(K1) and menaquinone (K2). K1 is concentrated in leafy greens and other green vegetables. K2 can be further subdivided into menaquinone-4 through -14. The number represents the length of the side chain attached to the napthoquinone ring.
Menaquinone-"X" can be abbreviated MK-"X". MK-4 is the type synthesized by animals for their own use from K1 (and from MK-7 in rats). MK-5 through MK-14 are synthesized by bacteria. MK-7 in particular is made in large amounts by the bacterium Bacillus subtilis that ferments the infamous Japanese condiment natto. It's also sold as a supplement. Animals concentrate MK-4 in a number of organs, with smaller amounts of K1. Certain organs such as the brain, pancreas and salivary gland show an overwhelming preference for MK-4 over K1 in rodents and humans. The liver is a notable exception; in some animals, including humans, it concentrates longer menaquinones to a greater extent than MK-4 if they're present in the diet.As far as I can tell, MK-4 is capable of performing all the functions of vitamin K. MK-4 can even activate blood clotting factors, which is a role traditionally ascribed to vitamin K1. Babies are often born clotting deficient, which is why we give newborns vitamin K1 injections in the U.S. to prevent hemorrhaging. In Japan, they give children MK-4 to prevent hemorrhage, an intervention that is very effective. Could that have to do with the fact that Japan has half the infant mortality rate of the U.S.?
Certain cultures would have had a predominance of MK-4 over other forms of vitamin K in the diet, which supports the idea that MK-4 can stand nearly alone. These cultures include heavy consumers of dairy like the Masai. Humans go through one of their most critical growth phases-- infancy-- with most of their vitamin K coming from MK-4. Colostrum, the first milk to come out, is particularly rich in MK-4.
Vitamin K is required to activate certain types of proteins, called Gla proteins. Gla stands for gamma-carboxyglutamic acid, a modified amino acid that's synthesized using vitamin K (by a reaction called gamma-carboxylation). Gla proteins are important: the class includes MGP, osteocalcin and blood clotting factors, important for keeping arteries clear, bones strong and blood clotting correctly.
I've said before that vitamin K's function is to carboxylate Gla proteins. In fact, that's a gross oversimplification. Research on vitamin K2 is turning up new functions all the time. One of the more exciting things that's been discovered is that it acts like hormone, activating a nuclear receptor called the steroid and xenobiotic receptor (SXR) and thereby influencing the expression of a number of genes. This puts it in the same category as vitamin A and D. It also acts as an antioxidant, a cofactor for sphingolipid synthesis in the brain, and an activator of protein kinase A signaling. These are all functions that have been studied in the context of MK-4, and for most of them, no one knows whether MK-7 has equivalent effects.
I'm always on the lookout for studies that can shed light on the question of whether MK-4 and MK-7 are equivalent. MK-7 is able to activate clotting factors and osteocalcin, so it can clearly function as a cofactor for gamma-carboxylation in some contexts. Osteocalcin is a Gla protein that's important for bone health. MK-7 supposedly hangs out in the blood for longer than MK-4 in humans, which is one of the things MK-7 supplement manufacturers like to mention, but these findings were conducted by MK-7 supplement vendors and the results have not been published. Interestingly, MK-4 and MK-7 have the exact same plasma half-life in rats, so I think the human experiment should be repeated. In any case, a longer plasma half-life is not evidence for superiority of one form over another in my opinion.
Today, I found another difference between MK-4 and MK-7. I was reading a paper about SXR-independent effects of vitamin K2 on gene expression. The investigators found that MK-4 strongly activates transcription of two specific genes in osteoblast cells. Osteoblasts are cells that create bone tissue. The genes are GDF15 and STC2 and they're involved in bone and cartilage formation. They tested K1 and MK-7, and in contrast to MK-4, they did not activate transcription of the genes in the slightest. This shows that MK-4 has effects on gene expression in bone tissue that MK-7 doesn't have.
I tend to think there's a reason why animals synthesize MK-4 rather than other forms of vitamin K2. Vitamin K2 MK-4 seems to be able to perform all the functions of vitamin K, including activating Gla proteins, participating in sphingomyelin synthesis, binding SXR, and activating transcription through protein kinase A. That's what you would expect for an animal that had evolved to use its own form of K2. Investigators haven't tested whether MK-7 is capable of performing all these functions, but apparently there's at least one it cannot perform.
