Vitamin K2
Vitamin K2 (menaquinone) is the vitamin that determines where calcium goes. It is the cofactor for the γ-carboxylation of osteocalcin, which binds calcium into the bone matrix, and of matrix Gla protein, which actively inhibits calcification of arteries and soft tissue.
That dual role is the entire argument for the nutrient: without adequate K2, calcium is deposited less reliably in bone and more readily in vessel walls — the direction nobody wants.
K1 and K2 are not interchangeable
- K1 (phylloquinone) — from green leaves; taken up preferentially by the liver for the clotting cascade. Most dietary vitamin K is K1.
- K2 (menaquinone) — from fermented foods and animal products; reaches bone and vessel tissue.
Within K2 the subtype governs the half-life, and the difference is large:
- MK-4 — half-life of hours. Occurs in animal tissue; the form the body makes by converting K1. Studied at pharmacological doses (45 mg/day) in Japanese osteoporosis trials.
- MK-7 — half-life of about three days. From Bacillus subtilis fermentation; nattō is the dietary source. Maintains a steady blood level from a single daily dose, which is why it is the form in most bone formulations, typically 90–180 μg.
MK-7's long half-life is the whole reason it displaced MK-4 in supplements: MK-4 at supplement doses is cleared before it does much.
Evidence
- Rotterdam Study — higher dietary K2 (not K1) associated with less coronary calcification and lower cardiovascular mortality. Observational.
- Knapen (2013), 3 years, MK-7 180 μg/day in postmenopausal women — reduced bone-mineral-density loss and reduced vertebral height loss.
- Japanese MK-4 osteoporosis trials at 45 mg/day are positive but at doses three orders of magnitude above supplement levels and have not consistently replicated outside Japan.
Reasonable summary: the mechanism is solid, the bone evidence is decent, the cardiovascular evidence is largely observational.
The one interaction that matters
Warfarin. Warfarin works by antagonising vitamin K. Adding K2 opposes the drug directly and changes INR. This is not a caution to be careful — it is a reason not to start it without the prescriber's involvement. It does not apply to the direct oral anticoagulants (apixaban, rivaroxaban, dabigatran), which do not act on vitamin K.
Other cautions
- Fat-soluble — take with fat; deficiency is likelier after bariatric surgery or with fat malabsorption.
- K2 is frequently combined with high-dose vitamin D, which raises calcium absorption. The pairing has a rationale — D brings calcium in, K2 directs it — but a high-dose D regimen has its own risks that K2 does not cancel.
- No established toxicity for K1 or K2 at supplemental doses; synthetic K3 (menadione) is a different matter and is not used in human supplements.
See also: Creatine · Chelated Minerals · Stack Substances