Vitamin K is an essential nutrient, best
known for its role in blood clotting. Plants make one form of vitamin K
(phylloquinone, or vitamin K1) for their use. But your body doesn't use
all of the K1 in your diet "as is." Instead, the body converts some of
this plant form of the vitamin into a different vitamin K molecule:
Menatetrenone, or MK-4, a form of vitamin K2. Tissues vary in their
vitamin K needs, and it's become clear that some tissues have a specific
need for Menatetrenone, which is not met by phylloquinone. For some
purposes (like blood clotting), phylloquinone works fine; but extensive
evidence shows that Menatetrenone has unique effects on bone health not
shared by phylloquinone.
•Fracture victims' levels of Menatetrenone are more depressed than are their levels of phylloquinone.
•Areas where more K2 is consumed in the diet have lower fracture rates.
inhibits the resorption (teardown) of bone caused by the local cellular
messenger prostaglandin E2 (PGE2). The same concentration of
phylloquinone has no effect.
- Menatetrenone also cuts down on the bone
cells' formation of PGE2 in the first place.
- Menatetrenone is able
to reduce the creation of osteoclasts (cells involved in the teardown of
bone tissue) out of early cell types - but again, phylloquinone has no
- Menatetrenone, but not phylloquinone, actually increases the programmed cell death ("apoptosis") of existing osteoclasts.
strengthens the bone-building legions of the osteoblasts (cells
involved in the manufacture of new bone), mildly increasing both their
numbers and their activity.
Over the course of the last decade, at least sixteen clinical trials
have been performed using Menatetrenone, and every single one has found
that K2 supplements protect bone health. Menatetrenone not only slows,
halts, or even reverses loss of bone mass: it dramatically reduces your
risk of suffering a fracture.
•In one trial, women who took an ultra-high dose Menatetrenone
supplement for 24 weeks increased their bone mineral density by an
impressive 2.2%, even as the women taking a placebo (dummy pill) lost
7.31% of their bone density.
•In another trial, Menatetrenone was put
to the test in a direct comparison against the bisphosphonate drug
etidronate (Didrocal®). Menatetrenone preserved bone mass, and also
slashed fracture risk by roughly two thirds over the course of two
•In a third trial, osteoporotic women taking Menatetrenone
supplements sustained nearly no bone loss over two years, while cutting
fracture risk by 64% as compared with non-supplementing women.
The ability of bones to withstand fractures is not just determined by
the quantity of bone (as measured by Bone Mineral Density (BMD)), but
also by the quality of bone - bone "microarchitecture," including
especially "trabecular connectivity." Evidence suggests that
Menatetrenone's most important effects are on bone quality, not bone
•Clinical trials have found that Menatetrenone provides as much
protection against fracture as drugs that have much more powerful
effects on BMD. Clearly, Menatetrenone's bone-protective effects extend
to aspects of bone health beyond the BMD numbers.
provides powerful protection against the loss of trabecular connectivity
in laboratory animal models of menopausal osteoporosis.
•Menatetrenone supplements increase bone quality in young, healthy animals.
To get the amount of Menatetrenone used to produce these effects in
clinical trials and experimental studies requires a specific
•Existing science shows that phylloquinone does not provide the same
benefits as Menatetrenone. No clinical trials using phylloquinone
supplements have been performed to show reduced fracture risk.
body's ability to convert phylloquinone into Menatetrenone is limited,
flattening out at levels far below what's used in clinical trials. This
ability is further reduced with aging.
•Very little vitamin K2 exists in the diet, even in the richest food sources.
•While the body's friendly bacteria produce some K2, little or none of this K2 is absorbed.
Menatetrenone's health benefits extend well beyond the skeletal
system. Emerging science is now documenting the role of vitamin K - and
specifically of Menatetrenone - in protecting our cardiovascular health,
and the health of that all-important organ, the brain.
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A, Morii H, Fujita T, Ohata M. "Effects of menatetrenone on the bone and
calcium metabolism in osteoporosis: a double-blind placebo-controlled
trial." J Bone Miner Metab 1998; 16(2): 106-12.
ii. Iwamoto J, Takeda T,
Ichimura S. "Effect of menatetrenone on bone mineral density and
incidence of vertebral fractures in postmenopausal women with
osteoporosis: a comparison with the effect of etidronate." J Orthop Sci.
2001; 6(6): 487-92.
iii. Shiraki M, Shiraki Y,
Aoki C, Miura M. "Vitamin K2 (menatetrenone) effectively prevents
fractures and sustains lumbar bone mineral density in osteoporosis." J
Bone Miner Res. 2000 Mar; 15(3): 515-21.
iv. Geleijnse JM, Vermeer C,
Jurgers LJ, Grobbee DE, Pols HA, Witteman JC. "Inverse association of
dietary vitamin K-2 intake with cardiac eventsand aortic
atherosclerosis: the Rotterdam Study." Thromb Haem. 2001 Jul; 85(Suppl):
v. Allison AC. "The possible
role of vitamin K deficiency in the pathogenesis of Alzheimer's disease
and in augmenting brain damage associated with cardiovascular disease."
Med Hypotheses. 2001 Aug; 57(2): 151-5.
vi. Vermeer C. "Prevention of
arterial calcification by vitamin K2." In Miki T (ed). "Vitamin K: A
Conference Record. Renewing Bone Metabolism." 2000; Tokyo: Intermedd