I'd bet my bottom dollar there are other important functions of MK-4 that have not yet been identified, and functions whose full importance has not yet been appreciated. There's no way to know whether MK-7 can fully stand in for MK-4 as long as we don't know all of MK-4's functions. I also think it's worth mentioning that MK-4 is the only form of vitamin K2 that's been shown to reduce fracture risk in clinical trials.
That being said, MK-7 may still have a place in a healthy diet. Just because it can't do everything MK-4 can, doesn't mean it has no role. It may be able to fill in for MK-4 in some functions, or reduce the dietary need for MK-4. But no one really knows at this point. Hunter-gatherers would have had a source of longer menaquinones, including MK-7, from livers. So it's possible that we're adapted to a modest MK-7 intake on top of MK-4.
42 comments:
I agree that we are mostly just ignorant, but I have developed this hypothesis based on what we know so far:
1. MK-4 and MK-7 are not analogues in the majority of respects. Situations where MK-7 can take MK-4's place will be the exception, not the rule.
1.a. I believe this because (another guess here) the liver rounds up and holds on to MK-7 to prevent it from interfering with MK-4 processes in the other tissues until the MK-7 can be flushed from the body. It's similar enough to mess things up.
1.b. Similarly MK-7 hangs out in the blood of humans because our tissues do not want it.
2. Rats have been eating rancid (meaning MK-7 rich) foods for much longer than primates, which has allowed them to evolve additional mechanisms for using this resource. Humans could theoretically evolve this mechanism too, but so far have not.
2.a. MK-7 depletes quickly from rat blood because they are converting it into MK-4 at the same rate as MK-4 depletion.
Brock,
Great set of hypotheses! Let's test one prediction by inhibiting the conversion of MK-7 to MK-4 in rats and see it affects blood plasma level of both and on their health.
All very interesting comments Brock.
From the standpoint of my pocketbook, I just wish that mk4 was as cheap and as easy to find as mk7.
StephenB
Stephan,
I just want to understand why you care so much about whether these two particular menoquinones are equivalent.
We are so early in discovering the Vitamin K story that it is impossible to tease out the exact most active ingredient and ingest it. I'm sure the nutriceutical industry will try to fund research proving that their particular patented Vitamin K is superior.
Even now I wonder how much money exchanges hands between the Dutch cheese board and the Dutch researchers.
My feeling is that time and again when we purify out the "true active" ingredient we ruin its nutritional value.
Perhaps your interest is more scientific in nature. Why do you care?
Brock, I'm not so sure rats have been eating rancid foods longer than primates, as both have been scavengers and opportunistic eaters for millions of years during their evolution. And this brings me to my next question:
Stephen, if bacteria are responsible for creating many of the menaquinones as well as certain vitamins both within our systems as well as those in foods we eat, how do you feel about the hygiene hypothesis?
http://en.wikipedia.org/wiki/Hygiene_hypothesis
Part of poor health in western society could also be related to refrigeration, antibiotics, freeze-drying and food preservation techniques, anti-bacterial soaps, and a general philosophy geared towards killing off bacteria science has written off as harmful, but with which we've actually developed a symbiotic relationship over millions of years.
Very good stuff. If all K's get metabolized to some extent via toxic menadione, however, in order to reduce the toxic load it might make sense to take the minimum needed to get the desired effect, which means MK-7 and not MK-4 (because less MK-7 is needed)??
Is MK-4 converted to MK-7 in the human body? Could this be part of the reason why MK-4 has a lower half-life in the blood because it is isomerized or converted to other menaquinones, namely MK-7? Have there been any studies that show that blood concentrations of MK-7 rise proportionally after ingesting MK-4? It's my understanding that MK-7 is said to be a more biologically active menaquinone.
Brock,
Sounds plausible. The thought has also crossed my mind that MK-7 could interfere with MK-4 function. I haven't seen any evidence to support that yet though.
Aaron,
That would be a good experiment. I wonder how you would block the conversion?
