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Vol.3 Issue 4:
Bone Health

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Peak K2 - Related Research

Label Info | Related Research | Magazine Article(s) | Related Abstract(s)


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.
Menatetrenone 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 such power.
Menatetrenone, but not phylloquinone, actually increases the programmed cell death (“apoptosis”) of existing osteoclasts.
Menatetrenone 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 years.
•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 quantity.

•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.
Menatetrenone 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 Menatetrenone supplement.

•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.
•The 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.


i. Orimo H, Shiraki M, Tomita 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): AbsP473.

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 Inc, 2-21.

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