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"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.? 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. 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. "

Research has uncovered the fact that vitamin K also plays a crucial role in maintaining bone health. It was found that the amount of vitamin K required to halt bone absorption leading to osteoporosis requires much greater intakes than that required for blood clot regulation. Further, it appears that bone and vascular tissue (like coronary arteries) maintain a preference for a different form of vitamin K than that required for blood clotting regulation. Rather than vitamin K1 needed for clotting, vitamin K2 is the form preferred by bones and arteries (Schurgers LJ et al 2001). It appears that much of the information generated over the years for vitamin K focused on the K1 form, ignoring the K2 form necessary for bone and vascular health. Normal deposition of calcium occurs only in bone and in teeth. Abnormal deposition of calcium in the body occurs in three places: the inner lining of the arteries of the body (the intima) that causes atherosclerotic plaque; the muscle layer of arteries ("medial calcification"); and heart valves. K2 appears to be the form of vitamin K responsible for controlling these phenomena.

Increased intakes of vitamin K2, but not vitamin K1, may decrease the risk of coronary heart disease in postmenopausal women, says a new study.\nFor every 10 microgram increase in the amount of vitamin K2 consumed, researchers from the Netherlands report a 9 per cent reduction in the risk of developing coronary heart disease (CHD).

Vitamin K2 is produced by animal tissues, including the mammary glands, from vitamin K1, which occurs in rapidly growing green plants. A growing body of published research confirms Dr. Price's discoveries, namely that vitamin K2 is important for the utilization of minerals, protects against tooth decay, supports growth and development, is involved in normal reproduction, protects against calcification of the arteries leading to heart disease, and is a major component of the brain. Vitamin K2 works synergistically with the two other "fat-soluble activators" that Price studied, vitamins A and D. Vitamins A and D signal to the cells to produce certain proteins and vitamin K then activates these proteins. Vitamin K2 plays a crucial role in the development of the facial bones, and its presence in the diets of nonindustrialized peoples explains the wide facial structure and freedom from dental deformities that Weston Price observe

Vitamin K-containing dietary supplements: comparison of synthetic vitamin K1 and natto-derived menaquinone-7.\nSchurgers LJ, Teunissen KJ, Hamulyák K, Knapen MH, Vik H, Vermeer C.\nBlood. 2007 Apr 15;109(8):3279-83. Epub 2006 Dec 7.\nPMID: 17158229 \nDOI 10.1182/blood-2006-08-040709\n

[Vitamin K2] Ishida Y. Clin Calcium. 2008 Oct;18(10):1476-82. Review. Japanese. PMID: 18830045 "Vitamin K2 has been approved for the treatment of osteoporosis in Japan since 1995. Vitamin K2 treatment in osteoporosis has been shown to inhibit the occurrence of new bone fractures and to maintain BMD. The uniqueness of the prevention of bone fractures by vitamin K2 is that there has been no direct evidence of the relationship between increase of BMD and a decrease in the occurrence of bone fractures. A recent systematic review of seven Japanese randomized controlled trials by Cockayne has also shown that supplementation with phytonadione (Vitamin K1) and menaquinone (Vitamin K2) , particularly menaquinone-4, is associated with increased BMD and reduced fracture incidence. To confirm these results, a larger well design RCT using fractures as the primary endpoint is clearly needed."

A study recently published by the European Prospective Investigation into Cancer and Nutrition (EPIC) has revealed that increased intake of vitamin K2 may reduce the risk of prostate cancer by 35 percent. The authors point out that the benefits of K2 were most pronounced for advanced prostate cancer, and, importantly, that vitamin K1 did not offer any prostate benefits.

Mechanisms underlying the biphasic effect of vitamin K1 (phylloquinone) on arterial blood pressure.\nTirapelli CR, Resstel LB, de Oliveira AM, Corrêa FM.\nJ Pharm Pharmacol. 2008 Jul;60(7):889-93.\nPMID: 18549675 \nDOI: 10.1211/jpp.60.7.0010\n

Conversion of phylloquinone (Vitamin K1) into menaquinone-4 (Vitamin K2) in mice: two possible routes for menaquinone-4 accumulation in cerebra of mice.\nOkano T, Shimomura Y, Yamane M, Suhara Y, Kamao M, Sugiura M, Nakagawa K.\nJ Biol Chem. 2008 Apr 25;283(17):11270-9. Epub 2007 Dec 14. \nPMID: 18083713 \ndoi: 10.1074/jbc.M702971200 \n\nOur results suggest that cerebral menaquinone-4 originates from phylloquinone intake and that there are two routes of accumulation, one is the release of menadione from phylloquinone in the intestine followed by the prenylation of menadione into menaquinone-4 in tissues, and another is cleavage and prenylation within the cerebrum.