Homertobias,
Like you, I think the bottom line is the same as always: eat food. I'm interested in this question because vitamin K2 has been getting a lot of attention lately. Supplement manufacturers are jumping on the bandwagon. People are taking K2 supplements and they're deciding between MK-4 and MK-7. MK-7 vendors have been making loud claims that MK-7 is superior to MK-4, so I felt the need to give a less biased assessment.
Gunther,
I think it's a plausible hypothesis. I don't feel totally convinced by it yet but I'm willing to be.
Micawber,
It depends on what effect you're after. If all you want to do is carboxylate serum osteocalcin, then take MK-7. If you want K2 that will do everything K2 is supposed to do, including activate PKA-dependent transcription, then MK-4 is what you want.
Jason,
I'm not aware of any evidence that MK-4 is converted to MK-7 in humans or rodents. In fact, rats will convert MK-7 to MK-4.
No one can make the statement that MK-7 is more biologically active than MK-4 at this point because most of MK-4's functions haven't been evaluated head-to-head with MK-7. We don't even know at this point if MK-7 can do a fraction of the things MK-4 can in the body. Maybe it can, but we just don't know.
MK-7 does carboxylate osteocalcin more than MK-4 at the same dose, but that's just one of MK-4's many functions. MK-7 isn't capable of activating PKA-dependent transcription in bone cells. So I don't think there's any foundation for the statement that MK-7 is more biologically active.
HI,
I guess my main point about Vitamin k2 is it is too soon to get polarized in one menaquinone camp. If you feel the need to supplement, please take both. OK, so we know alot about the coagulation pathways and Vitamin K. We know something about gla proteins and inhibiting/promoting calcification in bone or arterial walls. What do we know about undercarboxylation of endometriosis? How about malignant breast calcifications? What about Gas6? or PRGF 1 or 2. Or the konatopins?
Why, if K3 is toxic, does it effectively inhibit cancer cell growth?
If you feel the need to supplement, please hedge your bets. Theres alot more going on here than a dutch experiment comparing plasma levels or bone strength of Vitamin K1 (not mk4) to mk7.
Is MK7 consumed by the majority of the human race in significant quantities?
The only vitamin that we truly seem to require supplementation for as modern humans appears to be vitamin D just because we spend so much time inside. Everything else can be had from a varied, nutritious diet with an absence of anti-nutrients. One can spend a lot of money on supplements, but do they really improve your quality of life and/or lifespan, or is someone just selling you something? I'd rather spend $1-5 a day on higher-quality food than supplements.
It's interesting to note that many French people get a high intake of both -4 and -7, the former from foie gras (and other pate and liver containing charcuterie) and the latter via their cheese.
And, they're not afraid of the sun, either, if the view from my former terrace overlooking Pt. St Louis in Toulon was any indication (bare bresties, & all :)
I'll bet those factors have far more to do with explaining the "French Paradox" than red whine and resveritol.
Hey Stephen,
Fascinating blog. I enjoy reading it. However at the imminst.org forum we are also discussing the matter.
One particular user who is very knowledgeable has 2 counter claims in favor of MK-7 that I want your opinion on:
1. MK-7 has a much longer half-life because it's more fat soluble than MK-4. You thus get more bang for the molecule.
2. See PMID: 10084398. MK-7 gets converted to MK-4 in the tissues, so in vivo MK-7 will activate those genes.
And here is a third point to consider:
K1 reduces glutathione transferase activity, so I don't take any. All K's get metabolized to some extent to toxic menadione, so I take the minimum needed to get the desired effect, which means MK-7 and not MK-4. PMID: 19179058 found lower CHD risk in the Prospect-EPIC cohort mainly from MK-7, MK-8, and MK-9. I don't believe it was because MK-4 was lacking in their diets, because another study on this cohort reported MK-4 intakes higher than MK-7 and MK-8.
Semin Thromb Hemost. 1995;21(4):357-63.
Observations on vitamin K deficiency in the fetus and newborn: has nature made a mistake?
Israels LG, Israels ED.
Department of Medicine, University of Manitoba, Manitoba Institute of Cell Biology, Winnipeg, Canada.
