converted to trans fats), and fructose and sugar which cause arterial plaque.
It's now said that it is actually a Vit C deficiency which allows the arteries to be lined with plaque. That taking high dose L Lysine and Vitamin C can reverse arterial plaque problems as both combined literally clean the arteries and cardiovascular system over time.
I think its good that nature gives the body numerous ways in which to recover from disease.
Adding to all the K2 oddities out there is this study from 2012: http://www.ncbi.nlm.nih.gov/pubmed/23140417
They gave 420 μg of either MK-4 or MK-7 for seven days to healthy Japanese woman. Guess what? MK-7 blood levels rose significantly at 4h and 48h after the first dose and after 7 days of treatment.
MK-4 didn't rose at all, neither after the first dose nor after 7 days. It's not just that it didn't rose significantly, it wasn't even detectable!
So what's your take on this odd result? Does it explain why the Danish study supposedly found a protective effect for >MK-4 only? Or did the MK-4 got "suck up" by the tissues that fast (<4h)? Or maybe there measurement methods were faulty? Very strange result anyway...
OK, after following all the references provided by aforementioned study I have to say that today there seems to be conclusive evidence that MK-4 in normal dietary (sub-mg) amounts is probably very much worthless (that's probably the reason the Japanese bone density trials used a much higher, pharmacological dose of 45mg). Even vitamin K1 seems to raise MK-4 levels in the body much more efficently that MK-4 itself, whereas MK-7 appears highly efficient in raising blood and tissue levels of MK-4. Those findings fit right in with the observation of the Dutch (not Danish, sorry!) study, where only the longer chain forms - and not MK-4 - were associated with coronary risk reduction. We now know that only these forms are absorbable, whereas dietary MK-4 largely passes through the system unused.
Maybe this is a good example of how far astray our resoning sometimes goes, when we wear those paleo-eyeglasses. Everything makes perfectly sense as long as we gaze through them, but when we are forced to put them down we are confronted with a empirical reality that sometimes just doesn't fit in with our (our Weston A. Price's for that matter ;) romantic notions about a supposedly paradisiac paleolithic past.
The studies showing MK-4 useless typically use relatively small amounts of MK-4. Ive seen them try to use 45ug daily.
I'd like to see studies that use 45mg and higher daily doses of MK-4!
45mg is 100 times larger than 450ug.
The Dutch that eat the cheese are getting MK-4, not MK-7. The smaller amounts in the cheese appear to help them.
A vast majority of studies are flawed and/or have conflicts of interests.
Post a Comment