I'm always on the lookout for foods rich in vitamin K2 MK-4, because it's so important and so rare in the modern food system. I heard some internet rumors that marrow might be rich in fat-soluble vitamins. Google let me down, so I decided to look through the rat studies on K2 MK-4 in which they looked at its tissue distribution. I found one that looked at the K2 MK-4 content in different tissues of rats fed vitamin K1. Marrow was rich in K2, along with testes. It contains 10-20 times more MK-4 than liver by weight, and more than any of the other organs they tested (serum, liver, spleen, kidney, heart, testes, marrow, brain) except testes. They didn't include values for salivary gland and pancreas, the two richest sources.

In 1945, Dr. Weston Price described "a new vitamin-like activator" that played an influential role in the utilization of minerals, protection from tooth decay, growth and development, reproduction, protection against heart disease and the function of the brain. Using a chemical test, he determined that this compound-which he called Activator X-occurred in the butterfat, organs and fat of animals consuming rapidly growing green grass, and also in certain sea foods such as fish eggs. Vitamin K2 is produced by animal tissues, including the mammary glands, from vitamin K1, which occurs in rapidly growing green plants. A growing body of published research confirms Dr. Price's discoveries, namely that vitamin K2 is important for the utilization of minerals, protects against tooth decay, supports growth and development, is involved in normal reproduction, protects against calcification of the arteries leading to heart disease, and is a major component of the brain

Vitamin K2 is emerging as an exciting player in the control and possible regression of coronary atherosclerotic plaque. Only about 10% of dietary vitamin K intake is in the K2 form, the other 90% being the more common K1.

Vitamin K supplementation in postmenopausal women with osteopenia (ECKO trial): a randomized controlled trial. Cheung AM, Tile L, Lee Y, Tomlinson G, Hawker G, Scher J, Hu H, Vieth R, Thompson L, Jamal S, Josse R. PLoS Med. 2008 Oct 14;5(10):e196. Erratum in: PLoS Med. 2008 Dec;5(12):e247. PMID: 18922041 CONCLUSIONS: Daily 5 mg of vitamin K1 supplementation for 2 to 4 y does not protect against age-related decline in BMD, but may protect against fractures and cancers in postmenopausal women with osteopenia. More studies are needed to further examine the effect of vitamin K on fractures and cancers. Trial registration: ClinicalTrials.gov (#NCT00150969) and Current Controlled Trials (#ISRCTN61708241)

If you've been following the Track Your Plaque conversation, you know that, contrary to prevailing opinion among many cardiologists, there is an emerging notion that coronary calcification is an active process, a true part of the disease. Vitamin D3 is an important aspect of this question. So is vitamin K2. Not to be confused with K1 that plays a role in blood coagulation, K2 has an important role in calcium metabolism. Thus, vitmain K2 deficiency is related to osteoporosis and to coronary calcification.

High dietary menaquinone intake is associated with reduced coronary calcification.\nBeulens JW, Bots ML, Atsma F, Bartelink ML, Prokop M, Geleijnse JM, Witteman JC, Grobbee DE, van der Schouw YT.\nAtherosclerosis. 2008 Jul 19. [Epub ahead of print]\nPMID: 18722618 \ndoi:10.1016/j.atherosclerosis.2008.07.010 \n

A high menaquinone reduces the incidence of coronary heart disease in women.\nGast GC, de Roos NM, Sluijs I, Bots ML, Beulens JW, Geleijnse JM, Witteman JC, Grobbee DE, Peeters PH, van der Schouw YT.\nNutr Metab Cardiovasc Dis. 2009 Jan 27. [Epub ahead of print]\nPMID: 19179058 \ndoi: 10.1016/j.numecd.2008.10.004\n