The microsomal mixed function oxidase system metabolizes xenobiotics (Phase I) to products that, if not activated and conjugated for excretion (Phase II), are capable of forming conjugates with cellular macromolecules, including DNA, resulting in toxic, mutagenic, or carcinogenic events. Benzo(a)pyrene (BP), a polycyclic aromatic hydrocarbon, is a model carcinogen for this system. Vitamin K1 (phylloquinone) is a regulator of BP metabolism. These studies demonstrate that K1 is capable of increasing Phase I metabolism and decreasing glutathione transferase activity (Phase II) in chick embryo liver; that deprivation of K1 reduces BP/DNA adducts in mouse liver and reduces tumor formation in mice given intraperitoneal BP; and that K1 supplementation increases BP induced tumor formation in mice. However, epidemiologic studies indicate that children of mothers who smoke during pregnancy may not be at increased risk of cancer. It is known that the placentas from these pregnancies exhibit markedly increased levels of arylhydrocarbon hydroxylase induced by the polycyclic aromatic hydrocarbons in tobacco smoke, but there is no corresponding increase in this enzyme activity in the fetus in such pregnancies. We suggest that the low vitamin K level is a secondary protective mechanism for xenobiotics, such as BP, that may escape the primary placental screen. The recently described role of vitamin K-dependent Gla protein as ligands for receptor tyrosine kinases, also establishes K as a link in cell growth and transformation. It is proposed that the small total body pool of K1 in the adult, which is sufficient only to meet continuing needs, and the even smaller pool in the fetus are protective. This protective effect of low K1 levels is particularly important in the presence of the high mitotic rates and rapid cell turnover in the avian embryo and mammalian fetus.
PMID: 8747698
Br J Nutr. 2006 Feb;95(2):260-6.
Menadione is a metabolite of oral vitamin K.
Thijssen HH, Vervoort LM, Schurgers LJ, Shearer MJ.
Department of Pharmacology, Cardiovascular Research Institute Maastricht, University of Maastricht, PO Box 616, 6200 MD Maastricht, The Netherlands. h.thijssen@farmaco.unimaas.nl
Phylloquinone is converted into menaquinone-4 and accumulates in extrahepatic tissues. Neither the route nor the function of the conversion is known. One possible metabolic route might be the release of menadione from phylloquinone by catabolic activity. In the present study we explored the presence of menadione in urine and the effect of vitamin K intake on its excretion. Menadione in urine was analysed by HPLC assay with fluorescence detection. Urine from healthy male volunteers was collected before and after administration of a single dose of K vitamins. Basal menadione excretion in non-supplemented subjects (n 6) was 5.4 (sd 3.2) microg/d. Urinary menadione excretion increased greatly after oral intake of the K vitamins, phylloquinone and menaquinone-4 and -7. This effect was apparent within 1-2 h and peaked at about 3 h after intake. Amounts of menadione excreted in 24 h after vitamin K intake ranged, on a molar basis, from 1 to 5 % of the administered dose, indicating that about 5-25 % of the ingested K vitamins had been catabolized to menadione. Menadione excretion was not enhanced by phylloquinone administered subcutaneously or by 2',3'-dihydrophylloquinone administered orally. In archived samples from a depletion/repletion study (Booth et al. (2001) Am J Clin Nutr 74, 783-790), urinary menadione excretion mirrored dietary phylloquinone intake. The present study shows that menadione is a catabolic product of K vitamins formed after oral intake. The rapid appearance in urine after oral but not subcutaneous administration suggests that catabolism occurs during intestinal absorption. The observations make it likely that part of the menaquinone-4 in tissues results from uptake and prenylation of circulating menadione.
PMID: 16469140
Nutr Metab Cardiovasc Dis. 2009 Jan 27.
A high menaquinone reduces the incidence of coronary heart disease in women.
Gast GC, de Roos NM, Sluijs I, Bots ML, Beulens JW, Geleijnse JM, Witteman JC, Grobbee DE, Peeters PH, van der Schouw YT.
Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, The Netherlands; Department of Human Nutrition, Wageningen University, The Netherlands.
BACKGROUND AND AIM: Vitamin K dependent proteins have been demonstrated to inhibit vascular calcification. Data on the effect of vitamin K intake on coronary heart disease (CHD) risk, however, are scarce. OBJECTIVE: To examine the relationship between dietary vitamins K(1) and K(2) intake, and its subtypes, and the incidence of CHD. METHODS AND RESULTS: We used data from the Prospect-EPIC cohort consisting of 16,057 women, enrolled between 1993 and 1997 and aged 49-70 years, who were free of cardiovascular diseases at baseline. Intake of vitamin K and other nutrients was estimated with a food frequency questionnaire. Multivariate Cox proportional hazards models were used to analyse the data. RESULTS: After a mean+/-SD follow-up of 8.1+/-1.6 years, we identified 480 incident cases of CHD. Mean vitamin K(1) intake was 211.7+/-100.3mug/d and vitamin K(2) intake was 29.1+/-12.8mug/d. After adjustment for traditional risk factors and dietary factors, we observed an inverse association between vitamin K(2) and risk of CHD with a Hazard Ratio (HR) of 0.91 [95% CI 0.85-1.00] per 10mug/d vitamin K(2) intake. This association was mainly due to vitamin K(2) subtypes MK-7, MK-8 and MK-9. Vitamin K(1) intake was not significantly related to CHD. CONCLUSIONS: A high intake of menoquinones, especially MK-7, MK-8 and MK-9, could protect against CHD. However, more research is necessary to define optimal intake levels of vitamin K intake for the prevention of CHD.
PMID: 19179058
Thank you for the great posts, Stephan!
As for the supplement issue, with all the respect to many, I'm growing less and less comfortable on them, as sound as the theory may sound on each case. And this is why.
I've been on lowcarb for 8+ years. For the last 4 years it has been a diet high in animal fats, low in grains & Pufa - and totally without supplements (including fish oil and vitamin D). Furthermore I've been without fish all my life, due to allergy.
Before lowcarb I had all the flu's there were around, and most of them ended up as imflammations in respiratory channels, as a long afterplay. This happened several times every year, as can be seen in my old work diaries.
How about the last four years (on low carb which gets closer and closer to Kwasnievski OD)? No colds and no flus.
Yet I'm working at the office, live high up north (in southern Finland, to be exact), I don't excercise generally much - and none in winter.
So, how can an elderly lady who was very, very prone to imflammations the first 40 years of her life, now stay clear of those - even without pills? I'd blame it on the grainless diet and butterfat (which is my staple food). But that's only me :)
Regards,
LeenaS
LeenaS, I'm curious about the source of your butter. The Swiss people profiled by Weston Price ate butter (and cheese) from grass-fed cows as a staple during the winter, too. They certainly weren't getting vitamin D from sunlight either and did quite well. Thanks.
Hi, Scott. Butter and vitamin D is an interesting issue, at least locally :)
Before the cholesterol scare, a hint of acidity in the Finnish butter, due to fermenting, won many prices internationally. Almost ironically, our one and only Nobel prize in sciences was won on 1945 by a guy, who invented the way to preserve hay as green stuff, just for nurture of (dairy) cows during the winter (see wikipedia here) http://en.wikipedia.org/wiki/Artturi_Ilmari_Virtanen
So, dairy cattle here is kept indoor for most of the year, but it is sill largely fed with this AIV feed and not grains. Furthermore, butter is slightly fermented also nowadays. Weather this feed boosts vitamin D, is a good question. However, it might well preserve a good deal of vitamin K1, which could be transformed into K2. This is because preservation in human food seems to do that same trick.
So (sorry, long story), my high school textbook on household and cooking described butter as one of the big vitamin D sources. And that was in 1970's.
Then, thanks to the North Karelia project, butter was given extremely bad reputation (although at that time poor folks here were loaded with new, cheap margarine, not butter). So butter and especially its nutritional value was dismissed practically everywhere in text books - and it has never returned. Which makes me think that Orwell's changing of history or facts of 1984 may be a lot easier than we thought?
Regards,
LeenaS
First, I love your blog, and I have learned a lot from you.
Second, I know this was just a tangential throwaway line:
"Could that have to do with the fact that Japan has half the infant mortality rate of the U.S.?"
Nevertheless, as an American radiologist, I have gotten very tired of politicians and others using published infant mortality rates as a club to bash American health care. There are many shortcomings in American health care, but I don't think that infant mortality is one of them.
Infant mortality rates reflect many things, including the health and nutritional status of the mother. A large driver of infant mortality in the US is premature births. During my internship, the largest cause of premature labor in my hospital was acute cocaine toxicity. Many of these labors resulted in premature births and infant mortality. These deaths are certainly reflective of a problem in American society, but I don't think they are an example of a problem in American health care.
There are significant differences between the ways infant mortality is reported in different countries. The wikipedia article
http://en.wikipedia.org/wiki/Infant_mortality
discusses this quite well, including this bit about Japan:
This point is reinforced by the demographer Ansley Coale, who finds dubiously high ratios of reported stillbirths to infant deaths in Hong Kong and Japan in the first 24 hours after birth, a pattern that is consistent with the high recorded sex ratios at birth in those countries and suggests not only that many female infants who die in the first 24 hours are misreported as stillbirths rather than infant deaths but also that those countries do not follow WHO recommendations for the reporting of live births and infant deaths.[10]
I think that America does a great job in rescuing premature babies, and in counting our failures. Could we do better? Sure, but it isn't easy. Many expectant mothers are first seen by a physician when they are in labor. That would be a hard thing to change in our society.
Can we learn some things from Japan and other countries? I'm sure we can. Hopefully some American pediatricians are reading the article you reference and considering a change in how we give vitamin K to newborns.
Robert,
I tend to agree with what you said.
Richard,
I agree, I think resveratrol is a pathetic attempt to resolve the "French paradox".
Pieter,
I don't think MK-7's longer half-life has to do with its solubility. It gets transported differently by lipoprotein particles. Rats can and do convert MK-7 to MK-4, but it's not clear that happens in humans. Our menaquinone metabolism pathways seem to be less robust than rats'.
I wouldn't get too caught up in extrapolating health effects from biochemical studies in the medical literature. In my opinion, the only thing that's certain is that a diet rich in MK-4 is healthy. As far as supplements go, it's anyone's guess because the studies haven't been done. MK-4 supplements can effectively reduce fracture risk, but that's about all we know for sure about them. MK-7 hasn't been tested yet but it probably will be soon enough. I also don't have a lot of faith in the ability of observational studies to distinguish between the effects of the different menaquinones. Cheese contains all of the MKs they looked at so how well can they really separate them? And MK-4 is the one that reverses arterial calcification in rats. Just my opinion.
LeenaS,
Thanks for your observations. It seems like a good diet can have a remarkable effect on the immune system.
Dennis,
That infant mortality comment was actually a little joke, I'm not really suggesting that's why they have lower mortality. If I understood correctly, you were suggesting the relatively high rate of infant mortality in the U.S. is more due to the health of the mother/infant than medical care. I'm not an expert but I would tend to agree based on what I know. Mortality isn't the only problem we have, there's also premature births as you mentioned, low birth weight etc. that are unusually prevalent in the U.S. if I'm not mistaken. That would suggest to me that the problem started before the delivery itself.
I think the same can be said about our healthcare system in general. We have relatively poor health outcomes in this country relative to other affluent countries, especially considering our outrageously high healthcare spending. But I don't really blame that on the healthcare system so much as on the unhealthy people (outside of the problems of the insufficient/low-quality healthcare some segments of the population receive).
Pieter,
I meant to say "MK-4 is the only one that has been shown to prevent/reduce arterial calcification in rats up to this point"
I'm curious, there isn't much a mention that MK-7 9derived from Natto) seems to be better at preventing/reducing arterial calcificaiton than MK-4. Or at least that is what I understand the Rotterdam study indicated. Is this true?
dw8928,
The Rotterdam study didn't indicate which of the menaquinones was responsible for the association, although supplement manufacturers tried to twist the interpretation into supporting their product after the fact. All the Rotterdam study showed was that a higher K2 intake (all forms) was associated with a lower CHD risk and arterial calcification.
Brock and others,
The reason MK-7 has a longer half-life is because it has a longer side-chain, is thus more fat-soluble, and thus is located more in the core of the lipoproteins that carry it in the blood then the surface, thus having less interaction with enzymes that would bring it into the cells. I don't think the liver holds on to it; if it did, it wouldn't appear in LDL very much.
Interesting stuff on SXR, Stephan!
Chris
Stephan,
MK-4 is cheaper than MK-7! All of the MK-7 being sold comes in much lower doses. I think Thorne is the most cost-effective source of MK-4, especially with my suspicion that it has much higher bioavailability than solid capsules loaded with binders and fillers.
Chirs
Stefan,
You linked to a study showing MK-7 has superior osteocalcin activation compared to K1, but you wrote in your text that it was a comparison to MK-4. I have never seen a direct comparison of K1 and MK-4 on osteocalcin activation. I haven't been keeping up with the literature regularly since I wrote my activator X article, but up to that point there was no in vivo comparison between MK-4 and MK-7. As far as I know, there still isn't -- is there?
Micawber, what is the evidence that we need less MK-7 than MK-4?
Jason, probably not, since MK-7 never turns up in any mammals eating purified diets to which K1 is added, but tons of MK-4 turns up in many tissues on such diets. The reason MK-4 has a shorter half-life is apparently because it is less lipid-soluble due to its shorter tail and resides more towards the surface of the lipoprotein and is therefore more easily absorbed into cells. The reason you give, even if it happened, could not reduce plasma half-life because the conversion would take place in cells rather than in plasma.
Chris
Homertiobas,
Usually things that kill cancer cells are toxic!
Chris
Chris,
You are absolutely right! I misread that paper. Thanks for the correction, I'll edit the post.
I haven't seen any studies that compare MK-4 and MK-7 in vivo.
You have a good point that MK-4 is cheaper per dose. So if I understand correctly, you are also of the opinion that MK-7 is a questionable substitute for MK-4 given our current state of knowledge?
Stefan,
If there were an MK-4/MK-7 combo supplement, I'd probably take it, but I think it makes more sense to go for MK-4 given the choice between the two for the reasons you stated. The plasma half-life reason is utterly absurd, considering the reduction in plasma half-life is due to the MK-4 being delivered to the tissues where it carries out its functions! It's also much easier to get MK-7 from the diet in amounts comparable to the supplements, since fermented foods can be quite high in it and the supplements are quite low in it.
Chris
@ Chris Masterjohn.
Life Extension Foundation sells a K2 product with both MK-4 (1 MG) & MK-7 (100 mcg).
http://tinyurl.com/ddzsac
Stephan or anyone else,
Do you have an opinion on the use of formulated vitamin K in the (Life Extention Foundation-related) supplement developed by Dr Russell Blaylock for treatment of excitotoxic brain damage? It contains 1545 mcg of vitamin K in the following amounts:
Vitamin K1 500 mcg
Vitamin K2 1000 mcg (as MK-4)
Vitamin K2 45 mcg (as MK-7, as MenaQ7™)
http://www.whale.to/a/blaylock5.html
http://newportnutritionals.com/about.html
Does anyone have an opinion in general as to the relation of vitamin K in any form to the problem of excitotoxic neurodegenerative disease?
My own experience with that condition is that it can co-exist with a tendency to "normal" over-expression of bone formation (bone spurs, bony joints, tauri), and that it seemed to develop at the same time as a tendency to reactive hyperkeratosis, suggesting calcium metabolism is off (?). I experienced no positive change in my condition while taking the supplement Neprinol, containing nattokinase.
Pamela,
I don't know anything about using K2 to treat excitotoxic brain damage.
I think we are better off if we stay away from plant foods. Phylloquinone as it stands from the name is designed for plants. Phytosterols are for plants and they do interfere with mammalian cholesterol metabolism. I bet Vitamin k1 does the same in mammals. If you did not know about nutrition like our paleo people would you eat leaves in nature. No human would prefer plant foods over meat and fat if there was no brainwashing propaganda.
I'm tempted to take an MK-4 one day and an MK-7 the next to possibly get the best of both worlds.
Are there any suggestions of contraindications or other reasons that this might not work as well as it could do?
I have another good question that just about stays on subject:
Is there any advantage at all in taking in some K1 if getting a big dose of K2?
This question applies to K1 supplements or K1 rich foods (Yes, I know, assume you're getting all or more of the other nutrients of Kale elsewhere.)
My understanding is that K1 is a simple but ineffective precursor to K2 so K2 supplements outweigh any practical use of K1. I could be completely wrong though. Does K1 have any unique benefits when taken alongside K2?
Thanks.
This study concludes: "A high intake of menoquinones, especially MK-7, MK-8 and MK-9 could protect against CHD.".
-------------------------------------
A high menaquinone intake reduces the incidence of coronary heart disease.
Gast GC, de Roos NM, Sluijs I, Bots ML, Beulens JW, Geleijnse JM, Witteman JC, Grobbee DE, Peeters PH, van der Schouw YT.
Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, 3508 GA Utrecht, The Netherlands. g.c.m.gast@umcutrecht.nl
Abstract
BACKGROUND AND AIM: Vitamin K dependent proteins have been demonstrated to inhibit vascular calcification. Data on the effect of vitamin K intake on coronary heart disease (CHD) risk, however, are scarce. To examine the relationship between dietary vitamins K(1) and K(2) intake, and its subtypes, and the incidence of CHD. METHODS AND RESULTS: We used data from the Prospect-EPIC cohort consisting of 16,057 women, enrolled between 1993 and 1997 and aged 49-70 years, who were free of cardiovascular diseases at baseline. Intake of vitamin K and other nutrients was estimated with a food frequency questionnaire. Multivariate Cox proportional hazards models were used to analyse the data. After a mean+/-SD follow-up of 8.1+/-1.6 years, we identified 480 incident cases of CHD. Mean vitamin K(1) intake was 211.7+/-100.3 microg/d and vitamin K(2) intake was 29.1+/-12.8 microg/d. After adjustment for traditional risk factors and dietary factors, we observed an inverse association between vitamin K(2) and risk of CHD with a Hazard Ratio (HR) of 0.91 [95% CI 0.85-1.00] per 10 microg/d vitamin K(2) intake. This association was mainly due to vitamin K(2) subtypes MK-7, MK-8 and MK-9. Vitamin K(1) intake was not significantly related to CHD. CONCLUSIONS: A high intake of menoquinones, especially MK-7, MK-8 and MK-9, could protect against CHD. However, more research is necessary to define optimal intake levels of vitamin K intake for the prevention of CHD.
PMID: 19179058 [PubMed - indexed for MEDLINE]
Couls someone pease tell me where to purchase MK-4 supplements online? Thanks
Relentless Improvement sells MK-4, in 15 mg dosage.
Does anyone know which form of vitamin K is best to take in supplement form for bone metabolism between K1 and preformed K2? Which is best for directing calcium to the bones and teeth and keeping it from the soft tissues and from creating kidney stones?
Is MK-4 converted by the body from K1?
I have a supplement for bone health that has K1. What would be the reasoning behind creating a bone health supplement with K1 instead of K2 or MK-4?
My GUESS is that with another component in my supplement - gut specific lactoferrin which acts as a pre-pro biotic - helps with the absorption of the K vitamin in the right form but I need help understanding how all this works.
Any feedback would be much appreciated!
Hey guys, any drug interaction between K2's and Metformin/Glyburide/anti-diabetic Rx? Help! for my uncle thanks
gamma linoleic acid GLA?
Stephen,
I checked with NOW Foods (NOW Science & Nutrition Group)yesterday. Their K2 product Vitamin K-2 100 mcg - 100 Vcaps, in MK-4.
Assuming MK-4, has anyone seen a value for probable average daily consumption in a healthy native population?
Great blog. I've been fighting osteoporosis, calcification and migraines for years (prob due to ever increasing calcium and D) Think I'll now hedge my bets and take BOTH mk4 and mk7
BTW - latest study on mk7 by E. Theuwissen, M. Knapen, E. Smit, C. Vermeer (Maastricht, NL)
Results: It was found that low-dose supplemental MK-7 intake significantly reduced
age-related decline of BMC and BMD at the lumbar spine and femoral neck, but not of
the total hip. Calculated bone strength indices were favorably affected by MK-7
supplementation. Moreover, both the BMD of the lumbar spine and the impact strength
remained unchanged during the entire treatment period in the MK-7 group, and
declined as expected for age-associated bone loss in the placebo group.
Conclusion: We conclude that postmenopausal women can benefit from taking MK-7
supplements to prevent bone loss and optimize bone quality.
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